Vit D3>125nmol/L min in blood. FIRST SMALL STEP for pwMS

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Vit D3 is part of a complex answer

Postby MarkW » Fri May 31, 2013 11:21 am

NZer1 wrote:Some insights to why the Vit D supplementation is not a simple answer to a complex problem;
Quote,
"Gene transfer
The main problem in Th1/Th17 diseases is that the VDR, which controls much of the innate immune system, seems to be blocked by bacterial ligands. There are many types of bacterial species at work that can transfer genes horizontally, and focusing on just one is an error.
The L-form bacteria enter the cell via endocytosis or some other means. We think they have a way to block the vitamin D nuclear receptor (VDR) ligand with a protein antagonist (perhaps capnine). The problem is that the phagocytes, while successfully engulfing the bacteria, are unable to kill them.
Transcription for specific genes occurs when the correct promoters and enhancers are provided by the activated VDR to separate the DNA double helix at the correct gene location and make the complement mRNA coded for a protein. The mRNA then returns to the cytoplasm to be translated into protein by the cell ribosomes.
However, when an antagonist is attached to the VDR ligand, the VDR is not in the correct physical shape to enter the nucleus through the nuclear membrane pores to access DNA where it would normally transcribe 900+ genes into mRNA. Many of these proteins are critical to the function of the immune system.
One researcher, using computer molecular modeling and affinity calculations, has determined that Benicar is a VDR agonist (activates the VDR), and in high enough concentrations will dislodge the bacterial antagonist (which inhibit VDR function). Over time, Inflammation Therapy will allow the hormone 1,25-D to regain homeostasis with the VDR and reactivate the immune system on its own."
https://www.chronicillnessrecovery.org/ ... 5&Itemid=5
;)
Nigel

Hello Nigel,
I am not sure why you posted this in a Vitamin D3 thread. Unless you are suggesting pwMS should not increase their Vit D3 levels???
Vitamin D3 supplementation should be the FIRST SMALL STEP for pwMS. it is not the only step in this highly complex disease but if a pwMS has low Vit D3 levels and poor vein health then the CCSVI procedure is probably less likely to be a success. Also supplementing vit D3 is probably the cheapest option for pwMS.
Kind regards,
MarkW
Mark Walker - Oxfordshire, England. Registered Pharmacist (UK). 11 years of study around MS.
Mark's CCSVI Report 7-Mar-11:
http://www.telegraph.co.uk/health/8359854/MS-experts-in-Britain-have-to-open-their-minds.html
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Re: Vit D3>125nmol/L min in blood. FIRST SMALL STEP for pwMS

Postby NZer1 » Fri May 31, 2013 12:00 pm

Hi Mark,
I personally like to be informed by all reliable sources of information rather than an opinion, so for that reason I go looking and share what I find. I don't tell people what to think, quite the opposite I like to see and hear people thinking and coming to their own conclusions when they have the details in front of them.

So many times people have followed red herring assumptions and wondered at the end of time why they weren't told differently, and the answer is right there, they were told what to do, rather than assess their needs and progress their knowledge.

Just saying of course.

:)
Nigel
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Re: Vit D3>125nmol/L min in blood. FIRST SMALL STEP for pwMS

Postby Squeakycat » Fri May 31, 2013 12:57 pm

NZer1 wrote:Some insights to why the Vit D supplementation is not a simple answer to a complex problem;
Quote,
"Gene transfer

The main problem in Th1/Th17 diseases is that the VDR, which controls much of the innate immune system, seems to be blocked by bacterial ligands. There are many types of bacterial species at work that can transfer genes horizontally, and focusing on just one is an error.

The L-form bacteria enter the cell via endocytosis or some other means. We think they have a way to block the vitamin D nuclear receptor (VDR) ligand with a protein antagonist (perhaps capnine). The problem is that the phagocytes, while successfully engulfing the bacteria, are unable to kill them.

Transcription for specific genes occurs when the correct promoters and enhancers are provided by the activated VDR to separate the DNA double helix at the correct gene location and make the complement mRNA coded for a protein. The mRNA then returns to the cytoplasm to be translated into protein by the cell ribosomes.

