all things vitamin D

Discuss herbal therapies, vitamins and minerals, bee stings, etc. here

Postby jimmylegs » Tue Apr 19, 2011 4:13 pm

hey there do you also take zinc?

by the way 250 is the top end of the safe range, above which the *risk* of hypercalcemia is increased.

it's not like there's a hypercalcemia on/off switch between 249 and 250..
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Re: Tr1 Regulatory Cells and Vitamin D

Postby sou » Thu Apr 28, 2011 6:39 am

CVfactor wrote:
sou wrote:If MS ever proved to be autoimmune.


"ThisIsMS an unbiased multiple sclerosis community" Not so much.


Why not so much? Unbiased does not really mean that everybody have to agree with everything posted. I strongly disagree with the immunomodulatory approach to treatment and the autoimmune nature of the disease. I may be right, I may be wrong. What's the problem with that?

The forum would be biased if the moderators removed posts which disagree with the forum policies or financial interests. What we all like about this forum is that it is open to any opinion. Everyone may express their opinion freely, respecting the common sense rules. We are free to express ourselves. It does not necessarily mean that we have to agree, too.
Shortest joke: "We may not be able to cure MS but we can manage its symptoms."
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Postby CVfactor » Thu Apr 28, 2011 4:36 pm

O.K., I guess I am going to keep this thread up to date with information I find that supports the hypothesis that MS is a due to a regulatory T-cell defect.

This theory could be wrong, but I believe there is a lot of information to support this and it seems like this forum is the best place I have found to share ideas.

So, to answer Jimmylegs question, I do not monitor my magnesium levels, but I do eat a lot of nuts which are supposed to contain a lot of magnesium.

Now back to the subject at hand.

Here is another recent study that evaluates Regulatory T-cells in the Theiler's virus mouse model of MS. For those not familiar with this model it is not EAE, but is induced by a virus instead of an auto-antigen:

http://www.ncbi.nlm.nih.gov/pubmed/21273044

And the conclusions:

"In summary, our findings strongly indicate that differences in
the numbers and the ratio of CNS T effector:Treg cells during acute
TMEV infection control the efficiency of the anti-viral immune
response resulting in virus persistence and resulting long-lasting
effects leading to the eventual development and progression of the
autoimmune demyelinating disease. The preferential expansion of
Tregs in TMEV-infected SJL/J mice, as compared to disease-resistant
C57BL/6 mice, suggests the possibility that genetic susceptibility to
certain autoimmune diseases may be in some instances due to
‘regulatory mimicry’. This would encompass a situation wherein
a clonotype of nTregs expressing a self antigen-specific T cell
receptor selected on particular MHC backgrounds could be activated
to expand in response to a cross-reactive epitope expressed
on an infectious agent. This expanded population of Tregs would
then ameliorate or delay the clearance of the infectious agent in the
target organ of the autoimmune disease setting the stage for
promotion of the development of autoimmunity via mechanisms
such as molecular mimicry or epitope spreading. These findings
thus have important implications to our thinking about the
potential mechanisms underlying induction of human autoimmune
disease secondary to virus infection."

My takeaway is that this is further evidence that MS may be initiated by a viral infection which causes an inappropriate immune response that is not halted by self-tolerance due to a defect in the natural regulatory T-cell (nTreg) function.
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Postby jimmylegs » Thu Apr 28, 2011 6:41 pm

actually i asked about zinc. it affects how your body absorbs supplementary d3.

on the magnesium topic though, if you don't measure, you might at least be interested in this WONDERFUL resource with lots of detail on which seeds and nuts are best (raw is the best of all).

http://www.mgwater.com/rod09.shtml
my approach: no meds so far - just nutrient-dense anti-inflammatory whole foods, and supplements where needed
info: www.whfoods.com, www.nutritiondata.com
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Postby CVfactor » Fri Apr 29, 2011 6:06 am

Oh, yeah sorry you were talking about Zinc. So no I do not take any other supplements beside vitamin D. I know there could be other factors that influence how vitamin D functions but for now I have just decided to focus on vitamin D and eat a healthier diet (more fruits, vegetables and nuts).

Thanks for the information on the nuts and seeds. Right now I eat a lot of mixed nuts (almonds, wallnuts, pecans, hazel, brazils) all in shells.
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Postby CVfactor » Sat Apr 30, 2011 6:40 pm

Here is a recent paper that describes how vitamin D seems to induce Tregs in mice:

http://atvb.ahajournals.org/cgi/content/abstract/30/12/2495

This study was conducted by people working on atherosclerosis, but it does support the theory that vitamin D promotes development of regulatory T-cells.
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Anyone have a link for this article about Vitamin D?

Postby zanne10000 » Mon May 02, 2011 6:30 pm

I just saw my naturopath today and she said she went to an infectious disease conference recently and someone presented a study about Vitamin D, MS and a triggering infection (often EBV). I think the following info from the April 19th issue of Neurology is the article to which she's referring, but it costs $20 to access it. Does anyone have a free link to it? BTW, she has increased my Vit D to 40,000 IUs for 28 weeks based on what she heard at the conference. It's a high dose, I realize, but she said it was shown to be as effective as immune modulators. Thanks!



