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Re: Vitamin D3

Postby NHE » Wed Jul 06, 2011 1:36 am

Here's some more info on Vitamin D3.

Relapse frequency has been found to correlate inversely with vitamin D3 levels. 50-60 ng/mL (125-150 nmol/L) is a good target range. Note, the conversion factor for 25(OH) vitamin D3 ng/mL -> nmol/L = 2.496

post128403.html#p128403

higher 25-OH-D levels were associated with a reduced hazard of relapse. This occurred in a dose-dependent linear fashion, with each 10nmol/l increase in 25-OH-D resulting in up to a 12% reduction in risk of relapse. Clinically, raising 25-OH-D levels by 50nmol/l could halve the hazard of a relapse.


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Postby jimmylegs » Wed Jul 06, 2011 4:20 pm

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Postby CVfactor » Wed Jul 06, 2011 5:42 pm

I don't know why there is such an unwillingness to investigate vitamin D. It seems that the only work being done is by NIH grants on the basic science and a few initial trials from researchers outside of the U.S.

I think the National MS Society has really dropped the ball here. When I first got sick and found out that MS has a latitude gradient and this may be due to sunlight exposure and vitamin D levels, I had to ask myself why isn't this being researched more fully?

It would be a shame if the cure for MS (and many other autoimune diseases) is simply a matter of having the right level of serum 25OHD3. Something that could be taken care of from supplementation that is readily available at any drug store.

Personally, I think there is a revolution waiting to happen in healthcare and Vitamin D is the key.

Here is a good organization that also feels the same way:

http://www.vitamindcouncil.org/
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Postby CVfactor » Fri Jul 08, 2011 5:15 pm

Continuing on with the theory that regulatory Tcells (Tregs) provide a protective role against self reactive immune cells in many types of diseases here is a very recent paper that describes the state of Tregs in ALS or more commonly known as Lou Gehrig's disease.

http://brain.oxfordjournals.org/content/134/5/1293.abstract

"These observations were extended into the amyotrophic lateral sclerosis patient population where patients with more rapidly progressing disease had decreased numbers of regulatory T lymphocytes; the numbers of regulatory T lymphocytes were inversely correlated with disease progression rates. These data suggest a cellular mechanism whereby endogenous regulatory T lymphocytes are immunocompetent and actively contribute to neuroprotection through their interactions with microglia. Furthermore, these data suggest that immunotherapeutic interventions must begin early in the pathogenic process since immune dysfunction occurs at later stages."

So, it appears that Treg dysfunction and/or population reduction is key to many diseases outside of MS.
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Postby CVfactor » Sat Jul 09, 2011 5:05 pm

More information about regulatory T-cells as modulators of diseases besides MS, here is a paper that investigates Treg function in a mouse model of HIV-1 Enchephalitis:

http://www.ncbi.nlm.nih.gov/pubmed/20846730

Treg readily migrated across the blood brain barrier and were retained within virus-induced neuroinflammatory sites. In non-inflamed peripheral tissues (liver and spleen) Treg were depleted. These observations demonstrate that Treg migrate to sites of inflammation where they modulate immune responses.


In my view it appears the key is not the fact that immune cells target the bodies own tissue, it is the fact that the regulatory T cells (Tregs) are failing to shut-down the attack on the self.
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Postby CVfactor » Mon Jul 11, 2011 3:22 pm

It looks like there is a revolution happening in health science at this moment with the discovery of regulatory T-cells and diseases and self tolerance.

Here is a good video discussion Tregs and their application in transplant rejection as well as their role in autoimune diseases.

http://www.youtube.com/watch?v=PYHvVj2qaDE

And here is a video discussion regarding Tregs and Parkinsons disease:

http://www.youtube.com/watch?v=2ZJL5pAGTZo

It looks like Tregs will be the basis for future therapies in preventing many types of disease as well as transplant rejection.
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Postby CVfactor » Tue Jul 12, 2011 5:33 pm

Here is a new paper on vitamin D and MS:

http://www.ncbi.nlm.nih.gov/pubmed/21723567

Abstract
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 (MS) 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 MS. To gain more insight into putative regulatory mechanisms of Vitamin D in MS pathogenesis, we studied 132 Hispanic patients with clinically definite MS, 58 with relapsing remitting MS (RR MS) during remission, 34 RR MS patients during relapse, and 40 primary progressive MS cases (PP MS). Sixty healthy individuals matched with respect to place of residence, race/ethnicity, age and gender served as controls. Levels of 25(OH) Vitamin D and 1,25(OH)(2) Vitamin D, measured by ELISA were significantly lower in RR MS patients than in controls. In addition, levels in patients suffering relapses were lower than during remissions. By contrast, PP MS 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) Vitamin D. 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, VDR expression was induced by 1,25(OH)(2) Vitamin D in both activated and resting cells. Interestingly, T cells were able to metabolize 25(OH) Vitamin D into biologically active 1,25(OH)(2) Vitamin D, since T cells express 1α-hydroxylase constitutively. Finally, 1,25(OH)(2) Vitamin D also increased the expression and biological activity of IDO, triggering significant increase in the number of CD4+CD25+ T regulatory cells. Collectively, these findings suggest that 1,25(OH)(2) VitaminD plays an important role in T cell homeostasis during the course of MS, suggesting correction of its deficiency may be useful during treatment of the disease.


