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Prof Trevor Marshall
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A new study has just been published, where a micro-array was used to see which human genes were affected by infection with Borrelia burgdorferi. This adds to the data we have on HIV and M.tuberculosis down-regulating VDR expression.

http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1000444

(here is the relevant data table with VDR in it)

Live Borrelia burgdorferi reduced VDR expression in monocytes by 50 times, and lysates ('dead' Borrelia) reduced it by 8 times (these ratios are not directly comparable with the HIV and TB studies Amy and I cite in our presentations).

So now we can understand the contribution which Borrelia burgdorferi adds to the metagenome...



ps: I would note that M.tb and Borrelia reduce the number of VDRs, rather than block the binding pocket with a ligand, such as capnine. It is believed that VDR is expressed by Estrogen-receptor-beta, but this is still tentative... The bugs know their target better than we do :X
 

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Dr Trevor Marshall wrote: ps: I would note that M.tb and Borrelia reduce the number of VDRs, rather than block the binding pocket with a ligand, such as capnine. It is believed that VDR is expressed by Estrogen-receptor-beta, but this is still tentative... The bugs know their target better than we do :X
 


Trevor,

I was wondering about this. This week, you already mentioned that M.Tb's effect wasn't through blocking the VDR itself.

Yet, Wang's table 1 does mention that the VDR transcribes itself, which would make it extremely vulnerable: knock the VDR out and it is gone. It would make sense that other receptors transcribe it, since we know how important it is. I guess that is called functional redundancy in the genome?

Forever learning, Frans  :)

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http://tinyurl.com/lko755

Not sure, but this article seems relevant.

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Does this now suggest that bacteria not only compromise our Vitamin D Receptors but also make some receptors permanently redundant?

What is the consequence of this if indeed we have a permanent net loss of our VDR quota and diminished antibacterial peptides?  

 

                                                             Rick

Frans
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rick wrote: -1: Does this now suggest that bacteria not only compromise our Vitamin D Receptors but also make some receptors permanently redundant?

-2: What is the consequence of this if indeed we have a permanent net loss of our VDR quota and diminished antibacterial peptides?   

                                                             Rick


Rick:

-1: not redundant, but ineffective:  remember that rising levels of 25D and 1,25D start knocking out other receptors as well as the VDR and as we can tentatively conclude, the bacterial load shuts down other receptors as well as the VDR (in the case of Bb perhaps the Estrogen beta receptor, as shown above)

-2: you get a chronic disease ... However: the MP is designed to turn this around:  the actual DNA for the VDR, the other receptors and the antimicrobial peptides does not disappear, it is not being transcribed, so once things normalize again, transcription starts again, leading you to health

Hope this helps,

Frans

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Dr Trevor Marshall wrote:
I would note that M.tb and Borrelia reduce the number of VDRs, rather than block the binding pocket with a ligand, such as capnine.


This study says that M.tb downregulates expression:
http://www.cmj.org/Periodical/paperlist.asp?id=LW9156&linkintype=pubmed

Is there another study you're thinking of or did I misread this? I wouldn't ask were it not for the KB.

Paul

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@Paul: Are you looking for the reference Dr. Marshall provided in the first post of the thread maybe?

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Maybe the problem is that the implications of the paper Trevor references is too subtle for me to get.

The impetus for the question came from the fact that there is other research that shows Bb downregulates expression of the VDR. In the PLoS Pathogens paper Trevor refers to there is (at least according to Trevor) a different mode of action.

I was just wondering if:
1. Bb really cleaves the VDR in particular. There is no indication in the paper I can see beyond generic talk of cleaving and references to caspase-1, which belongs to a family known for cleaving receptors.
2. If yes, I was wondering if this action compliments/contradicts the research referred to here in which Bb downregulates VDR expression (downregulating and cleaving are different!):
http://mpkb.mp-dev.com/doku.php/home:pathogenesis:vitamind:metabolism#bacteria_disable_the_vdr

I'm trying to make a habit of not including anything in the KB that I don't get. Therefore, I would rather not include this paper until I see how it fits into its proper context.

Paul

Prof Trevor Marshall
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Paul,
If you look at the differential expression of the VDR on the second to last entry in Table S2 of the paper I cite you can see that expression of the VDR is downregulated by 50 times (0.02) and 8 times (.12) by the Borrelia infection :):)
 
Expression by the VDR may also be affected (eg by capnine etc) but that isn't clear by looking at the data they collected.
 

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Treor,

I just found this paper, the latest on VDR. VDR also seems to be downregulated by EBV.

Expression profile of nuclear receptors upon Epstein - Barr virus induced B cell transformation.  PMID:  19550398

I cannot access the full-text to see how manyfold it is downregulated, or by what mechanism, perhaps someone can look at it?

Frans

Last edited on Sat Jun 27th, 2009 03:52 by Frans

paulalbert
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Great find, Frans!

Here's the full text:
http://www.exp-oncology.com.ua/download/755.pdf

Paul

Last edited on Sat Jun 27th, 2009 06:33 by paulalbert

Frans
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Thanks Paul,

Patrick was even faster in sending a link to the full-text  :D

I am trying to figure out how manyfold the VDR was downregulated, but concentration is lacking.

There are, however, some things that occurred to me.

1: it seems as if bacteria and viruses that have been implicated in a lot of autoimmune (chronic TH1) diseases, like EBV and borrelia ALL act through downregulating the VDR;  of course, this makes sense, considering the role the VDR plays in innate immunity ...  This might in fact be WHY they are always implicated ... and now we understand why

2: this might also give an indication of why infection by these critters pushes people over the brink, right into th1 disease

3: this particular paper might also give an insight as to why EBV infection (I am thinking of Pfeiffer's disease as we call it (you guys call it the Kissing disease?) is so hard to conquer;  innate immunity is severely compromised, so healing takes a long time

Something else just occurred to me:  I have seen in pubmed that MicroRNA's play a role in VDR transcription. Wiki tells me EBV encodes several microRNA's, for what it is worth ..  Perhaps those microRNA's are involved in the machanism by which EBV downregulates the VDR. Of course, this a reaching a little ...  ;)

Frans

Edit:  EBV does NOT cause cold sores. EBV is a Human herpes virus (number 4), but not all Herpes viruses are EBV's ... If I am not mistaken, cold sores are caused by Herpes simplex. Not EBV.  concentration on MP remains an issue...

Last edited on Sat Jun 27th, 2009 12:54 by Frans

Prof Trevor Marshall
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Frans,
The 3D-graph is plotted as Log(concentration ratio) and I estimate about 5 times for VDR.You might like to cross-check my numbers.
 