However, when an antagonist is attached to the VDR ligand, the VDR is not in the correct physical shape to enter the nucleus through the nuclear membrane pores to access DNA where it would normally transcribe 900+ genes into mRNA. Many of these proteins are critical to the function of the immune system.

One researcher, using computer molecular modeling and affinity calculations, has determined that Benicar is a VDR agonist (activates the VDR), and in high enough concentrations will dislodge the bacterial antagonist (which inhibit VDR function). Over time, Inflammation Therapy will allow the hormone 1,25-D to regain homeostasis with the VDR and reactivate the immune system on its own."

https://www.chronicillnessrecovery.org/ ... 5&Itemid=5

;)
Nigel

Jimmylegs there is some very good info on vits and mins regarding the deficiency and synthesis as well!
Nigel,
While all of this may well turn out to be true, I'm not sure that it says anything about vitD supplementation as it stands.

Clinical practice requires that we get beyond terms such as "seems," "think," and "computer molecular modeling" to actual proof that can be and is replicated by other scientific groups.
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Re: Vit D3>125nmol/L min in blood. FIRST SMALL STEP for pwMS

Postby NZer1 » Fri May 31, 2013 1:15 pm

Ed,
the same issue happens time and again where technology has to follow theories!

The number of anecdotal outcomes and theories invented pushes Science into new holes in understanding, sooner the better I say!

Bring on some new tools!

:)
Nigel
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Vitamin D Studies at CMSC/ACTRIMS Joint Meeting

Postby Squeakycat » Sun Jun 02, 2013 12:11 pm

Source URL: https://cmscactrims.confex.com/cmscactr ... r1448.html
Journal Date: 2013/05/30
Article Title: 25-Hydroxyvitamin D and MS Activity During Therapy with Interferon Beta-1b

25-Hydroxyvitamin D and MS Activity During Therapy with Interferon Beta-1b

Thursday, May 30, 2013
Alberto Ascherio, MD , Harvard University, Boston, MA
Kassandra Munger, ScD , Harvard University, Boston, MA
Claire Simon, ScD , Harvard University, Boston, MA
Ludwig Kappos, MD , University Hospital, Basel Neurology, Basel, Switzerland, Basel, Switzerland
Chris H Polman, MD , VU Medical Center, Amsterdam, Netherlands
Mark Freedman, MD , University of Ottawa, Ottawa, ON, Canada
Hans-Peter Hartung, MD , Heinrich-Heine University, Dusseldorf, Germany, Dusseldorf, Germany
David Miller, MBChB, MD, FRCP , UCL Institute of Neurology, London, United Kingdom
Xavier Montalban, MD , Hospital Universitari Vall d’Hebron, Barcelona, Spain
Gilles Edan, MD , CHU-Hôpital Pontchaillou, Rennes, France
Frederik Barkhof, MD, PhD , VU Medical Center, Amsterdam, Netherlands
Rupert Sandbrink, MD , Bayer Pharma AG, Berlin, Germany
Karl Kochert, MD , Bayer Pharma AG, Berllin, Germany
Christoph Pohl, MD , Department of Neurology, University Hospital of Bonn, Berlin, Germany
Background:
Recently, various studies have been dissecting possible beneficial effects of 25-hydroxyvitamin D (25[OH]D) in reducing disease burden and MRI detectable disease activity in multiple sclerosis (MS).

Objectives:

We studied the impact of 25(OH)D levels under interferon beta-1b (IFNB-1b) treatment on global gene expression levels with respect to the activity of MS.

Methods:

BENEFIT studied IFNB-1b in patients with a clinically isolated syndrome (CIS). Within the first 2 years of the study, contrast-enhanced cerebral MRI scans and 25(OH)D were obtained at the CIS and after 6, 12, and 24 months. In addition, gene expression profiles in peripheral blood mononuclear cells (PBMC) were determined using Affymetrix HGU 133 plus 2 arrays at the CIS and after 2/3, 12 and 24 months. The association of ~19,000 genes with enhancing lesions, with 25(OH)D, and with IFNB-1b treatment was modeled with negative binomial and Gaussian generalized linear models. Gene set enrichment analysis (GSEA) was performed to test the association of previously described gene sets relevant for the function of IFNB-1b and 25(OH)D with the number of enhancing MRI lesions. For naïve, threshold based gene-function classification, the Database for Annotation, Visualization and Integrated Discovery (DAVID ) v6.7 was used.