In Focus Robert A. Gross
Spotlight on the April 19 Issue Neurology April 19, 2011 76:1367

...data for diagnoses of multiple sclerosis (MS) and infectious mononucleosis were analyzed...provides support for interactions between vitamin D and Epstein-Barr virus in determining the prevalence of MS, which should be taken into account for...
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Postby jimmylegs » Mon May 02, 2011 8:13 pm

i'll look and let you know if i can get it.
my approach: no meds so far - just nutrient-dense anti-inflammatory whole foods, and supplements where needed
info: www.whfoods.com, www.nutritiondata.com
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Postby zanne10000 » Mon May 02, 2011 8:53 pm

Thanks, jimmylegs! I'm wondering if this might be the study to which she was referring:

http://www.webmd.com/multiple-sclerosis ... s-relapses

It's several years old, though... but it does mention the 40,000 IUs for six months and then tapering, which is what she wants me to do.
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Re: Anyone have a link for this article about Vitamin D?

Postby NHE » Tue May 03, 2011 2:24 am

zanne10000 wrote:I just saw my naturopath today and she said she went to an infectious disease conference recently and someone presented a study about Vitamin D, MS and a triggering infection (often EBV). I think the following info from the April 19th issue of Neurology is the article to which she's referring, but it costs $20 to access it. Does anyone have a free link to it? BTW, she has increased my Vit D to 40,000 IUs for 28 weeks based on what she heard at the conference. It's a high dose, I realize, but she said it was shown to be as effective as immune modulators. Thanks!



In Focus Robert A. Gross
Spotlight on the April 19 Issue Neurology April 19, 2011 76:1367

...data for diagnoses of multiple sclerosis (MS) and infectious mononucleosis were analyzed...provides support for interactions between vitamin D and Epstein-Barr virus in determining the prevalence of MS, which should be taken into account for...


If you have a university near you, then take a flash drive and head off to their research library. At my local university, I can save the pdf's to a flash drive and then print them out at home.

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Postby CVfactor » Thu May 05, 2011 4:50 pm

To expand a little more on the concept of molecular mimicry, this is in essence the possibility that fragments of a virus (peptide) have a similar structure to that of autoantigens (fragments of your tissue such as Myelin Basic Protein).

Here is a good example showing this:

Image

You can see that in picture C, a E-coli peptide is structurally similar to a Myelin Basic Protein peptide.

And here is a good overview from Wikipedia on the Molecular Mimicry theory:

http://en.wikipedia.org/wiki/Molecular_mimicry

So basically your immune system T-cells could attack its own tissues because it believes it is a foreign antigen. This is known as cross-reactivity.

So as many may know, MS is more prevalent in women. Here is a paper that looks at cross-reactivity in male and female mice in EAE:

http://www.ncbi.nlm.nih.gov/pubmed/20950867

The conclusions are that female mice have a higher propensity for cross-reactivity than male mice.

But this goes back to there is increasing evidence that in healthy individuals, regulatory T-cells should be able to differentiate self from non-self.
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Re: Tr1 Regulatory Cells and Vitamin D

Postby NHE » Fri May 06, 2011 3:32 am

Thank you for posting the interesting image discussing the peptide structures and how this might influence molecular mimicry. In addition to physical structure, the chemistry of the various amino acid residues is also important when considering antibody and/or receptor cross reactivity. There are several residues where the chemistry is markedly different between the two peptides and I suspect that these differences might influence how the immune system responds to them. For example, ARG to VAL is a polar/basic to hydrophobic substitution, SER to LYS is a polar/neutral to polar/basic substitution, ALA to ASN is a nonpolar to polar substitution and HIS to VAL is a polar/acidic to nonpolar substitution. As you're likely aware, such substitutions, especially polar to nonpolar, will affect the three dimensional structure of the peptide in aqueous media thereby affecting antibody and receptor recognition. Not having read the full paper, I do not know if the authors address these differences though they are important when considering the homology of two different structures.

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Postby CVfactor » Sat May 07, 2011 5:28 pm

NHE,

Yes, I think molecular mimicry can have many aspects of mechanism. It sounds like you are more familiar with the intricacies than I am.

But I found another very interesting article about T-cells and multiple sclerosis:

<shortened url>

This article is very good in my opinion because it goes into great detail about all of the different types of T-cells and their function.

