all things vitamin D

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

Postby mrhodes40 » Sat Apr 11, 2009 9:14 am

The scary thing about this particular protocol is the low, low vitamin D. I mean, getting people down under 10 8O

Here's a good reason not to do that
Association of vitamin D metabolite levels with relapse rate and disability in multiple sclerosis.Smolders J, Menheere P, Kessels A, Damoiseaux J, Hupperts R.
School for Mental Health and Neuroscience, Maastricht University, Maastricht, The Netherlands. j.smolders@mumc.nl

BACKGROUND: Multiple Sclerosis is associated with low serum levels of 25-hydroxyvitamin D (25(OH)D). We investigated the association between serum levels of 25(OH)D and 1,25-dihydroxyvitamin D (1,25(OH)2D), the biologically active metabolite, and clinical MS severity as expressed by EDSS-score and relapse rate. STUDY-DESIGN: Cross-sectional study. PATIENTS AND METHODS: Serum samples from 267 MS patients were collected for 25(OH)D and 1,25(OH)2D measurement. Clinical MS parameters at the date of serum sampling were determined. Results: Both metabolite levels were significantly lower in the progressive forms compared to the relapsing remitting (RR)MS phenotype. In RRMS patients (disease course < or = 5 years), high 25(OH)D levels were associated with a high chance of remaining relapse-free. Low 25(OH)D levels were associated with high EDSS-scores. 1,25(OH)2D was not directly associated with relapse rate or EDSS-score, and was dependent of age and 25(OH)D level. CONCLUSION: Serum levels of 25(OH)D were associated with both relapse rate and disability in MS patients. These results are suggestive for a disease modulating effect of the serum concentrations of 25(OH)D on MS. The low circulating 1,25(OH)2D levels in progressive MS are due to older age and lower 25(OH)D levels. The potential consequences for vitamin D supplementation in MS will be discussed.

FROM HERE

The MP claims the proof that MS is a "TH1" disease according to their vitamin d parameters is that they say MSers all have low 25D and high 1,25D. What is happening, according to their theory, is that the germs are making 1,25D directly in the body. 1,25d is the active metabolite and is actually a hormone, a well known fact.

The computer model comes into play here again because Marshall says that according to is computer simulation, 1,25D, is able to bind and activate the steroid receptors in the same way prednisone or something like that would.

Ergo, they claimthat all MSers are walking around as if on steroids all the time. They say that's why taking vitamin d seems to help MS, it is as if taking a steroid. They claim that this is why MSers have this theoretical germ rampant in our bodies that we canoot defeat, our immunity is severely hampered by this theoretical chronic steroid stimulation and we will never get better unless we get rid of the vitamin D.

But high 1,25D is not what is seen in studies on MS and vitamin D like the examples above and below, which checked both metabolites.

So the claim that the 25D is being converted into 1,25D by germs in your body thus leaving the 25D low and the 1,25D high is not supported.

ANOTHER PAPER HERE LOW 1,25d AND 25D

As an added element it is absurd to imagine that the body could function if it willy nilly could allow one hormone, 1,25d, to activate the receptors of another hormone, corticosteroids. How oculd yor body function at all it that were true?

There is not one peer reviewed medical paper anywhere that shows that 1,25D can bind and activate the steroid receptors.

Additionally, the molecular genomic shape of a hormone is not the only thing that allows it to bind and activate a particular receptor pocket, there are additional proteins involved:CLICK FOR PAGE ON RECEPTOR PROTEINS HERE

These threads live for a long time I wanted to add enough that some future person looking at this marshall protocol and coming to TIMS for material would have what they need. As I said I almost went for this once...scary

I know I saw a study last year that showed supplementing with vitamin D reduced lesions on MRI...can anyone add that to this thread as well? I can't find it :oops:
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Postby SarahLonglands » Sat Apr 11, 2009 9:58 am

Marie, this has just been published in Brain:
http://tinyurl.com/cowjzg Is it what you were looking for?

9321461 [PubMed - as supplied by publisher]

Department of Neurology, Institute for Neurological Research Dr. Raúl Carrea, FLENI, Buenos Aires, Argentina.