Results:

Higher 25(OH)D levels (p=0.0013) and IFNB-1b treatment (p<0.0001) were significantly associated with a lower number of enhancing lesions. 63 genes were significantly associated (p<0.05) with 25(OH)D levels; all but one of them were also associated with IFNB-1b treatment, which was significantly associated with 770 genes. GSEA showed that 25(OH)D gene sets reflecting the impact of vitamin D receptor binding on respective target genes as well as some IFNB-1b response gene sets were highly significantly associated with enhancing lesions. IFNB-1b and 25(OH)D regulated similar genes and first-line immune regulatory processes as shown by DAVID-based gene-function classification.

Conclusions:

The results show a beneficial role of 25(OH)D on MS activity. On a molecular level in PBMCs, the mechanistic explanation for this effect is a systemic gene regulation by 25(OH)D which is part of a larger systemic gene response to IFNB-1b therapy. Genes associated with either of the 2 are mainly steering immunological processes that impact on the inflammatory activity of MS.


Other presentations involving Vitamin D
Source URL: https://cmscactrims.confex.com/cmscactr ... %7Cpge%7C1

Does Low Vitamin D3 Confer a Greater Risk For Relapse In ADEM: A Pediatric Case Series
Thursday, May 30, 2013 Allen DeSena, MD, MPH , Neurology & Neurotherapeutics - MS Clinic, UT Southwestern Medical Center, Dallas, TX Donna C Graves, MD , Neurology & Neurotherapeutics - MS Clinic, UT Southwestern Medical Center, Dallas, TX Benjamin Greenberg

The Role Of Vitamin D In Optic Neuritis
Saturday, June 1, 2013 Jodie M Burton, MD, MSc, FRCPC , Clinical Neurosciences, University of Calgary, Calgary, AB, Canada Jessie Trufyn, BSc , University of Calgary, Calgary, AB, Canada Cheslia Tung, BSc candidate , University of Calgary, Calgary, AB, Canada

Vitamin D and RNFL Thickness in MS Patients without a History of Optic Neuritis
Thursday, May 30, 2013 Cecilie Fjeldstad, PhD , MS Center of Excellence, OKLAHOMA MEDICAL RESEARCH FOUNDAT, Oklahoma City, OK Gabriel Pardo, MD , MS Center of Excellence, OKLAHOMA MEDICAL RESEARCH FOUNDAT, Oklahoma City, OK Background: Vitamin D deficiency has been

Ancestry Is a Key Determinant Of Vitamin D Status In Children With Demyelination
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Viral and Genetic Risk Factors For Pediatric Neuromyelitis Optica
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Risk factors for transverse myelitis compared with multiple sclerosis, neuromyelitis optica, and other neurologic disorders in pediatric patients
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25-Hydroxyvitamin D and MS Activity During Therapy with Interferon Beta-1b
Thursday, May 30, 2013 Alberto Ascherio, MD , Harvard University, Boston, MA Kassandra Munger, ScD , Harvard University, Boston, MA Claire Simon, ScD , Harvard University, Boston, MA Ludwig Kappos, MD , University Hospital, Basel Neurology, Basel, Switzerland, Basel, Switzerland

HHV6 IgG Response and Genetic Factor rs11154801 Associate With Relapse Rate in Children
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Translational Research in Psychological Practice: Assisting Clients to Take Control while Attempting to Adapt
Friday, May 31, 2013: 2:20 PM Lake Eola AB Sally Shaw, DPsych , MS Clinic, Eastern Health, Victoria, Australia Simone Buzwell, PhD , Learning Transformations, Swinburne University, Victoria, Australia Background: The provision of psychological support services to people with MS

Mitigation of Adverse Effects On Hispanics While Using Titration On Fingolimod
Saturday, June 1, 2013 Angel R Chinea, MD , San Juan MS Center, San Juan, PR Background: Based on my clinical experience with Fingolimod, probability of developing adverse effects is variable from patient to patient. Fingolimod is a first oral

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Re: Vit D3>125nmol/L min in blood. FIRST SMALL STEP for pwMS

Postby MarkW » Thu Jun 06, 2013 6:04 am

Hello Nigel,
In my professional opinion there is sufficient evidence on Vitamin D3.