As for micro-RNAs, note that the Estrogen-beta receptor is not down-regulated. Since VDR is believed to be expressed primarily by Er-beta, that implies (for me) that the mechanism of downregulation is a ligand targeting Er-beta. Micro-RNAs are an unlikely ligand, although I admit I haven't tried to dock them...
 

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Trevor,

Somehow transcription of VDR and transcription by VDR keeps confusing/eluding me. PMID: 19437538  shows miRNA influencing transcription by VDR, not of VDR. My mistake.

But if I am not mistaken, ER beta is also downregulated by EBV ? It is mentioned in table 1 under receptors being downregulated.

In graph 2a VDR and ER beta show a similar slope, going up a little, until about 48 hours, but ending lower. ER-beta is the green one :)

5 times downregulation is a serious impact btw.

As for checking your numbers: I don't think I have the capability or knowledge at this time, to say the least :?   Ah well, MP is not endless  :D  Life after it might very well be, hehe :cool:

Frans

Russ
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Reading this thread makes it clear to me that VDR blockage (from bacterial ligands and from ingested Vitamin D) is not the only way in which the immune system of a patient with TH1 disease is compromised.  The pathogens mentioned in this thread downregulate the expression of the VDR itself (by targeting receptors responsible for VDR expression) and there are probably other pathogens that have evolved even more creative ways for disrupting the immune system.

The main part of the MP, activating the VDR with Benicar and avoidance of ingested Vitamin D, will counteract blockage of the VDR with bacterial ligands, but my understanding is that it would not have a direct affect in combating downregulation of the VDR or other mechanisms the bacteria might employ.  This brings a number of questions into my mind...

Is the expectation that though there are other ways in which the immune system is weakened, that VDR blockage is the main one, and that once this blockage is removed, even if the number of VDRs is reduced thru downregulated expression, that this will restore immune function enough that it can start to go to work on all pathogens, regardless of the mechanisms they are employing?

Is it fair to say that the degree to which all the various immune system weakening mechanisms are employed by a particular patient's bacterial soup (how much is bacteria that block the VDR with ligands, how much is bacteria that downregulate expression of the VDR, etc.) would be a key factor in how they respond to the MP?

Might a patient with a bacterial soup that has a high degree of down-regulation of the VDR require more help from antibiotics than a patient who has a bacterial soup that is mainly just blocking the VDR with ligands?

Thanks!

- Russ

p.s. I only partially take for granted the fact that we have a scientist "working for us", who is completely on top of all the new studies that come out and can explain them to us.  :)

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Russ wrote:
Might a patient with a bacterial soup that has a high degree of down-regulation of the VDR require more help from antibiotics than a patient who has a bacterial soup that is mainly just blocking the VDR with ligands?


Unless I misunderstand your question, Russ, I think they're the same thing. Excepting the effects of viruses such as EBV, how else does a VDR get downregulated??? Certainly not by itself.

Paul

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Hi Paul.  I probably didn't word that well.  These are the two mechanisms I was trying to differentiate between:

1. Bacteria that produce a ligand (e.g. capnine) that blocks the VDR.  Benicar is effective at displacing this ligand from the VDR and re-activating it.

2. Bacteria that produce a ligand that blocks, for example, the Estrogen-beta receptor which Dr. Marshall has said is likely responsible for VDR expression.  The result here would not be a blocked VDR but a VDR that is not expressed.  I don't think Benicar would be directly effective in combating this down-regulation...I would think you'd need an agonist of the Estrogen-beta receptor to displace the ligand that is blocking that.

I may be missing something, but this is how I was understanding the difference between blocking a receptor and down-regulating it's expression.

- Russ

Prof Trevor Marshall
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Russ,
The two things will both be happening at once. Some species doing one thing, some species the other. Benicar will always be useful in trying to start the process of disease reversal.

The extreme case, of course, is the chronic phase of HIV/AIDS. Murdoch University has one of the world's leading research teams in HIV/AIDS, and I spent some time working through these issues in my mind while I was visiting Murdoch last week :):)
 
http://www.murdoch.edu.au/About-Murdoch_old/Murdoch-discoverers/Professor-Simon-Mallal/
 
http://www.genesiis.murdoch.edu.au/simon_mallal.html
 

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Hi Frans,
I think you are not off-base by suspecting that RNA interference and related RNA mechanisms are likely involved in the processes by which the human microbiota exert their profound influence on its host.  Micro-RNAs are single-stranded RNAs that primarily downregulate protein production by inhibition of protein translation from messenger RNAs (mRNAs).  Thus, production of microRNAs that target either or both of the the estrogen receptor or the VDR could reduce VDR production and activity.  Researchers are beginning to document the production of micro and siRNA (small interfering) double-stranded RNA molecules in pathogenic bacteria, their operation in host cells and their association with disease (cancer, in particular).

The mechanisms by which the small RNA classes can affect gene expression are amazing and still being discovered; they can disrupt both protein translation and transcription, and even affect protein function and longevity post-transcriptionally.  They are involved in alternate forms of host protein splicing - different 'splice variants' of the same protein can function very differently in the host.  I am not aware of small RNAs that act as ligands for host receptors, but anything is possible. 

The researchers at West China hospital have the molecular expertise and equipment to help sort things out at the intracellular level in the human host.  I am also hopeful that Amy will be pursuing these matters in her graduate work.  There are exciting things to come in the next few years,
Ruth


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I am having a follow-up appt with my Endo who is also a bone specialist (Ha!) on Mon Dec 7th..(I am 44 rys old and have osteopenia, so she is monitoring me.)

She is going to "freak" :shock: when she sees how low my 25-D levels are now this year..So I would like to take just 1-2 mins of her time to explain in point forms, why I am avoiding Vit D and why my 25-D levels need to stay low at this time...etc.

Can someone please help me with this...This is my understanding of it all, but I may have my facts mixed up.

1. The VDR controls the innate immune system.

2. People who have Th1 diseases have CWD bacteria (in their phagocytes) which block some enzyme?  This is turn causes a rise in the levels of 1-25D in the body.

3. Elevated levels of 1-25 D (above what level?), cause the innate immune system to shut down, so it can no longer fight the intracellular bacteria.

4. When the 1-25 D goes up the 25-D tends to go down.

5. We need to keep the 25-D below 12 ng/ml because taking in any Vit D will cause a conversion into 25-D which in turn will cause 1-25 to rise, which if goes too high (above what number?) will cause the innate immune system to shut down again.

