all things vitamin D

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

Postby patientx » Fri Apr 10, 2009 4:40 pm

By the way, Marshall uses a program available for free on the internet.


That's not so damning; I got a whole operating system for my PC for free over the internet.

But I'm glad you took the time to read through his theory and figure out where it is flawed. The guy can throw some medical jargon. I'm open to non-conventional theories; but I read enough to think this is crackers. Relying only on computer simulations clinched it for me. He even coined a new phrase (at least his website is the only place I've seen it): "in silico."

I'm an electrical engineer by trade. And we use computer simulation software on a daily basis. It's easier to change things and try them in software before you actually build something. But the accuracy depends on the models. And, in the end, we also verify on the bench with a real piece of hardware.
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Postby CureOrBust » Fri Apr 10, 2009 5:58 pm

his "theory" is specifically for another medical condition
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Postby sou » Sat Apr 11, 2009 4:08 am

Hi.

We have had a course in computer assisted molecular modeling and simulations. One important conclusion was that algorithms of today give different results compared to the algorithms of yesterday. We can easily assume that algorithms of tomorrow will give different results from those of today.

At the rise of bioinformatics, big pharmas thought that simulations could replace classic lab research. But that didn't happen. Even worse, molecules tested with older algorithms will have to be tested again and again with newer. I wonder how many drugs have been erroneously thrown to the rubbish bin.

In conclusion, simulation is a very useful tool for evaluating probabilities. But just like you can't use a hammer to unscrew, you can't simulate and expect to have a 100% accurate model of the functionality of a cell, not to mention a zillion cells that make up a human body.

sou
Shortest joke: "We may not be able to cure MS but we can manage its symptoms."
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Postby Wonderfulworld » Sat Apr 11, 2009 4:09 am

Computer and mathematical models are easily controlled....well, easier than live humans :lol: . I don't feel that this theory is a runner for me.

JL :
No boron in my multi but the new cal/mag/d3 tablet I got recently includes boron in it. My current daily D3 is 5000iu, has been since November. Calcium 1400mg, Mag 750-1000mg.

Off topic, but an interesting one for you JL! - found that migraines are linked to D3 deficiency/insufficiency. Also Cal/Mag. So I upped my magnesium this month and for the first time in 6 months I got through a month without a migraine. For some reason I can tolerate up to 1000mg mag at the moment but in 3 doses during the day.

Due to visit neuro on 20th April, will be getting D3 test then, my gp is at a loss as to what to do so I'll check with neuro. The dept is doing work on vit D receptor genes; see: http://www.stvincents.ie/E.R.C/Neurology_Group.htm

Sorry for wandering off topic to the rest of the people on the thread :oops:
~~~~~~~~~~~~~~~
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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Testing your children for D3 levels?

Postby Wonderfulworld » Sat Apr 11, 2009 4:23 am

Having read so much about vitamin D3 and MS recently I got my now 14 month old son tested for D3 levels.

The rest of you MS-D3-fans will be happy for us when I tell you that his level is 76nmol, just into the normal range. Yay!

The reason I'm posting is in case any of you MS parents are interested in getting your children tested for D3 levels, based on this news from Feb this year. http://www.sciencenews.org/view/generic ... ncy_and_MS

I am a sun-fan and have been taking 200% RDA vitamin D for the years prior to my pregnancy. I also got as much sun (albeit very limited in Ireland) as I could during the pregnancy. During the pregnancy I chose a pre-natal supplement with vitamin D in it.

DESPITE all this I was insufficient in vitamin D after I gave birth and have continued until last Nov at my last test.

**I was concerned about my sons' level of Vitamin D as he would inherit my levels of the vitamin. **

I have been giving him approved Vit D3 drops (see: http://www.fsai.ie/details.aspx?id=6984) and I got him tested at 1 year, so that his GP and I could see how his levels were.

I find it very interesting that despite the supplementation he is just inside the normal range. His GP advises he continue the drops and get tested again in a few months. I am so grateful to other ThisisMS'er's for the information about all this and I am hoping that I have reduced my son's risk for MS a bit.
~~~~~~~~~~~~~~~
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 jimmylegs » Sat Apr 11, 2009 5:57 am

that is great ww. cheerleader fixed her migraines with magnesium (among other things) also. pretty neat huh!
hope you hear that d3 is improving on the 20th :) maybe the boron will help.
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Postby jimmylegs » Sat Apr 11, 2009 6:00 am

good job ww, very important.
see if you can get the level up over 100, for lowest ms risk!
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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 Anecdote » 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 people).
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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

Thank you, my friends, for your research and answers.
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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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