NZer1 wrote: I personally like to be informed by all reliable sources of information rather than an opinion......

As Ed has pointed out already you are not giving us facts but opinions of the writers of one paper.

NZer1 wrote:I don't tell people what to think, quite the opposite I like to see and hear people thinking and coming to their own conclusions when they have the details in front of them.

I don't tell people what to think. I am just giving advice that increasing Vit D3>125nmol/L min in blood should be FIRST SMALL STEP for pwMS. I have weighed the evidence and the economics and my message is simple: SPEND A FEW CENTS A DAY ON RAISING YOUR D3 LEVEL.

NZer1 wrote:..............I like to see and hear people thinking and coming to their own conclusions when they have the details in front of them.
So many times people have followed red herring assumptions and wondered at the end of time why they weren't told differently, and the answer is right there, they were told what to do, rather than assess their needs and progress their knowledge.

There is too much information around MS for any human being to assess, so I advise on a small area which interests me. I think that the writers of the paper you cite have forgotten that receptors (including VDR ones) are less prone to interference if their primary ligand (vit D) is in a plentiful supply. Binding to the receptor is a competitve situation and the receptor has a preference for its primary ligand. However this is far beyond a general Vit V3 and MS thread.
You appear to be the one following the proverbial red herring around vitamin D3 and MS. However you are not alone as most MS neuros appear to have missed the simple economics of vit D3. Medical science has missed the widespread impact of low Vit D3 levels in humans in general since discovering Ricketts.

The paper cited by Ed must be adsorbed if you want to discuss Vit D3 and genes.

Kind regards,
MarkW
Mark Walker - Oxfordshire, England. Registered Pharmacist (UK). 11 years of study around MS.
Mark's CCSVI Report 7-Mar-11:
http://www.telegraph.co.uk/health/8359854/MS-experts-in-Britain-have-to-open-their-minds.html
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Re: Vit D3>125nmol/L min in blood. FIRST SMALL STEP for pwMS

Postby Squeakycat » Thu Jun 06, 2013 6:46 am

MarkW wrote:However you are not alone as most MS neuros appear to have missed the simple economics of vit D3. Medical science has missed the widespread impact of low Vit D3 levels in humans in general since discovering Ricketts.
Mark,
I think it very interesting that there was so much discussion of Vit D at this recent neuro conference. I think this bodes well for neuros incorporating awareness of this into clinical practice, far faster than they embracing CCSVI anyway.
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Re: Vit D3>125nmol/L min in blood. FIRST SMALL STEP for pwMS

Postby NZer1 » Thu Jun 06, 2013 12:31 pm

MarkW wrote:Hello Nigel,
In my professional opinion there is sufficient evidence on Vitamin D3.

NZer1 wrote: I personally like to be informed by all reliable sources of information rather than an opinion......

As Ed has pointed out already you are not giving us facts but opinions of the writers of one paper.

NZer1 wrote:I don't tell people what to think, quite the opposite I like to see and hear people thinking and coming to their own conclusions when they have the details in front of them.

I don't tell people what to think. I am just giving advice that increasing Vit D3>125nmol/L min in blood should be FIRST SMALL STEP for pwMS. I have weighed the evidence and the economics and my message is simple: SPEND A FEW CENTS A DAY ON RAISING YOUR D3 LEVEL.

NZer1 wrote:..............I like to see and hear people thinking and coming to their own conclusions when they have the details in front of them.
So many times people have followed red herring assumptions and wondered at the end of time why they weren't told differently, and the answer is right there, they were told what to do, rather than assess their needs and progress their knowledge.

There is too much information around MS for any human being to assess, so I advise on a small area which interests me. I think that the writers of the paper you cite have forgotten that receptors (including VDR ones) are less prone to interference if their primary ligand (vit D) is in a plentiful supply. Binding to the receptor is a competitve situation and the receptor has a preference for its primary ligand. However this is far beyond a general Vit V3 and MS thread.
You appear to be the one following the proverbial red herring around vitamin D3 and MS. However you are not alone as most MS neuros appear to have missed the simple economics of vit D3. Medical science has missed the widespread impact of low Vit D3 levels in humans in general since discovering Ricketts.