6.We take Benicar b/c it unblocks the VDR from 1-25D? and it allows the innate immune system to wake up and see and attack the CWD once again.

How did I do..yes?  no?   :D

I will also be leaving her some research papers etc...for her to read...Ha..like that's going to happen? :P

Thanks!!

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Good luck with your doc. Be sure to print out the article on Amy Proal's website http://www.bacteriality.com re: Vitamin D. She explains it in simple terms.

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Everything you say is pretty much right except re: #5, we are also concerned that 25-D will bind and inactivate the VDR. Also, re: #6, when Benicar binds the VDR it turns it on transcribing enzymes which reduce high levels of 1,25-D, which reduces the chances that high 1,25-D interferes with other receptors - many of which also play key roles in immune function.

If you want to know what Marshall says about what is happening to cause your vitamin D metabolites to be out of whack, check out this article:
http://mpkb.org/doku.php/home:pathogenesis:vitamind:mechanisms

That said, I wouldn't go too deep into the molecular biology or the bacteria. You could say that it has been our experience that people simply do not get better when they have high levels of 25-D. You could also point out that MP patients take a medication that binds to and activates the Vitamin D Receptor, so you are in a completely different boat than most other people with an inflammatory disease. And then say, if you have any questions, have a look at this peer-reviewed paper.
http://autoimmunityresearch.org/transcripts/AR-Albert-VitD.pdf

Paul

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3,4, and 5 seem to leave out the suppression of the immune system by the VDR itself being blocked.  Here is a summary I put together for Bill-K in the TH1 questions forum:

"A) The VDR is responsible for a great deal including
  1) part of innate immunity
  2) a feedback system controlling the level of 1,25D

B) Several other nuclear receptors are responsible for many things including
  1 )part of innate immunity

C) 25D (and D2 & D3  also) blocks the VDR and shuts it down resulting in, among other things
  1) From A1, suppression of the immune system to a degree 
  2) From A2, disregulation of 1,25D allowing 1,25D to go too HIGH resulting in
      a)1,25D docking in other nuclear receptors where it does not belong shutting them down resulting in
             1) From B1, further suppression of the immune system

So you see, high 1,25D does suppress the immune system and is accounted for in the MP.  And unfortunately, as you can see, 25D has a double whammy effect on the immune system."

Cynthia

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Okay I am getting my notes together and constructing a document I can read to my Endo at my next appt.

Is it the 1-25 being too high that causes the innate immune system to shut down?

If so, at what level does it start to do this...or what level is considered acceptable and by whose standards?  I remember reading something in the past about the Merck Manual...Is this where we are getting our numbers from or is this the standard book in medicine?

I ask b/c when I first mentioned the MP to her in 2005 (on the recommendation of my G.P. at the time)...As he felt of all the info, I have ever brought to him on treatments for chronic Lyme /CFS.....he said this (MP) makes the most sense to me as it is scientifically based..

Anyways back in 2005, I had my first 1-25 D levels checked and they were 173 pmol/L (or 72.08 pg/ML) which is HI as the range here in Canada at that time was 30 - 120 pmol/L

At that time my Endo said my levels weren't really that high as labs were now changing the acceptable levels of 1-25 D to be up to 150 pmol/L.

As of Sept 2008 (8 months of being on Olmesartan & NO Minocin) my 1-25 levels dropped to 73 pmol/L , which is 30.41 pg/ML and my 25-D is now 14 nmol/L or 5.6 ng/ML

Is my 1-25D level too low now?

Thanks!!!:D


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Both a high 1,25-D and a high 25-D can contribute to suppression of innate immune function according to the MP perspective.

I discuss this in the NY Annals paper (Waterhouse et al, see http://mpkb.org ).

Your 1,25D is fine now and so is your 25D.  Yes, we use the Merck manual limit.  I think others raise the limit because they don't understand what a high 1,25D means.  You might also show your doctor the paper by Blaney et al (also in the KB).

Joyce Waterhouse


PS  The MP perspective is that it is not necessary to measure 1,25-D once one has started the protocol.  One might review the KB with regard to measuring D metabolites and related documents for more on this.

Last edited on Sun Nov 22nd, 2009 12:10 by jcwat101

Joyful
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Lisa, this article, " Test: 1,25-dihydroxvitamin D (1,25-D)", in the MP KB gives some information on the lab ranges also.

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Joyce,
Thanks so much for mentioning your article here. I had printed out the "six key papers" and have been working through reading them all but hadn't finished yours yet. Now I have and....wow--what a great explanation of the impact of VDR dysregulation all in one place. I've been flipping around between 4-5 different links to information and trying to piece it all together. Each link covered part of it, and some were more detailed than I could fully grasp.
You and your "et al partners" (Tom Perez and Paul Albert) did a great job explaining it all in a very readable format. For anyone who hasn't read it yet, here is a direct link to the full 11-page preprint:

Reversing Bacteria-Induced Vitamin D Receptor Dysfunction is Key to Autoimmune Disease
Pages 5-7 in particular cover the impact of high vitamin D levels on innate immunity and using serum levels for diagnostic purposes.

Thanks again for all your hard work.:)
Marysue

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When you see so many reports in the news about how Vit D is good for your immune system and that it can help reduce cancers etc...

Is there actual research proving this?  OR....Are the researchers just making a conclusion (without any proof) that low levels of 25- D contribute to/cause cancer....because they find that so many people who get cancer, have these low levels of 25-D and thus are making an assumption.

Just wanting to get my facts accurate...As I know the Endo is probably going to say to me, that everything I am telling her is wrong and incorrect about our high 1-25D & low 25-D's and that we need Vit D to prevent cancers etc....

Thanks!! :)

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Here's the ol' KB article on cancer and vitamin D:
http://mpkb.org/doku.php/home:pathogenesis:vitamind:cancer

This article may also be helpful:
http://mpkb.org/doku.php/home:pathogenesis:vitamind:mechanisms

Best,
Paul

thelymelight
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Tanks Paul..will take a look!!

Joyful
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Lisa,

Paul has written some other good articles in the MP knowledge base too...

See especially:
Mistaking correlation for causation in vitamin D studies
(http://mpkb.org/doku.php/home:pathogenesis:vitamind:correlation)
Also:
Assessing the published literature
Immunosuppression and insufficient followup in vitamin D studies
Koch's postulates
Latitude studies on vitamin D and disease
Palliative vs. curative treatments

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Joyful, thanks for those extra links.
In the "Assessing the published literature" section, #5 states, The concept of the “blood-brain barrier” has lost meaning in today's world of molecular genomics.2
And, there is a link to this pubmed article/abstract:
http://www.ncbi.nlm.nih.gov/pubmed/19228962
Could someone (maybe Paul:)) explain this article to me. I get that it has something to do with contradicting current thinking about the blood-brain barrier since you referenced it, but I don't understand what the article is saying enough to make the connection.