And again, more evidence that Vitamin D promotes Treg cell function/population.
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Re: Vitamin D

Postby NHE » Wed Jul 13, 2011 2:12 am

CVfactor wrote:Here is a new paper on vitamin D and MS:

http://www.ncbi.nlm.nih.gov/pubmed/21723567

...T cells were able to metabolize 25(OH) Vitamin D into biologically active 1,25(OH)(2) Vitamin D, since T cells express 1α-hydroxylase constitutively. Finally, 1,25(OH)(2) Vitamin D also increased the expression and biological activity of IDO, triggering significant increase in the number of CD4+CD25+ T regulatory cells. Collectively, these findings suggest that 1,25(OH)(2) VitaminD plays an important role in T cell homeostasis during the course of MS, suggesting correction of its deficiency may be useful during treatment of the disease.


And again, more evidence that Vitamin D promotes Treg cell function/population.


Here's a good review paper on vitamin D. The full paper is free. It discusses many aspects of the activity of vitamin D so don't be dissuaded by the abstract.

http://www.ncbi.nlm.nih.gov/pubmed/15951480


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Postby CVfactor » Wed Jul 13, 2011 5:51 pm

NHE,

Good find. I hadn't read this paper. I think the important thing to realize is that the active form of vitamin D (1.25 OH2D3)can be generated directly by immune cells.

So, I believe that at the cellular level this is very important for modulation of immunity/autoimmunity at the site of inflamation by regulatory T-cells.

But since the "normal levels" of the form of Vitamin D that is circulating in your blood (25OHD3) from which the active form is derived is based on bone health instead of immune health, there could be a disconnect here.

This is where the problem lies. We need to have recommended blood serum levels based on immune health which seems to be a much higher level than is required for bone health.

I know when I became sick, I found out that my vitamin D level was deficient, but the doctors really didn't think this was a cause of concern.

The NIH and the National MS Society really need to push for more realistic values for vitamin D levels. This would cause food to be fortified with higher values such that vitamin D deficiency could all but be eliminated thus sparing many people from conditions such as MS and related diseases.

Sadly though I don't think this is going to happen unless people start to realize how important this is.
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Postby Dev29 » Thu Jul 14, 2011 8:08 am

I am a bit of lurker here but my main question w/ vitamin d is whether or not it impact men and women equally. I don't have any paper reference handy, but that it doesn't "work" in men or at least not as well.

Does anyone here have any information?
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Postby jimmylegs » Thu Jul 14, 2011 9:46 am

AFAIK it's more about age, skin colour, and amount of clothing and sunscreen use.

i found optimizing my zinc level improved my d3 synthesis/absorption. women tend to be lower in zinc than men.

that's about all i got at the moment :)
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Postby CVfactor » Fri Jul 15, 2011 2:25 pm

Dev29 wrote:I am a bit of lurker here but my main question w/ vitamin d is whether or not it impact men and women equally. I don't have any paper reference handy, but that it doesn't "work" in men or at least not as well.

Does anyone here have any information?


I think the optimum amount to supplement with is different from person to person.

But here is a good graphic showing the relationship between supplementation with Vitamin D3 and your blood serum level:

Image

You can see that blood serum level of 25OHD that is considered "toxic" by many doctors is 250 nmol/L. According to this data, taking 10,000 IU's of vitamin D3/day would raise your blood serum levels to around 200 nmol/L.

However, in a recent high dosage study involving people with MS and vitamin D, the treatment group received an average of 14,000 IU's over a 52 week period with a maximum dosage of 40,000 IU's (I posted this information previously, but I'll post it here again for conveinance):

http://www.ncbi.nlm.nih.gov/pubmed/20427749

And here is a graphic from this paper:

Image

So you can see from the chart in the lower right that the highest levels of 25OHD blood serum for the treatment group ranged from about 250-550 nmol/L for the same dosage of 40,000 IU's.

Personally, I take 40,000 IU's/day and have a 25OHD blood level of 250 nmol/L. I am not recommending that anyone take this amount, but this is what I have to take to reach the lower end of the "toxic" range. Please note: Toxic in conventional medicine means that you become hypercalcemic which means you have too much calcium in your blood. However, the people in the trial had normal calcium levels even though they were supplementing with 1200mg/day. To me, this means that high doses of vitamin D does not cause hypercalcemia, and in my case my blood calcium levels are on the low end of the normal range (9 mg/dL) without supplementation.