Although Vitamin D is best known as a modulator of calcium homeostasis, it also has immune modulating potential. A protective effect of Vitamin D on multiple sclerosis is supported by the reduced risk associated with sun exposure and use of Vitamin D supplements. Moreover, high circulating levels of Vitamin D have been associated with lower risk of multiple sclerosis. In this study, we measured 1,25 (OH)(2) Vitamin D and 25 (OH) Vitamin D levels in multiple sclerosis patients separated into different clinical subgroups according to disease status. In addition, direct effects of 1,25 (OH)(2) Vitamin D on ex vivo CD4+ T cells and myelin-peptide specific T cell lines were investigated to gain more insight into putative regulatory mechanisms in the disease pathogenesis. One hundred and thirty-two Hispanic patients with clinically definite multiple sclerosis were studied, 58 with relapsing remitting multiple sclerosis during remission, 34 during relapse and 40 primary progressive multiple sclerosis cases. Sixty healthy individuals matched with respect to place of residence, race/ethnicity, age and gender served as controls. Levels of 25(OH)D(3) and 1,25(OH)(2)D(3), measured by ELISA were significantly lower in relapsing-remitting patients than in controls. In addition, levels in patients suffering relapse were lower than during remissions. In contrast, primary progressive patients showed similar values to controls. Proliferation of both freshly isolated CD4+ T cells and MBP-specific T cells was significantly inhibited by 1,25(OH)(2)D(3). Moreover, activated Vitamin D enhanced the development of IL-10 producing cells, and reduced the number of IL-6 and IL-17 secreting cells. Notably, Vitamin D receptor expression was induced by 1,25(OH)(2)D(3) in both activated and resting cells. Interestingly, T cells were able to metabolize 25(OH)D(3) into biologically active 1,25(OH)(2)D(3), since T cells express alpha1-hydroxylase constitutively. Finally, 1,25(OH)(2)D(3) also increased the expression and biological activity of indoleamine 2,3-dioxygenase, mediating significant increase in the number of CD4+CD25+ T regulatory cells. Collectively, these data suggest that 1,25(OH)(2)D(3) plays an important role in T cell homeostasis during the course of multiple sclerosis, thus making correction of its deficiency may be useful during treatment of the disease.


Sarah :?:
An Itinerary in Light and Shadow Completed Dr Charles Stratton / Dr David Wheldon abx regime for aggressive secondary progressive MS in June 2007, after four years. Still improving with no relapses since starting. Can't run but can paint all day.
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Postby mrhodes40 » Sat Apr 11, 2009 11:14 am

:D Thanks Sarah a most excellant paper! Did you notice this little section?

Proliferation of both freshly isolated CD4+ T cells and MBP-specific T cells was significantly inhibited by 1,25(OH)(2)D(3). Moreover, activated Vitamin D enhanced the development of IL-10 producing cells, and reduced the number of IL-6 and IL-17 secreting cells



that's reason enough right there to not do the MP; 1,25D is not acting like a steroid, it is slowing down the parts of the immune system that need slowing down in MS....and increasing the parts that need increasing.

Now if an MPer was here they would tell an elaborate story about how this does not count because it was done in a lab dish, as if fresh blood behavior in a lab dish is completely different than in the body.

they would point to this section as support for themselves though
Interestingly, T cells were able to metabolize 25(OH)D(3) into biologically active 1,25(OH)(2)D(3), since T cells express alpha1-hydroxylase constitutively


What that says is that the t cells turned 25D into 1,25d, they have been claiming this is because the germs are making this happen. In fact activated macrophages can convert 25d to 1,25d in a local area like that, that is known. But that does not result in overall high 1,25d as the other papers show and it also is not a bad thing for the 1,25d to be there as it modultes the immune system in a very positive way for MS.

this little bit
Notably, Vitamin D receptor expression was induced by 1,25(OH)(2)D(3) in both activated and resting cell


is important because note that the VDR was activated no problem by the 1,25d. This is another aspect of vitamin D activity the MPers say is not working in MS because the VDR, they say, is inactivated by 25d. No evidence of that either.

All in all I hope pwMS who are considering this marshall protocol learn what they say over there then read this thread. Many people who never studied the MP will find this information a little confusing, but to those who already drank the koolaide, the more detailed infor will be welcome.
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Thank you, RuSmolikova

Postby lyndacarol » Sat Apr 11, 2009 12:19 pm

RuSmolikova--

Thank you for posting the link to the WEALTH of information on the vitamin D/MS connection. I have only started reviewing the information, but already it raises old questions. The first one concerns the Lapps or Lapplanders. They live VERY far north in Scandinavia with very little sunshine (i.e. vitamin D); caribou makes up the majority of their diet; yet, MS is virtually nonexistent among these people. Why is that?

Under the vitamin D hypothesis, MS should be rampant in that population. Likewise, among the Eskimos (Inuit). EDIT: I now know that their diet is rich in vitamin D.
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Postby jimmylegs » Sat Apr 11, 2009 12:40 pm

http://www.baiki.org/content/glossary.htm
The Sami diet is simple and healthy. It consists of fish caught in lakes, rivers and the ocean, reindeer meat that is dried in the sun, smoked, or cooked in a stew with potatoes, and cloudberries and mushrooms gathered from the forests and bogs. Shredded carrots, sliced peppers amd bok choy often accompany a Sami meal as do bread, cheese and coffee.

http://en.wikipedia.org/wiki/Inuit_diet#Seal
Seal meat is the most important aspect of an Inuit diet and is often the largest part of an Inuit hunter’s diet.[1] Depending on the season, Inuit hunt for different types of seal: harp seal, harbor seal, and bearded seal. Ringed seals are hunted all year, while harp seals are only available during the summer.[2]

http://cat.inist.fr/?aModele=afficheN&cpsidt=17514649
The trace-element content of seal meat is very high, particularly iron (379 μg/g muscle in hooded seal) and zinc (30 μg/g muscle in harp seal), as also is the vitamin content, especially vitamins A, D3 and B12.
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Postby mrhodes40 » Sat Apr 11, 2009 12:50 pm