Marysue

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Marysue,

Well, according to Trevor and co., the blood-brain barrier is this idea that all types of stuff - chemicals, drugs, bacteria - are incapable of passing the barrier, but this study and various others suggest the opposite.

Here's the Wikipedia article repeating some of the folklore:
http://en.wikipedia.org/wiki/Blood-brain_barrier

Best,
Paul

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Thanks Paul.

The descriptions of the various diseases associated with the blood-brain barrier listed there (in Wikipedia) are interesting. Hmmmm....more examples of "bacterial involvement" regardless of whether the blood-brain barrier actually exists as stated or not.

Marysue

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My recollection is that the point is that the barrier is not totally absent but that it is just not as effective as previously thought.  Some things don't get through very well, but others do.  And how much of a barrier it is may also vary according to the individual and the circumstances and what substance or cell type is at issue.

Joyce Waterhouse

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Good point, Joyce. I didn't mean to imply that everything gets through.

Paul

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Thanks Joyful for the additional links to articles

thelymelight
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UPDATE with BONE SPECIALIST :

Okay folks, here’s how my appt went with the Bone Specialist.

She actually took the time to listen to me explain some of the info behind the MP and she did take a quick look at some of the research papers I brought her…(this is a step forward from when I saw her last year).

While she may still not quite understand all the workings of the VDR & innate immune system etc..She still disagrees with me keeping my 25-D (Vitamin D stores so low).

She acknowledges that 1-25 is what build bones/density…But she said I will develop SOFT BONES without enough D stores, which is what the body needs to assist in absorbing Calcium….This is different than having less dense bones, which is where the 1-25 D comes in.

She has had patients who have had normal 1-25 D levels, yet still had ‘fractures and when they went in and did a bone biopsy their bones were all MUSHY (Soft Bones) So she said just because you have a normal 1-25 D, doesn’t mean you are not a risk for developing Osteomalacia…soft bones….

She also said you can’t rely on the Merck Manual for 1-25 D levels, as each lab uses a different assay for their test, they are not all the same…

She also made some rude comment that b/c Dr. Marshall is not an M.D., he really doesn’t understand how all the physiology works (or something to that affect, can’t remember the word she used right now)..So then I said well the Dr. who is overseeing my care while on the MP, is very knowledgeable of the protocol and “IS” an M.D….She then said, Yes, but he isn’t a bone specialist…..I think no matter what I say, she would have an answer for everything.:X

While I respect Dr. Marshall’s discoveries & research very much,  I feel I also need to respect and be open to where she is coming from ie - her education, knowledge and first hand experience dealing with patients, as a Bone specialist/calcium disorders clinician… 

When I looked up info on the Knowledge Base site under “Concerns for Physicians” I see concern #4 is  re: “Avoiding consumption of Vit D leads to Osteoporosis” when I explored the link further,  there are only 3 studies quoted, that dispute Vitamin D supplementation can prevent Osteoporosis etc…But there is no mention of Vitamin D preventing SOFT BONES…which I would suspect is an entirely different thing…

My concern is: Does my Bone Specialist have a valid point about keeping my Vitamin D stores up, to assist with calcium absorption so as to prevent developing SOFT BONES?

If not, then why?


Is it possible we are overlooking something important here? :?

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Bone matrix is dependent on estrogen homeostasis, not on Vitamin D. The estrogen receptor is expressed by the VDR. If your bone specialist did not stress the importance of estrogen to bone matrix then she is way out of her depth.

We have already been there, done that, years ago.

Get another bone specialist :)

..Trevor..


http://www.nsbri.org/HumanPhysSpace/focus6/ep_development.html
 
http://endo.endojournals.org/cgi/content/abstract/138/7/2919

http://www.ncbi.nlm.nih.gov/pubmed/12682916
 

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I wonder if bone marrow is too?

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We now know that the brain controls the formation of bone (12/22/2009)
http://www.physorg.com/news180708867.html

Just plucked this off of Ray Kurzweil's RSS feed. 

"The brain acts as a profound regulatory centre, controlling myriad processes throughout the body in ways we are only just beginning to understand. In new findings, Australian scientists have shown surprising connections between the brain and regulation of bone mass."

This quote struck me as being interesting: 

"It is now clear that the neural network which controls appetite and energy also alters bone density. When we are starving, our brains don't allow us to waste energy by reproducing, making fat or creating new bone. When we are eating too much, on the other hand, our brains make it easier to reproduce, store fat and create bone."

It seems to me that the body downregulates a lot of bodily processes in response to stress, however defined.  Inflammatory cytokines like TNF alpha for example can lead to cachexia (weight loss/wasting), bone loss and other sick behaviours including depressive disorders, etc.

So to me the real question (in the context of this article) is what signalling pathways are involved in the modulation of NPY measured by the researchers?  It doesn't just happen on its own.  TNF aplha, IL-6, IL-1b, AT2?  The reseachers indicate that NPY is modulated in response to stress, presumably infections are part of that equation.

Last edited on Thu Dec 24th, 2009 07:14 by Phillyguy

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Thank-you for your reply and the links to the following papers...I will check them out when I have a moment.:)

I take it when you mention bone matrix, that this includes soft bones...

Yes, she has mentioned once before, that keeping estrogen levels up is important too, but never mentioned it in the context of 'soft bones'....She measures my estrogen yearly and it is just fine, so no peri-menopause for me..:P

I suspect she is on a bit of an EGO trip here (being affiliated with two hospitals and one University) and not use to patients questioning or challenging her...and perhaps she doesn't want to see (via my treatment results down the road) that her beliefs about Vitamin D stores are incorrect or outdated...:shock:

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Dr.Marshall perhaps you could speak to this:

I just remembered the other day..that during my childhood whenever I got ill, the Dr.'s never really knew quite what I had...It was like I never got a full blown case of anything.

For Example: They thought I had the measles but weren't 100% sure..same with the mumps I believe...and they thought I might have Scarletina, but didn't know for sure.
Then when I was 18 yrs old, I got this severe flu-like illness, w/alot of dizziness, weakness, fatigue, excessive sleep, nausea, weight loss, light sensitivity, (possibly the start of Lyme disease) and again they didn't know for sure what I had...I was told it was "probably" a virus and that I would slowly recover over time...(which I did) but was never really the same after this episode....