The paper cited by Ed must be adsorbed if you want to discuss Vit D3 and genes.

Kind regards,
MarkW


Hi Mark,
rather than make this a personal issue I'll put the communication in another way so that you might get to understand what I am saying from a different angle.
In Science there is no black and white, there is the proverbial 50 shades of that other colour.
So when you see at the end of most if not all research papers the statement "there will have to be more studies to ...", that in simple words is a disclaimer to say that the article has some potential and there is room for more understandings to appear from different research and reviewers.

So my approach to all the hundreds of theories and insights with Vit D involvement is along the lines that you will find what you are looking for, you will skim over other details because they don't fit your paradigm or the outcome that fits the theory you support.

I'm not saying PwMS have to have Vit D or that they don't, I am aware that there are many reasons that Vit D is important and there are many reasons that Vit D shows as depleted. So finding to the best of your ability what is best for your situation is important and even more insightful is that the situation can have a different reason than we assume.
The supplementing can have different outcomes than one would assume, so to also assume that a blanket supplementation program will be the best for all is naive in my humble opinion.
It takes a small amount of questioning to find the safe way of learning what is happening from positive and negative outcomes in MS and there are many reasons that can be fathomed with discussion. In all aspects of our Health as Ed has taught us there are back up systems in our functions and as Jimmylegs has taught us there is synergistic effects that occur, which mean one supplement is not the complete method for improving Ill Health.

Old thinking is not always good thinking as knowledge grows!

:)
Nigel
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Re: Vit D3>125nmol/L min in blood. FIRST SMALL STEP for pwMS

Postby NZer1 » Thu Jun 06, 2013 11:23 pm

I believe that Gluten like Vit D is an important consideration to all PwMS.

Which makes me also wonder if dry Cat Food has gluten Ed?

Gluten sensitivity is a common issue in MS and it may be a compounding
effect issue!!!!
"Abstract
Coeliac disease (CD) is an autoimmune disease of small intestine associated
with sensitivity to gluten. The clinical manifestations are often of
gastrointestinal nature, although the disease may be present
asymptomatically as well. It is a chronic disease and in the absence of
overt neurological involvement, extended gluten exposure may give rise to
silent or subtle morphological and white-matter changes in central nervous
system. The present study investigates such changes using brain volumetry
and the assessment of white-matter tissue in CD patients without
neurological symptoms. Seventeen CD patients without any neurological
involvement were included in the study and went under neurological
evaluation and anatomical MRI. Individual gray- and white-matter, and
subcortical structure volumes were acquired for using automated volumetric
analyses. The observed white-matter hyperintensities (WMH) evaluated using
Age-Related White-Matter Changes scale. Findings show a bilateral decrease
in cortical gray-matter and caudate nuclei volumes in CD compared to
controls. Negative correlations were found between the duration of the
disease and the volumes of the affected regions. Cerebellum was seemingly
unaffected. In addition, significantly higher proportion of WMH was found in
CD patients, specifically in bilateral frontal and occipitoparietal
cortices. We observed a significant gray-matter and caudate nucleus atrophy
in the CD patients in the absence of marked neurological symptoms. Present
findings point out to a need for histopathological investigations
potentially focusing on anti-TG2 antibodies, and serial volumetric analyses
on the CD-related cortical and subcortical changes."
http://www.ncbi.nlm.nih.gov/pubmed/23615718

RESEARCHERS FIND INCREASED ZONULIN LEVELS AMONG CELIAC DISEASE PATIENTS


Researchers at the University of Maryland School of Medicine have found that
the human protein zonulin, which regulates the permeability of the
intestine, is at increased levels during the acute phase of celiac disease.
The discovery suggests that increased levels of zonulin are a contributing
factor to the development of celiac disease and other autoimmune disorders
such as insulin dependent diabetes, multiple sclerosis, and rheumatoid
arthritis. The findings are published in the April 29 issue of the journal
Lancet.


