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Upcoming paper (end 2007?)
 Moderated by: Prof Trevor Marshall
 

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Frans
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 Posted: Fri Oct 26th, 2007 07:40

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Trevor, I have some questions. I understand that a new paper is coming up hopefully sometime later this year.

I understand that it is going to be a review paper, but will there be any new stuff in it? I mean 25D's role in shutting down the VDR, Ki and Kd values of 25D and 1,25D for the others receptors. Things like that. Other than a summary of things in other papers I mean.

Furthermore I am wondering if I, living here in europe, might be able to order a copy of the magazine that publishes it ?

Sincerely, Frans



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Prof Trevor Marshall
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 Posted: Fri Oct 26th, 2007 10:56

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Frans,
The key new element (for MP folk) is the diagram detailing the genes/enzymes/proteins and receptors which regulate the Vit D metabolism. This is important to get out to you all. Unfortunately the editor of the journal which had initially invited the review, asked me to put in a section about how Vitamin D was desirable in low dosage, but not at high levels. I know that to be untrue, Homo sapiens needs no exogenous intake, and no UVB exposure (as you are all demonstrating), and I refused to commit scientific fraud to satiate the publisher. So I am having to look for another journal. The behavior of this editor was very unprofessional, especially as the paper had passed peer review.
 

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 Posted: Fri Oct 26th, 2007 12:09

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It 'almost' sounds unethical...  or at least it sounds disgusting



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Russ
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 Posted: Sat Oct 27th, 2007 14:54

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Dr Trevor Marshall wrote: Homo sapiens needs no exogenous intake, and no UVB exposure (as you are all demonstrating)

Is the same true for light exposure to the eyes - that the eyes/brain don't need any more light than the minimum necessary to see? 
 
I know at one point the thinking was that light to the eyes was capable of generating 1,25D (is that still the thinking?) and while not being enough to be immuno-suppressive systemically, might have some immuno-suppressive effect within the eyes.  So since my eyes seem to be very infected with TH1 bacteria, I've been going with the bare minimum needed to navigate/read/cook/etc. in my apartment, which turns out to be wearing 10% NOIRs in around 20 lux lighting. 
 
Is there any downside to being this strict with light avoidance?  I'm convinced I have more immunopathology in my CNS (e.g. neck pain) when I am strict like this.

Thanks.

- Russ

p.s. I am glad to hear that some people still have principles that they are willing to stand by.

Last edited on Sat Oct 27th, 2007 15:34 by Russ



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Rico
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 Posted: Sat Oct 27th, 2007 16:40

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Sorry to hear you had to face such an act, Trevor.
In light of that, I'm glad to see that your act was the right one.

Good luck finding a more professional editor and journal.



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Prof Trevor Marshall
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 Posted: Sat Oct 27th, 2007 16:43

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I am not sure whether the 1,25-D generated in the eyes is important at all.

There are a number of retinal protein genes which are transcribed by the VDR, which is the reason eyesight fails as these Th1 diseases advance, and with advancing age.

I know of no downside to strict light avoidance.

Fish and nocturnal animals have active VDRs, and active endogenous Vitamin D synthesis. For example, the Lamprey:
http://endo.endojournals.org/cgi/content/full/144/6/2704

Clearly many of these have little or no UVB exposure.

tickbite
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 Posted: Tue Oct 30th, 2007 09:56

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Dr Trevor Marshall wrote: I am not sure whether the 1,25-D generated in the eyes is important at all.

There are a number of retinal protein genes which are transcribed by the VDR, which is the reason eyesight fails as these Th1 diseases advance, and with advancing age.

I know of no downside to strict light avoidance.

Fish and nocturnal animals have active VDRs, and active endogenous Vitamin D synthesis. For example, the Lamprey:
http://endo.endojournals.org/cgi/content/full/144/6/2704

Clearly many of these have little or no UVB exposure.


There is one thing very important that you have taught us recently Dr. Marshall, and that is homo sapiens vitamins D metabolism and associated receptors are quite different than other animals including fish and nocturnal animals. We are not fish or nocturnal and haven't been. I'm not arguing your statement of "i know of no downside to strict light avoidance." Simply, pointing out the obvious. I think you are correct on the redundancy of gene transcription. None the less, the eyes still pose a Th1 conundrum for me. Please don't take this harshly. You know me, i'm just trying to get to the bottom of this :)
~Greg



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Prof Trevor Marshall
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 Posted: Tue Oct 30th, 2007 10:39

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What is the conundrum, Greg? I don't understand your concerns.

The primary function of the retina is to act as host for the Rhodopsins, which are GPCR receptors which sense light. A molecule of Retinal is bound into Rhodpsin, and it undergoes a conformational change when hit by a photon. The charge shift resulting from this phase change is conducted through the retina and aggregated so that at some threshold, most experts seem to think about 5 triggered receptors, a sensory signal is then sent along the optic nerve to the brain.

1,25-D binds into Rhodopsin, and will competitively displace Retinal (unpublished modeling work by yours truly). Thus excess 1,25-D can directly interfere with the process of vision.

Additionally, several key retinal proteins are transcribed by the VDR, giving another pathway for the Th1 bacteria to inhibit the proper operation of the eyes.