Is this not presenting with full blown sxs (thus Drs' not knowing what I had) a good indication of a poorly functioning immune system (VDR) right from a very young age/perhaps birth?   (Oh, and I was born 2 wks premature)

If so, would that be from inherited bacteria from the mother?

Does this only come from the mother or can it come from the father (via sperm) as well?

I say this b/c my mother is fairly healthy except for some osteoarthritis in her knees..Where as my father has had alot of health problems for many many years now...Heart disease (with a triple by-pass 9 years ago), now the start of Macular Degeneration (which I heard Dr B. say is a Th1 disease), 3 hernia operations, polyps in the colon, prostate cancer a few years ago, gall bladder removed... 

Both he and I are very much a like immune system wise...we are both very sensitive and react to alot of medications, herbs etc..

Your thoughts would be greatly appreciated!:)

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http://mpkb.org/doku.php/home:special:pregnancy
 
http://mpkb.org/doku.php/home:publications:marshall_chlamydia2_2009
(slide #27)

Mothers with low Vit D status (and Th1 disease) typically deliver pre-term :)
 

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CMV downregulates VDR 2.2 Fold

http://www.jimmunol.org/cgi/content/full/181/1/698

Take a look at the data supplement for the full transcriptome: 

http://www.jimmunol.org/cgi/content/full/181/1/698/DC1

-------------------------------------------------------------------

CMV dramatically increases the expression of inflammatory cytokines.  Per the transcriptome, IL-6 is increased 280 fold!  The TNF family is also significantly upregulated.

--------------------------------------------------------------------

This little nasty also significantly downregulates TLR1 and TLR6.

The primary known ligand for TLR1 are bacterial triacyl lipopeptides while the primary known ligand for TLR6 are diacyl lipopeptides from mycobacteria.

Most TLR's function as homodimers, however, TLR2 forms heterodimers with TLR1 or TLR6, each dimer having a different ligand specificity.  CMV directly hits TLR1 & 6 and indirectly hits TLR2 via VDR.

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Dr Trevor Marshall wrote: Live Borrelia burgdorferi reduced VDR expression in monocytes by 50 times, and lysates ('dead' Borrelia) reduced it by 8 times (these ratios are not directly comparable with the HIV and TB studies Amy and I cite in our presentations).

So now we can understand the contribution which Borrelia burgdorferi adds to the metagenome...
 

Trevor-
 
Finally dug up this discussion thread that you initiated back on 6/14/09 regarding Bb and VDR suppression, as you can imagine it had caught my attention.  The 50:1 VDR suppression rate, in the presence of live Bb, might account for the level of co-infection I was burdened with when I began the MP March '08.  With that in mind would you please, on a scale of 1-5, rank this statement's merit:

"If HIV (Human Immunedeficiency Virus) suppresses VDR 200:1 then is it not plausible that Borrelia.burgdorferi, at a 50:1 suppression rate, be viewed as a form of Human Immunedeficiency Bacteria, or HIB."
 
Look forward to your most serious thoughts on that comment/observation....


R/TB

Last edited on Tue Jun 7th, 2011 19:51 by TikBitten

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Borrelia does not persist as the complete organism, unlike HIV, they are not comparable.

There is no need to focus on Borrelia. Some of our most seriously ill members have never had a Borrelia infection. It is part of the mix, not a causal factor.

The size of the 50X factor was due to the assay method this study used. There is no reason to suspect there is any major difference in suppression effectiveness between Mycobacterium tuberculosis and Borrelia burgdorferi.

That said, I have long pointed out that HIV profoundly downregulates VDR, but new knowledge is suggesting that it also has a key action on MAF, also called DBP, which the other primary pathogens do not exhibit. So the situation re HIV's virulence is becoming clearer as the years go by.
 
A lot has changed in our scientific understanding  since I started this thread :) Sometimes it is tough to understand the pace of progress. Change it is, but it is also progress.
 

Last edited on Wed Jun 8th, 2011 01:28 by Prof Trevor Marshall

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Dr Marshall, if one organism affects VDR in a stronger degree and other organism affects it in lesser degree... Will standard olmesartan dosing work for all these organisms ?

Could there be a pathogen that affects VDR so strongly, that olmesartan won't be able to reverse this process ?

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Yes good point...What about Babesia? 

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Indeed, what about Babesia? What harm does it do? I am not interested in what ILADS says it does, I want to know what harm, and by what pathways...

Babesia survives in weakened immune systems.  The organism is impressive under a microscope, but it lives within red blood cells, and therefore does not significantly affect proteome interference. Easy to see, easy to diagnose, and exaggerated as a pathogen, IMO :) :)
 

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wrotek wrote: Dr Marshall, if one organism affects VDR in a stronger degree and other organism affects it in lesser degree... Will standard olmesartan dosing work for all these organisms ?

Could there be a pathogen that affects VDR so strongly, that olmesartan won't be able to reverse this process ?

Actually, Borrelia doesn't directly block the VDR like other organisms.  Instead it downregulates it's expression which is a different way of interfering with the immune system and one which Olmesartan does not directly counteract.

In order for the VDR to be "working", the receptor has to be expressed and there needs to be an agonist that binds to it and turns it on.  The way I think of it, a receptor is expressed when it is present in the cell and available for something to bind to it.  It is then turned on when something binds to it and that something is an agonist that turns it on (1,25D, Olmesartan) and not an antagonist that turns it off (25D, bacterial substances). 

Some organisms produce substances that bind to the VDR and block 1,25D from turning it on.  The VDR is still present in the cell, it is still "expressed", but it is not turned on.  Olmesartan, with it's high affinity for the VDR, is able to displace the bacterial substance and turn the VDR on. 

Other organisms - like borrelia, m. tuberculosis, and EBV - prevent the VDR from even being expressed in the first place.  So there is no receptor present for Olmesartan to bind to and therefore Olmesartan does not directly counteract this bacterial survival mechanism.  But I guess the idea is that though borrelia reduces the number of VDRs that are expressed, it does not prevent *all* VDRs from being expressed, so there are still some VDRs out there and by taking Olmesartan you are ensuring that the remaining VDRs re turned on. 

I imagine that in severely infected tissues, borrelia might reduce VDR expression so much that it is very difficult for Olmesartan to work it's magic.  This might be where antibiotics are more necessary, since they would likely interfere with whatever mechanism borrelia uses to prevent VDR expression.  Also, I suspect that carbohydrates/glucose are a key part of the ability of borrelia to do whatever it is that it does, and so eating low-carb would also help and this would explain why some people get much higher IP from lower carb intake.