So, it is not just a matter of taking a certain amount of vitamin D/day. You have to monitor your blood serum levels. From my own personal point of view I have decided to not believe in conventional medicine and increase my blood serum level to the upper end of normal because there is a lot of evidence that vitamin D prevents auto-immunity by promoting regulatory T-cell development. Since I have been on this dosage, I feel better than I have ever since I became sick and have not had any relapses like I used to. But my situation is anecdotal. We really need to find out what are the optimum blood levels to prevent autoimmunity. Unfortunately this is just starting to happen now and I fear it may take a decade or two before this testing is completed.

Here are the conclusions from the high dose vitamin D study I posted above:

Image
Last edited by CVfactor on Sat Jul 16, 2011 3:52 pm, edited 2 times in total.
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Postby jimmylegs » Fri Jul 15, 2011 2:44 pm

CV can you please shrink those a bit, thanks.

also the amount for each person to supplement does differ, depending on how far they are from optimal.

BUT, dose response also varies among individuals. you can optimize absorption for your age, skin colour, and level of exposure.

take a base line d3 level. select a daily dose for ex amount of time and test again for the amount of increase. helps to keep in mind there's a lag time from exposure to max serum level.

a few years back while zinc deficient i took d3 50,000IU/d x 10d and went from 72 nmol/L to 149 nmol/L. a few years later while zinc replete i took d3 50,000IU/d x 8d and went from 103 nmol/L to 271 nmol/L.

so with replete zinc my dose response to d3 more than tripled. i never megadose the way i used to now. above 250 you get into the zone for increased risk of hypercalcemia (it is hypercalcemia that kills rats when vit d3 is used as rat poison)
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Postby CVfactor » Sat Jul 23, 2011 5:26 pm

Here is a recent review article about Vitamin D and what potential it has in fighting many diseases:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3066777/

Despite the recent expansion in vitamin D research, an immense gap remains in our knowledge of its multiple functions in the variety of cell types where the presence of vitamin D receptors and paracrine production of calcitriol have been established. However, it is now generally accepted that a strong connection between vitamin D and the immune system exists as suggested by several key findings: (a) the presence of VDR in activated human immune cells, (b) the ability of these cells to produce calcitriol, and (c) the ability of calcitriol to inhibit the proliferation of T cells. In addition, it has become increasingly evident in recent years that calcitriol plays a significant role in modulating the function of the immune system. Furthermore, many epidemiological studies strongly suggest that vitamin D deficiency and certain VDR polymorphisms may be linked to immune system related diseases such as multiple sclerosis, SLE, DM type I, alopecia (areata or universalis), and psoriasis.


And to expand a little more about the different forms of Vitamin D in the body, here is a graphic from this paper:

Image

This is a good graphic becuase it shows that many cells in the body produce 1,25(OH)2D3 a.k.a. Calcitriol at the local level from the main circulating form of 25(OH)D3. It is kinda of difficult to distinguish between the three types of Vitamin D because they are all referred to as Vitamin D, but they are distinct from each other.
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Postby CVfactor » Thu Aug 04, 2011 6:03 pm

Here is a recent article that proposes the concept of the biography of the immune system which links infections such as Epstein-Barr with defective regulatory T-cells which are a characteristic of PWMS:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2708340/

The immunoregulatory pathways are based on populations of lymphocytes, termed regulatory T cells (Tregs), in which there is currently considerable interest. In the case of infectious disease, such populations may lead to rapid resolution, the establishment of latent or persistent infection or to tissue damage by autoimmune processes [28]. Accordingly, Tregs have been termed ‘a dangerous necessity’ [29]. This term implies that Tregs are neither ‘good’ or ‘bad’ per se but may, according to the overall pattern of responsiveness, participate in appropriate immune reactions leading to resolution of disease or in inappropriate ones resulting in immunopathology.

The temporal sequence of infections, especially initial and early ones, is crucial to the development of patterns of immune reactivity as prior contacts with other antigens may have induced cross-reactive T-helper cells competing with Tregs. As a consequence Tregs normally induced by the second pathogen may be marginalized or even eclipsed. The latter phenomenon, also known as lateral inhibition, has many parallels in biology, particularly in neurology. The locking of an immune response into an eclipsed state seems to involve an active deletion of clones of T-cells occurring as a result of reinfections or reactivations [28]. In the case of MS, infections such as those with HHV-6 [30, 31] and, possibly, with CP [12, 26] occurring before or at the time of initial or reactivated EBV infection could have such an effect.
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