But Inuits vitamin D intake wasn’t dependent upon the sun. They get all that they need from their diet, heavy on types of fatty fish that are naturally rich in vitamin D. The plentiful amounts of the vitamin kept them from developing less melanin. In fact, before milk was fortified with D, people living outside of Northern Canada and Alaska loaded their diets with fishy products, such as cod liver oil, to get their daily supplement. So despite their chilly climate and lack of sun exposure, it’s the Inuit diet that has kept them in their natural glow.

from http://scienceline.org/2007/06/18/ask-d ... iteskimos/
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Thank you, friends

Postby lyndacarol » Sat Apr 11, 2009 1:03 pm

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Postby mrhodes40 » Sat Apr 11, 2009 4:53 pm

My, good job WW!! I am so glad for your son! it is good to ear someone si following up the d link with something positive to do. And gee, this is spring when our d levels are lowest. Probably be great in the fall!
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Postby Wonderfulworld » Sun Apr 12, 2009 12:15 pm

Thanks JL and MrR...yes I'm keeping on with the "drops" for him and am allowing him about 10 mins sun exposure a day without sunscreen - hopefully his levels will rise even further and by the next time of testing in June he will be in a really healthy range.

He even knows what I mean when I say "can you find your drops?" and fishes them out for me, hands them to me and then lies still with his mouth open. He thinks they are a treat and grins afterwards!

I am just so happy to at least try to help reduce his risk from this *%$*@#* disease, IYKWIM.
~~~~~~~~~~~~~~~
Concussus Resurgo
~~~~~~~~~~~~~~~
RR-MS dx 1998 and Coeliac dx 2003
~~~~~~~~~~~~~~~
Copaxone, Cymbalta. EPO, Fish Oils, Vitamin D3 2000 IU daily, Cal/Mag/Zinc, Multivitamin/mineral, Co-Enzyme Q10, Probiotics, Milk Thistle.
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Postby Wonderfulworld » Sun Apr 12, 2009 12:21 pm

The Sami diet is also naturally gluten-free.... as a coeliac MS'er I noticed that a few years ago when I watched a documentary on them. They are, in essence, following a mesolithic diet - one that predated the farmers in the neolithic and the introduction of gluten (oats, wheat, barley, rye), chicken eggs, dairy etc. The BBD in effect.

Although I think the coffee was probably not around in mesolithic times :lol:
~~~~~~~~~~~~~~~
Concussus Resurgo
~~~~~~~~~~~~~~~
RR-MS dx 1998 and Coeliac dx 2003
~~~~~~~~~~~~~~~
Copaxone, Cymbalta. EPO, Fish Oils, Vitamin D3 2000 IU daily, Cal/Mag/Zinc, Multivitamin/mineral, Co-Enzyme Q10, Probiotics, Milk Thistle.
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Postby sou » Mon Apr 13, 2009 7:51 am

Hi.

Just a clarification, with the risk of repeating somebody else.

The term "steroids" refers to a class of fat soluble molecules capable of crossing cell membranes. Steroid hormones activate receptors at the interior of the cell, which can do several things, usually promoting expression of certain genes, altering parameters of the metabolism and behavior of the cell.

Not all steroids act on the same receptors. Each has its very own specific role.

sou
Shortest joke: "We may not be able to cure MS but we can manage its symptoms."
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Postby mrhodes40 » Mon Apr 13, 2009 1:34 pm

Thanks Sou! :D

I can always use clarification. I often get lost in the weeds explaining myself trying to make it simple I can lose clarity, please feel free to help me out if you can! :oops:
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Re: Thank you, RuSmolikova

Postby RuSmolikova » Mon Apr 13, 2009 3:34 pm

lyndacarol wrote:...but already it raises old questions. The first one concerns the Lapps or Lapplanders. They live VERY far north in Scandinavia with very little sunshine (i.e. vitamin D); caribou makes up the majority of their diet; yet, MS is virtually nonexistent among these people. Why is that?


I have a similar Q: Why there is so many MS patients in Australia? A lot of sun, and perhaps plenty fish oil in their food...
The fact that MS is rare around the exuator is connected with the sunshine only, isn´t it? Could there be a difference in parasite rates (hook worms) in different regions?
How about Lapps and Escymos and possible parasites? Do they eat raw meat or the hung one?
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Postby peekaboo » Mon Apr 13, 2009 3:49 pm

Ru -

The fact that MS is rare around the exuator is connected with the sunshine only, isn´t it?


not just sunshine but civilization environmental toxins industry etc.
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Postby jimmylegs » Mon Apr 13, 2009 4:56 pm

to my understanding population in oz is mainly in the southeast spreading up the east coast in a narrow band, with a dense little population pocket in the southwest also.
in northern oz you're about as far from the equator as, say, mexico. in the southeast of australia you can get to be as far from the equator as parts of the northeastern US and the southernmost parts of canada.
as to diet.. i was only there for a few months but certainly plenty of fish and chips seem to get consumed in australia.. and on my work crew we were big fans of tinned tuna.. not the best options available, but certainly widespread and cheap.
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