So I would think that the MP treatment, and especially Olmesartan alone, would be most effective for people with a pathogen mix that leans more towards VDR blockage than one that leans more towards VDR downregulation, since Olmesartan directly counteracts the former but not the latter. 

That is my layman's understanding of it.

Last edited on Sun Jul 10th, 2011 11:56 by Russ

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Interesting. We would have to know how borrelia reduces vdr expression to reverse this .

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This might be where antibiotics are more necessary, since they would likely interfere with whatever mechanism borrelia uses to prevent VDR expression
We really don't know that bacteriostatic antibiotics directly act on the intracellular organisms. We do know that Mino and Clindy definitely affect the human immune system directly. So the answer is likely even more complex than 'antibiotics', Russ :X

Further, it is believed that VDR is expressed by estrogen-receptor-beta, and in turn the VDR expresses the estrogen receptor precursor protein, so we have a ying-yang feedback/feedforward there.

But you have hit upon the reason I don't talk much about Capnine any more - the complete answer is getting a lot more complex than I contemplated just a  few years ago...
 
 

Last edited on Sun Jul 10th, 2011 12:23 by Prof Trevor Marshall

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Wrotek & Trevor wrote: Dr Marshall, if one organism affects VDR in a stronger degree and other organism affects it in lesser degree... Will standard olmesartan dosing work for all these organisms? Could there be a pathogen that affects VDR so strongly, that olmesartan won't be able to reverse this process?
Further, it is believed that VDR is expressed by estrogen-receptor-beta, and in turn the VDR expresses the estrogen receptor precursor protein, so we have a ying-yang feedback/feedforward there. 
Wrotek & Trevor-

IMO, I believe there are two primary levels of concern, at a minimum, in addressing microbacterial persistence:  

 i. The first, of course, as stated above, pathogenic effect on VDR expression but, also;

ii. Each pathogen's inherent ability (genetic makeup) for biofilm persistence, cyst formation, sequestering and immune system evasion. 

Case in point, me....

After three plus years on the MP I am far more comfortable discussing the topic as it appears this is the exact diagnostic scenario that’s unfolding in my treatment of Late Stage Lyme Disease, the result of an underlying long standing Borreliosis (Bb) condition.  Just as a comparison, much like AIDS is the disease state of HIV, Lyme Disease is the disease state caused by Borreliosis. 

As way of some background, the major concern when embarking on the MP was that, although the MP had the potential of clearing much of the micro-bacterial and other pathogenic load, in the end, a Borrelia infection would be far too resilient to roll back entirely.  And, unfortunately, at this point in time, my test results indicate just that scenario.

When I started on the MP in March 2008 it was difficult to know, due to a plethora of positive fungal/viral/bacterial test readings, if Lyme Disease was in fact the primary diagnosis.  By April of 2010, however, the underlying “pea-soup” condition became far clearer and the only detectable IGenex western blot signature left, kdA bands 31 & 41, was that of Borrelia.  Again, the causative agent underlying Lyme Disease.  Please know that when only those two bands are present (31 & 41) the likelihood of a positive Borreliosis diagnosis (Specificity & Sensitivity) reaches a 97% confidence level -- and additionally confirmed as positive with further 31 kDa epitope Igenex testing.

To make matters worse, as another confirmation, I recently performed a new, more comprehensive test panel from NeuroSciences Labs, Inc. that scanned not only western blot bands but also looked for key markers of Bb biofilm formation.  So as of March 23rd 2011, my results remain weakly positive for kDa bands 31 & 41 but, more alarmingly, a key marker (DbpA) for Bb extracellular matrix binding (i.e. biofilm formation) was identified and off the scale.  Thus leading my physician to believe that, although the MP was likely successful at clearing out much of the pathogenic pea-soup, much work is still needed to fully address the in-vivo biofilm life cycle of Bb.   

While I have surely improved greatly from 2008, at this point in time, the underlying causative pathogen, Bb, is proving to be very, very resilient.  At present I am working with my physician to develop additional layers of therapy, come December, that will compatibly overlay the MP and breakdown or interfere with ongoing Bb biofilm formation.

So net, net, in contrast to Dr. Marshall’s beliefs, I am definitely not of the opinion all bacteria are created equal and, hence, evenly susceptible in-vivo to the MP – at least not yet!!JJ

My 2 Cents,
TB

Last edited on Sun Jul 10th, 2011 13:42 by TikBitten

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a new, more comprehensive test panel from NeuroSciences Labs, Inc. that scanned not only western blot bands but also looked for key markers of Bb biofilm formation
Is that an FDA-approved test, or are you placing your fate in the hands of pseudo-science, TB? :) :) :)
 

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Dr Trevor Marshall wrote:
"We do know that Mino and Clindy definitely affect the human immune system directly".
What exactly do we know about Clindy in that respect ? Quite a bit of info on Mino has been posted (Bane, Phillyguy), but Clindy ??? Nil specific in the MPKB either.
Thx, Leo.

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This is off topic(I dont want to start new thread), but perhaps it could be possible to clone a conference countdown timer to http://marshallprotocol.com and mpkb.org websites ?
I have just realized that i missed 3 conferences and tomorrow i have 3 hours to catch up :D

Last edited on Sun Jul 10th, 2011 21:44 by wrotek

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My response was a bit terse TB. Sorry about that. I get very upset over the way that the"Lyme" industry drains every penny from members by convincing them they have "Lyme" and then coming up with bogus test after bogus test until both the patients, and their families, have been bankrupted.

The new test you mentioned has (at least) the following flaws:
Firstly, it is based on antibodies which have not been demonstrated to be specific for Borrelia, with a real risk of false-positive against other components of the microbiota. If you watch Amy's presentation at the Intl Congress on Antibodies:

http://www.youtube.com/watch?v=SGe9UTQJdHM

you will hear her explain how useless the average 'antibody' is, as they are non-specific, and hit hundreds of targets. None of the experts in the audience challenged this. Another paradigm shift for clinical medicine to leap, I am afraid :X

Second, biofilms are not what are making you ill. If you have any Borrelia in your bloodstream it is because of the combined load of all the intra-phagocytic  pathogens weakening your immune system, thereby allowing "cysts" and whatever, to persist in the blood and tissues. The concept of "Borrelia cysts" in-live- Homo-sapiens is junk science anyway, for a host of other reasons which I have enumerated over the last decade.