Here is a good summary of what the authors believe about T-cells and MS:

"The importance of T-cells in the pathophysiology of MS is suggested by several
lines of evidence. T-cells are located at the active edge of MS lesions, and the presence
of perivascular infiltrates of T-cells throughout the CNS is a consistent feature
in all stages of the disease (Prineas 1975). Patients with MS have a higher frequency
of activated T-cells in their peripheral blood, specifically a higher percentage of
activated myelin-reactive T-cells (Hafler et al. 1985; Zhang et al. 1994). The strongest
genetic risk allele for the development of MS is in the class II HLA-DR locus, and
recently another risk allele has been identified in the class I HLA locus (Yeo et al.
2007), suggesting that antigen presentation to CD4+ and CD8+ T-cells plays a causal
role in the development of disease. In the EAE model, adoptive transfer of myelinreactive
T-cells into the peripheral blood of a previously healthy animal is sufficient
to transfer disease (Zamvil et al. 1985). Together, these findings have led to the
hypothesis that MS is a T-cell-mediated autoimmune disease.
Advances in our understanding of T-cell physiology have expanded our understanding
of their role in MS pathophysiology. It is becoming increasingly clear that
T-cells are not a monomorphic population differing only in their T-cell receptor
(TCR) specificities, but rather they are a diverse mix of proinflammatory and antiinflammatory
subtypes, whose reciprocal interactions we are just beginning to
understand. In this chapter, we review what is known about the specificity and functional
state of T-cells in MS patients. To understand more fully the physiology of
these cells, we examine the factors that enhance or inhibit T-cell activation and the
effector profiles T-cells assume after they are activated. We explore in detail the
regulatory role certain T-cells play in inhibiting autoimmune and other inflammatory
processes and the functional deficiency of these cells in MS. Finally, we discuss how
T-cells specifically affect, and are affected by, the local environment of the CNS."

And here is what the authors conclude about Tr1 regulatory cells and vitamin D:

"Unlike FoxP3+ Treg, Tr1 lineage fate is not determined in the thymus, but rather
Tr1 cells are induced from naïve cells by activation in the setting of the appropriate
conditioning signals. Several stimuli have been shown to result in the induction of
Tr1 cells in vitro. Activating T-cells with CD3/CD28 crosslinking in the presence
of IL-10 and IFNa, or with the combination of dexamethasone and 1-,25-(OH)2
Vitamin D3, both result in Tr1 induction (Levings et al. 2001; Barrat et al. 2002).
The latter combination has been of interest as low levels of Vitamin D have been
identified as an environmental risk factor for MS (Munger et al. 2004). Tr1 cells
can also be induced by crosslinking CD3 with the alternative costimulatory
receptor CD46 (Kemper et al. 2003). Finally, the combination of IL-27 and TGFb
also induces Tr1 cells, and this combination is thought to be the mechanism
through which FoxP3+ Treg modified dendritic cells induce Tr1 formation
(Awasthi et al. 2007)."

So, I believe from my own experience Vitamin D is definitely helping me with my disease. But of course this is only anecdotal. I would think future Vitamin D research on patients with MS is a promising approach to investigate.
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Pregnancy and Vitamin D may protect against MS - studies

Postby MSUK » Fri May 20, 2011 2:27 am

Image

Tasmanian researchers have found that delaying pregnancy may increase the likelihood of women getting multiple sclerosis.

A yet to be published study looking at MS over the last 60 years has found the frequency of the disease has risen dramatically and it's largely been driven by women.

The Menzies Research Institute's Associate Professor, Bruce Taylor, says delaying pregnancy could be having an impact.

"We think that having children is protective for having MS, He said.... Read More - http://www.msrc.co.uk/index.cfm/fuseact ... ageid/1936
MS-UK - http://www.ms-uk.org/
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Postby Leonard » Sat May 21, 2011 6:09 am

Hallo America, wake up! Start to think wider, more conceptual, don't get lost or trapped in technical details of MS lesions, in biological processes in areas where things have already gone terribly wrong.

What is the common factor of pregnancy and Vitamin D: exactly, the micro-cellular feeding is improved. The whole pregnancy is about nothing else than micro-cellular feeding. The Vitamin D enhances the grips of the insulin on the cells and thereby improved the micro-cellular feeding. Both have anti-inflammatory properties? Of course not, they improve the feeding of the cells and the neuro signalling pathways calm down.

In this same context, this is interesting:

In 1949, Dr. Hench first applied steriods for a purpose other than the substitution in people who have a deficiency of this hormone creation. She gave it to patients with polyarthritis, with good results. In fact they had seen that women who are pregnant and have rheumatism problems, during pregnancy usually have less or no rheumatism.

On the other hand it was known that during pregnancy the adrenal glands produce more cortisol. Dr. Hench found that the arthritis may have been suppressed by increased cortisol production and that proved right. Gradually it was discovered that cortisone has strong anti-inflammatory properties and the knowledge about steroids and their action was developed further...

From this time onwards, the anti-inflammatory aspects have been seen. I guess also by the neurologists who's discipline started to develop around more or less the same timeframe.

But is this true? Is this conceptually correct? Perhaps, it is the other way around. Perhaps this is not anti-inflammation by suppression but neuro-signalling pathways that calm down because of better nutrition of the cells. Most certainly, if seen in the context of a pregnancy which is all about feeding of the unborn child, or if seen from a more conceptual point of view, this much morelikely to do with enhanced feeding of the cells.

If you look at it like this, so many things just fit together so neatly...
see also http://www.thisisms.com/ftopic-15188-da ... c-150.html
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