So it all makes sense to me... :)

Russ
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 Posted: Wed Oct 31st, 2007 06:54

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Thanks Dr. Marshall.  That makes a lot of sense.  One follow-up question though, in terms of 1,25D being generated in the eyes upon exposure to light, is that something that you are fairly certain happens, or is that an older theory that doesn't hold as much weight based on the new discoveries you've made such as 1,25D binding to the Rhodopsin receptors?

Thanks a ton for helping me understand this. 



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 Posted: Wed Oct 31st, 2007 07:18

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Russ,
I think you are asking whether exposure of a Th1 patient' s eye to light generates excess quantities of 1,25-D which then enters the brain or systemic circulations.

There is no data on this, and very little we can use to try and guess at the probabilities involved. Even the circulations are somewhat in question at the moment.
As you surmise, earlier statements we made about this issue have been difficult to sustain with data, and I would, in general, back away from them. The biggest single problem is that it is becoming clear to me that what 'modern medicine' knows about the brain is very limited indeed, with many pragma, such as the blood-brain barrier, vanishing as the molecular biology becomes better defined.

It is important for folk who exhibit photosensitivity while they recover their health (which is nearly everybody) to protect their eyes fastidiously. The exact mechanism(s) remain(s) clouded, however.
 

eClaire
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 Posted: Sun Nov 11th, 2007 07:53

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Sorry about the lost journal opportunity Trevor; I had no doubt that you'd do the right thing.  :)

Thanks also for the update about the eyes; I'd sort of reached that conclusion given the change last year in the MP advice about light protection.

I have a neuro reaction to light in my eyes if my NoIRs are too dark (I do not have neuro sxs if it is too dark without my NoIRs) or too light and so I have to protect my eyes in both directions if I want to limit sxs.  I don't know what this means, but I will keep my "eyes peeled" along the way for whatever discoveries make sense of that interesting sx.

Thanks so much for keeping us up to date on your efforts.  Claire



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Frans
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 Posted: Mon Dec 3rd, 2007 04:55

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Trevor, from what I understand, the paper is coming soon.

Do you think I will be able to order a copy to be sent to The Netherlands?

Sincerely, Frans



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Prof Trevor Marshall
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 Posted: Mon Dec 3rd, 2007 06:47

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eClaire,
We have sorted things out, the paper has been accepted and is 'in press'. An early Christmas present for us all:) I will put a preprint online as soon as I can (probably before Christmas).

Frans,
Check your email for a preprint :)
 

Last edited on Mon Dec 3rd, 2007 07:06 by Prof Trevor Marshall

Russ
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 Posted: Tue Dec 18th, 2007 02:14

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Dr Trevor Marshall wrote: It is important for folk who exhibit photosensitivity while they recover their health (which is nearly everybody) to protect their eyes fastidiously. The exact mechanism(s) remain(s) clouded, however. 

I think about the whole light sensitivity thing a lot because I am extremely light sensitive.  Light exposure to my eyes causes me symptoms that can last up to a week and it seems like it induces IP/herx.  One thought I had is that perhaps light to the eyes and the resulting stimulus thru the optic nerve and the brain somehow cause the exposure of bacteria which in turn causes IP/herx.  This would be similar to how massage can result in increased IP/herx due to causing the exposure of bacteria in tissues. 

Is something like this possibly part of the explanation of the effect of light to the eyes or does the data indicate that the symptoms of light exposure to the eyes have nothing to do with increased killing of bacteria?  Thanks.



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Prof Trevor Marshall
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 Posted: Tue Dec 18th, 2007 02:57

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Russ,
The rod receptors in the eye are GPCR, similar to Angiotensin-II receptors. There is an Xray model available for Bovine Rhodopsin, and I used that to show that not only are the receptors activated by Retinal, but 1,25D has a high affinity for them too. I am guessing that the receptors are activated by 1,25-D (rather than de-activated), but we don't know enough about the eye to say that just yet.

It is believed that when a pool of about 5 adjacent receptors are simultaneously activated, the electrical signal so produced is sufficient to produce a pulse on the optic nerve. So sight is not based on a single receptor, but on a pool of adjacent receptors. When receptors are activated by 1,25-D (being formed in the eye by incident radiant energy), it will activate vision, but presumably by providing a continuous random stimulus. The optic nerve and brain  then have to try and sort out where an image is, based on a consensus of false and true signals from the receptors in the retina.

Additionally, 1,25-D has the role of activating the VDR to produce several key proteins for the retina, without which the retina cannot remain strong and functional. The bacteria in the eye will obviously affect this process of transcription, which is probably why ocular symptoms (floaters, etc) are so common in these diseases.

We continue to explore the issues surrounding photosensitivity, but meanwhile, I hope that helps your understanding.
 

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 Posted: Thu Jan 10th, 2008 09:34

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Dr Marshall

Is your new paper available? If so, where can I read it. I am very interested.

Thanks



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 Posted: Thu Jan 10th, 2008 11:12

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I am at a conference at the moment. I expect that the paper will hit PubMed before the end of the month. You will see notice here as soon as it is available :)
 
 


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