"Zonulin works like the traffic conductor or the gatekeeper of our body's
tissues," says lead author Alessio Fasano, M.D., professor of pediatrics and
physiology at the University of Maryland School of Medicine, and director of
Pediatric Gastroenterology and Nutrition at the University of Maryland
Hospital for Children. "Our largest gateway is the intestine with its
billions of cells. Zonulin opens the spaces between cells allowing some
substances to pass through while keeping harmful bacteria and toxins out,"
explains Dr. Fasano.


Earlier research conducted by Dr. Fasano discovered that zonulin is also
involved in the regulation of the impenetrable barrier between the blood
stream and the brain, known as the blood-brain barrier.


Celiac disease offered Dr. Fasano and his team a unique model for
understanding the dynamic interaction between zonulin and the immune system.
Celiac disease is a genetic disorder that affects one out of every 300
people in Europe, but its prevalence in the United States is not fully
known. People who suffer from the disorder are unable to eat foods that
contain the protein gluten, which is found in wheat and other grains. The
gluten sets off a reaction that can cause diarrhea, abdominal pain,
malabsorption of nutrients, and other gastrointestinal problems. Celiac
disease can be easily treated by avoiding foods with gluten.


With celiac disease, the body reacts to gluten by creating antibodies that
attack the intestine and cause severe damage over time. Unlike other
autoimmune disorders, scientists also know that celiac disease is triggered
by a specific antigen, which is the protein gluten. Celiac disease is also
known to cause increased permeability of the intestine. In addition, many
people who suffer from celiac disease also suffer from other autoimmune
disorders.


The research team examined the intestinal tissue of seven people with celiac
disease, and six patients without the disease. Patients with active celiac
disease showed higher levels of zonulin and anti-zonulin antibodies compared
to non-celiac patients and patients in remission, who were eating a
gluten-free diet.


"With celiac disease, we could never understand how a big protein like
gluten was getting through to the immune system. Now we have the answer,"
explains Dr. Fasano. "People with celiac have an increased level of zonulin,
which opens the junctions between the cells. In essence, the gateways are
stuck open, allowing gluten and other allergens to pass. Once these
allergens get into the immune system, they are attacked by the antibodies,"
adds Dr. Fasano.


"I believe that zonulin plays a critical role in the modulation of our
immune system. For some reason, the zonulin levels go out of whack, and that
leads to autoimmune disease," explains Fasano.


Dr. Fasano adds that more research is needed. He is currently conducting
experiments with diabetic rats. Preliminary results from his experiments
show that insulin dependent diabetes occurs in lab rats about three to four
weeks after increased intestinal permeability. The researchers believe the
increased intestinal permeability is associated with increased levels of
zonulin.


"We are at the threshold of exciting discoveries in this field," says Dr.
Fasano. "We now have a new way of looking at our cells. Our cells are not
stacked together like bricks. They are a dynamic field, which is constantly
in flux."


http://www.umm.edu/news/releases/zonulin.htm







http://en.wikipedia.org/wiki/Blood-brain_barrier

Quote:

The blood-brain barrier (BBB) is a separation of circulating blood and the
brain extracellular fluid (BECF) in the central nervous system (CNS). It
occurs along all capillaries and consists of tight junctions around the
capillaries that do not exist in normal circulation. Endothelial cells
restrict the diffusion of microscopic objects (e.g. bacteria) and large or
hydrophilic molecules into the cerebrospinal fluid (CSF), while allowing the
diffusion of small hydrophobic molecules (O2, hormones, CO2). Cells of the
barrier actively transport metabolic products such as glucose across the
barrier with specific proteins. This barrier also includes a thick basement
membrane and astrocytic endfeet.


Thick basement membrane? Astrocytic endfeet? Brain extracellular fluid? And
that's only the first paragraph....







Zonulin is increased in our blood when we eat foods that contain glutens--

http://journals.lww.com/jpgn/Fulltext/2 ... n.232.aspx


EVEN IF YOU DO NOT HAVE CELIAC DISEASE OR A GLUTEN ALLERGY, ZONULIN WILL
AFFECT YOU.


Zonulin works as a gatekeeper in the intestine and also in the blood brain
barrier. The more zonulin you have in your blood, the more permeable the
tight junctions of your blood vessels become. Not a good thing, if we want
to maintain a healthy lining in our guts, and blood brain barrier.