While you have any immune system at all, it will deal with blood-borne flotsam and jetsam. If your immune system is too weak to do this you will die because of the accumulating apoptotic cells, quite apart from any pathogenic issues.

I hope that helps.

IMO it is always best to ask before spending money on what the Lyme-financial-ecosystem is pushing at you :)
 
 

Last edited on Sun Jul 10th, 2011 16:05 by Prof Trevor Marshall

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Leo,
Clindy has been reported as a CYP3A4 enhancer, and it was reported that this was achieved via the PXR.

http://www.ncbi.nlm.nih.gov/pubmed/18505790

Although I did confirm (in-silico) the PXR activity of mino, I was unable to confirm that clindy was a PXR agonist, and so there is a question in my mind about the pathway, but I will accept the researcher's observations that clindy enhanced the expression of CYP3A4, which, among other things, breaks down 1,25-D into inactive metabolites :)
 

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TikBitten, I think Dr. Marshall is right about antibody tests being non-specific and not a good marker of the level of infection.  I had a bunch of blood work done shortly after starting the MP and all sorts of antibody tests that had been negative prior to the MP were now positive because my immune system was working and killing pathogens.

As far as your main point about whether the MP alone will allow recovery in all cases, regardless of severity of disease and pathogen mix, I have wondered the same thing.  It's hard to think that it would, given the infinite number of pathogen combinations and ways in which the pathogens affect the body.  I guess only time will tell. 

And I also think that biofilms play a role.  Or at least some mechanism in which they are able to go into "hiding" when the environment is not right. 

Last edited on Mon Jul 11th, 2011 01:15 by Russ

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Russ,
The key thing to understand is that a pathogen living in a biofilm outside a cell (for example, a biofilm on a hip-joint) can evoke an immune reaction, while a pathogen living inside a nucleated cell can change the way the body works. In particular, an intra-phagocytic pathogen can change the way that the immune system works.

So a pathogen in tissue or the bloodstream has to survive by evading the immune system, while a pathogen inside a cell can modify the immune system itself to survive - eg by dysregulating the VDR.

It is the second function - changing the way the body works - which causes chronic illness.

I did write a paper in 2003 explaining the importance of pathogens getting inside a cell, but it is such an old paper now, with so many poorly developed ideas (heck, that was nearly a decade ago) that I don't cite it much :)
http://www.ncbi.nlm.nih.gov/pubmed/15246025

Proteomic interference, genomic interference, the actual chronic disease mechanisms, can only occur when a pathogen survives phagocytosis and persists within the nucleated cell.

I hope that helps,
Trevor
 

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That is a nice, concise description of chronic disease and the fundamental differences between the effects of microbiota persisting inside a nucleated cell and those gathered in colonies outside.

Many times I read or hear about biofilms in general being the big issue in chronic disease,never much about intraphagocytic microbiota.

That being said....can we assume biofilms that exist in outside these nucleated cells are probably persisting because of the changes that the intracellular bacteria have made to the immune system?

I wish there was a better way to limit the exaggerated immune responses to extracellular bacteria and proteins while the innate immune system clears.

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Hi Dr. Marshall......that was a great explanation!  Helped me a lot!  Graduated college without ever having to take a biology course so this is a hard learning experience for me,  but between you and Google I'm doing O.K.   Have decided to be an immunologist in my next life.  Never really knew in this life!!!!!!!!!!!!

Dian

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Reading this thread about Borrelia burgdoferi is interesting.  Since I watched Lida Mattman's presentation from the 2005 Chicago Conference about ALS being basically a late-stage Lyme disease I have wondered if I have borrelia causing my ALS.  While I had tests two years ago from the recognized leader in Lyme testing, and those tests came back negative for borrelia, I wonder if that pathogen is what ultimately tips the scales to ALS as Dr Mattman surmised. 

If, as described on this thread, borrelia downregulates the VDR and does not BLOCK it .. and that olmesartan may not be effective for pathogens that work by down-regulating the VDR ... then I wonder how effective my current regimen of just Benicar is going to be?  I have been on the MP now for almost two years and have not seen any neurological improvement yet.  Also Scott K was on the MP for over two years with ALS and did not get much improvement.  Given these facts, I wonder if a Benicar only approach is the correct path for ALS that possible could have borrelia as a main component of the microbiota that ultimately causes ALS! 

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Lida Mattman was using (her own) antibodies to determine if a species was Borrelia. The poor selectivity of antibodies probably explains why everything she saw identified itself to be Borrelia :) :)

As for the scare mongering about people being too-ill to recover on the MP there is NOTHING, nothing at all, which would indicate that is true. Stop worrying, stress will definitely make the disease worse...

It is important to recognize the way that the disease, and IP, can change the way you think..
 

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Thanks Dr Marshall.. it is always reassuring to hear your positive attitude!  I am TRYING very hard to stay positive and not get under too much stress ... trust me on that.  But I must admit it is difficult to remain stress free given how much motor function I am losing and how close to be totally bed ridden I am coming!   I want to believe all this is just IP and part of the healing process.  But it is hard not to wonder and worry about the terrible consequences if it is NOT IP but just the normal progression of ALS.  Hopefully the pure olmesartan study can get underway SOON as I think that may help me considerably. 

As always I do really appreciate your reassuring advice!! 

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It is almost certainly not the normal progression of ALS. Mean survival is 18 months after diagnosis :X Your cardiac and pulmonary status has not deteriorated at that rate...

I know it is tough losing so much neurological function, and it is also tough waiting for the body to regenerate. I thought your chess had been improving recently?
 

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Well now that you mentioned my chess ... that remains the lone bright spot in my life!  I just won my 15th game in a row last night!  And this is from a group of expert chess players that in the past I would have been lucky to break even with!  That is another thing I wonder about.. how is it that I have avoided the "brain fog" that so many others report as part of the IP. 

But it is known that ALS does not really affect the logical thinking processes much if at all.  It for whatever reason goes after primarily the motor CNS of the brain and spinal column.  And while it is true the mean time for ALS to mortality is startlingly short.. for some it can take years and years.   The neurologist that was my doctor's predecessor as head of the UCSF ALS center, Dr Olney, has had ALS now for 8 years and is just now reaching the fatal end stages.

You are correct that my pulmonary and cardiac function remain strong and healthy at this point.. exactly two years to the day from my ALS diagnosis!  So that is very encouraging indeed and something my neurologist stresses when I meet with her. 