Dr. Hubbard discussed research into zonulin in his presentation at the
conference. As many of you know, the Hubbard Foundation recommends a
gluten-free diet to maintain endothelial integrity and a healthy blood brain
barrier.


So, what is gluten?? Gluten is a special type of protein that is commonly
found in rye, wheat, and barley. Therefore, it is found in most types of
cereals and in many types of bread. Not all foods from the grain family,
however, contain gluten. Examples of grains that do not have gluten include
wild rice, corn, buckwheat, millet, amaranth, quinoa, teff, oats, soybeans,
and sunflower seeds.

http://www.youtube.com/user/HubbFound
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My Vit D3 levels in my blood

Postby MarkW » Fri Jun 07, 2013 5:33 am

Hello All,
I don't just pontificate about taking Vit D3, I take it.
For 6 months of the English winter I took 10,000 IU a day the result was 244 nmol/L.
Then I reduced to 5000 IU/day this spring and my level was reduced to 185 nmol/L.
I plan to get sun this summer and will get rechecked in 6 months time.
My results only apply to me as I supplement many vits and minerals and am taking the Wheldon CAP regime but thought someone may be interested.
Kind regards,
MarkW
Mark Walker - Oxfordshire, England. Registered Pharmacist (UK). 11 years of study around MS.
Mark's CCSVI Report 7-Mar-11:
http://www.telegraph.co.uk/health/8359854/MS-experts-in-Britain-have-to-open-their-minds.html
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Re: Vit D3>125nmol/L min in blood. FIRST SMALL STEP for pwMS

Postby Squeakycat » Fri Jun 07, 2013 7:02 am

NZer1 wrote:I believe that Gluten like Vit D is an important consideration to all PwMS.

Which makes me also wonder if dry Cat Food has gluten Ed?

As far as cat food, probably. To make dry cat or dog food, you have to get the material to stick together. Gluten is a very good way to do that.

But on the subject of vitD.

While gluten may be an issue, in all the areas you discuss, vitD is an issue because it is crucial in cell replacement and the creation of tight junctions between cells.

My initial interest in vitD was because of a skin disease that runs in my family which is characterized by a lack of tight junctions in epithelial cells. The disease is genetic and the gene involved is expressed by regulatory hormone vitD as the first step in the cell replacement cycle. The defect leads to a lack of tight junctions of epithelial cells.

It is clear that MS results from a lack of tight junctions in endothelial cells, breaches in the BBB, whatever the cause.

It is also characteristic of many cancers and auto-immune diseases such as celiac, Crohns and so on.

Vitamin D manages cell replication and the creation of the tight junctions between cells designed to prevent things from going where they shouldn't. Inadequate levels of vitD may well play a significant role in this which is why there is so much research interest in this area today.
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Re: Vit D3>125nmol/L min in blood. FIRST SMALL STEP for pwMS

Postby NZer1 » Sat Jun 08, 2013 2:20 pm

chronic-cerebrospinal-venous-insufficiency-ccsvi-f40/topic22308.html

Some more info that again helps us understand the whole spectrum regarding Vit D and Sun Light!

;)
Nigel
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Re: Vit D3>125nmol/L min in blood. FIRST SMALL STEP for pwMS

Postby MarkW » Sun Jun 09, 2013 6:46 am

Squeakycat wrote:
MarkW wrote:However you are not alone as most MS neuros appear to have missed the simple economics of vit D3. Medical science has missed the widespread impact of low Vit D3 levels in humans in general since discovering Ricketts.
Mark,
I think it very interesting that there was so much discussion of Vit D at this recent neuro conference. I think this bodes well for neuros incorporating awareness of this into clinical practice, far faster than they embracing CCSVI anyway.

Hello Ed aka Squeakycat,
I am very happy that the MS Neuro community is thinking about Vit D3. The problem they face is that much of the research only supplements Vit D3 to a blood level of 75-100 nmol/L. Then the researchers conclude that Vit D supplementation does not impact MS at all. I think that acheiving 150-250 nmol/L is required but evidence for this is lacking. The Berlin group is using 10,000 iu/day as high dose in their study. I am very interested to see what blood level are acheived. I suspect that the range will be large as some pwMS are lacking important co-factors. My training as a business consultant says do not wait for full medical results on D3 just give 5000 IU/day to everyone at risk of MS. Its an economic decision not a medical one......one diagnosis of MS in the UK has a lifetime cost of 1 million pounds and Vit D3 costs pence. The sums are simple for me but not for most Neuros.
Kind regards,
MarkW
Mark Walker - Oxfordshire, England. Registered Pharmacist (UK). 11 years of study around MS.
Mark's CCSVI Report 7-Mar-11:
http://www.telegraph.co.uk/health/8359854/MS-experts-in-Britain-have-to-open-their-minds.html
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Re: Vit D3>125nmol/L min in blood. FIRST SMALL STEP for pwMS

Postby NZer1 » Sun Jun 09, 2013 11:11 am

MarkW wrote:
Squeakycat wrote:
MarkW wrote:However you are not alone as most MS neuros appear to have missed the simple economics of vit D3. Medical science has missed the widespread impact of low Vit D3 levels in humans in general since discovering Ricketts.
Mark,
I think it very interesting that there was so much discussion of Vit D at this recent neuro conference. I think this bodes well for neuros incorporating awareness of this into clinical practice, far faster than they embracing CCSVI anyway.

Hello Ed aka Squeakycat,
I am very happy that the MS Neuro community is thinking about Vit D3. The problem they face is that much of the research only supplements Vit D3 to a blood level of 75-100 nmol/L. Then the researchers conclude that Vit D supplementation does not impact MS at all. I think that acheiving 150-250 nmol/L is required but evidence for this is lacking. The Berlin group is using 10,000 iu/day as high dose in their study. I am very interested to see what blood level are acheived. I suspect that the range will be large as some pwMS are lacking important co-factors. My training as a business consultant says do not wait for full medical results on D3 just give 5000 IU/day to everyone at risk of MS. Its an economic decision not a medical one......one diagnosis of MS in the UK has a lifetime cost of 1 million pounds and Vit D3 costs pence. The sums are simple for me but not for most Neuros.
Kind regards,
MarkW


There are different models of thinking on the Vit D issues. I have noticed that Neuro's are 'blamed' as being the reason that Vit D isn't acknowledged in diseases. Funny in a way as they are not the ones that create and undertake research.
The Sun Light benefits have been known for some time, but the supplement benefits are not proven, which is interesting when you consider who funds the research and what the risks are if the outcome says that UV rays are the key factor. Patenting UV could be a challenge.
The recent Functional Medicine Conference attended by Terry Wahls had some interesting insights to the synergy factors of UV and also the involvement of Vit D in body chemical and genetic functions.

It's what you learn that is important rather than what you are taught!

;)
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Re: Vit D3>125nmol/L min in blood. FIRST SMALL STEP for pwMS

Postby NZer1 » Wed Jun 12, 2013 12:33 pm

Some of us may not 'feel' the benefits of supplementing Vit D one reason may be;

The magnesium and Vitamin D Connection That Most People Do Not Know

Magnesium and Vitamin D work together and most people are unaware of that. Almost 8o% of Americans are magnesium deficient because of the processed foods we eat. Vitamin D can not be used by the body unless you have the proper levels of magnesium. Lack of vitamin D in the body causes pain and disease. Vitamin D deficiency, is the cause of probably 60% of the diseases in the U.S. and the world today. Although there has been a lot of talk about Vitamin D in the mainstream media the lack of knowledge of how the body uses Vitamin D is doing more harm than good. The key to getting your Vitamin D levels to where they need to be is not as simple as taking a Vitamin D supplement. They say if it is too easy or to good to be true it normally is! So let’s learn about how Vitamin D can be used by the body so you can have less pain and disease!



Magnesium is the key factor in converting vitamin D-3 into 1,25D? the only form of vitamin D the body can use. Magnesium from supplements does not work well because the body has a difficult time metabolizing minerals that are not combined with food. Because of this, magnesium rich vegetables are the simplest, easiest, and most efficient way for the body to build up a sufficient store of magnesium to meet the body’s various every day needs. Having a deficiency of magnesium is not only harmful to the body, it is wasteful; your body will not be able to convert all of the vitamin D-3 you are getting, from supplements or sun, into its useable form.

Read More Below:

http://fibrotv.com/2012/09/the-magnesiu ... -not-know/

;)
Nigel
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