I guess the only way of knowing the outcome of this long difficult journey is ... one foot in front of the other ... step by step ... til the end!  But be assured I AM willing to take this ALL THE WAY though to the end.  You will NOT see me giving up on the MP as others have done!  I intend to either prove it works for ALS.. or vice versa.  At least I have that to reassure me that my efforts will not be in vain and will help others in the future no matter my ultimate outcome.


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What exactly is the difference between the VDR being blocked and being downregulated?

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Hi Chris,

I guess you are in good smart company with Stephen Hawking! I know it is hard to wait around for progress but I am seeing some good results too after almost 2 years. My lungs feel so clear this summer in the middle of allergy season, so I am hanging onto that. It sounds like you have some excellent signs from what the experts have said.

Deb

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seanlane wrote: What exactly is the difference between the VDR being blocked and being downregulated?
Blocked: a ligand, like 25D,  binds to VDR itself and shuts it off (number of VDR's stays the same)

Downregulated: upstream of VDR, Estrogen Receptor transcribes VDR, if a microbe blocks the Estrogen receptor, VDR will not be transcribed, ergo: downregulated  (number of VDR's goes down)

Hope this helps,

Best Frans

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Frans wrote:

Downregulated: upstream of VDR, Estrogen Receptor transcribes VDR, if a microbe blocks the Estrogen receptor, VDR will not be transcribed, ergo:



And if the Estrogen Receptor is blocked, Osteoporosis may be the consequence, isn´t it ?

Thus the correlation between chronic infections, blocked VDR and Osteoporosis could be explained via ER ?

Alex

Last edited on Thu Jul 14th, 2011 12:03 by Alejandro

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Thanks for the encouragement Deb ... I appreciate it!

And Frans, thanks for the nice example of how upstream from the VDR the estrogen receptor can affect the expression of the VDR.  This makes me wonder about some studies I read recently that show some benefit for traumatic brain injuries by giving massive doses of progesterone.  Could it be that this helps the immune system clean up not only infected cells.. but also damaged cells? 

I guess I can only hope that IF borrelia does play a key role in ALS, and Dr Marshall has said it probably does NOT ... and if borrelia does downregulate the VDR somehow, that olmesartan will impact the proper receptors enough to eventually turn the tide against this terrible disease.

But it is interesting to speculate and wonder if this difference of blockade of a receptor versus downregulation of a receptor might account for the different rates of recovery for different chronic illnesses that we see on the MP.  Maybe there are pathogens that can still evade olmesartan's reactivation of the VDR ... by downregulating the VDR so that there are not many VDR expressed in those infected cells. 

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Maybe there are pathogens that can still evade olmesartan's reactivation of the VDR ... by downregulating the VDR so that there are not many VDR expressed in those infected cells
But Olmesartan hits many receptors, at least a half-dozen strong-hits that I know of :) It apparently has just the right profile to do the job :)

Progesterone reduces inflammation, because it is immunosuppressive. Hence, the patient would feel better, and there would be less swelling (in the short-term) :)
 
 

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Thanks Dr Marshall!  Good to have it reinforced that olmesartan hits those other receptors also. 

Could this difference of VDR blockade vs VDR down regulation be the reason why the recovery rate for some chronic illnesses, i.e. neurological, take longer than others on the MP?  It would seem like a plausible reason why the recovery takes a lot longer in some illnesses.

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Indeed, variation from patient to patient, from microbiota to microbiota, is what causes the variable length of recovery (IMO). But I have seen no evidence to date that recovery does not come incrementally for all those who manage to stick with the IP for long enough...
 

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Music to my ears Dr Marshall!!  :D:D:D

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Chris,
If it is any consolation to you, I did not have any neurological improvements until I was well into my 4th year of the MP. Many times I felt much worse than I had before starting the MP....I believe it is IP you are dealing with.

Even knowing this does not make it any easier to go through.

It certainly seems to me that with your chess game improving things are looking up.

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Thanks Aunt Diana for your encouragement! 

I guess I just have to be patient and wait for that turning point where I realize some neurological improvement.  But I do know if I continue on this trajectory for another two years ... it is going to get VERY difficult on me and my loved ones!  I was hoping that due to being relatively healthy back when I started in Aug 2009, that I'd have a faster recovery time.  Now that does not look like it is the case.

But as I said in an earlier post on this thread... I am in this til the end! ... whatever the ultimate outcome!   I intend to help prove that the MP either works or doesn't work for ALS!  You will NOT see me giving up on the MP to try some other crazy cure out there.  I have spent two years now studying and learning the science behind the MP.  The science is too strong to give up on.  And I feel strongly the MP gives me the BEST chance at defeating this terrible disease called ALS!! 

If I am fortunate enough to defeat this normally terminal disease with the MP ... you'll see me working as hard as I can to assist Dr Marshall's efforts to spread that victory as far and wide as possible!  That is a goal that helps me keep my sanity and focus when I am feeling down and tempted to doubt things. 

Chris

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Now Armin Alaedini at Weill Cornell Medical College in New York and his colleagues have found that patients diagnosed with post-Lyme disease syndrome have antibodies that suggest they carried the infection for an unusually long time. The finding, published in Clinical Immunology1, might help the syndrome to be better understood, diagnosed and treated.
Alaedini's team looked at antibodies made in response to a protein called VlsE, which is found on the surface of Borrelia burgdorferi, the tick-borne bacterium that causes Lyme disease.
The antibodies recognize a snippet of the protein called an epitope, and recruit the immune system to attack the bacterium. The researchers found that post-Lyme sufferers have a greater variety of antibodies to this epitope than patients whose infection cleared up quickly.
This finding suggests that patients with chronic symptoms have experienced a prolonged infection, caused by microbes that have evaded the immune system by varying the epitopes they carry. As a result of these variations, the body makes new antibodies targeting the modified protein. The longer the microbe manages to keep changing, the more diverse its host's antibodies become.

http://www.nature.com/news/2011/110805/full/news.2011.463.html#B1

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The group at Weill Cornell did not consider the possibility that their testing procedures might be confused by the thousands of other species present along with the Borrelia. I read this report, and although not junk science, it is of little practical use until their procedures become more precise, IMO. They really don't have much of a clue.
 
Rule #1 - whenever you see the word "antibodies" the research is most probably suspect.

..Trevor..
 

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Interesting Frenchie..thanks for posting this..:)

wrotek
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Dr Marshall, I saw in Your patent, that on page 3 there is information olmesartan docks into borrelia GPCR receptor.

Is this knowledge current ?
Do we know what this receptor does for borrelia ?

patent link
http://tinyurl.com/62oakzb

Last edited on Fri Sep 16th, 2011 01:41 by wrotek



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