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re the omission of salad related to potential interference with iron absorption. can you clarify what it was specifically about salad that had you concerned?http://www.healthtestingcenters.com/vitamin-d-1.aspx. (Incidentally, that's the online lab service I used).Concentration of vitamin D 25-hydroxy is the best indicator of your vitamin D status. It reflects vitamin D produced and obtained by your body and has a half-life of 15 days. However, vitamin D 25-hydroxy levels do not indicate the amount of vitamin D stored in your bodys tissues. Vitamin D, 1, 25-hydroxy is a better indicator of stored vitamin D but because it has a short half-life of 15 hours levels in the blood do not typically decrease until an individuals vitamin D deficiency is severe.
I'll try to do some 'splainin'.Anonymoose wrote:'Splain this...http://www.healthtestingcenters.com/vitamin-d-1.aspx. (Incidentally, that's the online lab service I used).Concentration of vitamin D 25-hydroxy is the best indicator of your vitamin D status. It reflects vitamin D produced and obtained by your body and has a half-life of 15 days. However, vitamin D 25-hydroxy levels do not indicate the amount of vitamin D stored in your bodys tissues. Vitamin D, 1, 25-hydroxy is a better indicator of stored vitamin D but because it has a short half-life of 15 hours levels in the blood do not typically decrease until an individuals vitamin D deficiency is severe.
So what do serum vitamin d levels really tell us? Is it just how much vitamin d is being let out of storage? Are we really deficient if we have plenty of storage? Where is all of that vitamin d going if our blood levels don't budge? Could my high calcitriol be a result of maxed out storage? Did my liver/kidneys change the d to calcitriol to dump the excess? Does anyone really know what is going on there since we can't measure vitamin d stores? And if we can't measure stores, how can they make that statement about 1,25oh being the best indication of stores???
Blerg! How can anyone make any recommendations if they really don't know what's going on?
Source URL: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3497336/
PMID: 23202962
DOI: 10.3390/ijms131013461
Journal Title: International Journal of Molecular Sciences
Journal Date: 2012
Journal Issue: 10
Journal Volume: 13
Journal First Page: 13461
Abstract URL: http://www.ncbi.nlm.nih.gov/pmc/article ... t=abstract
Article Title: Effect of High-Dose Vitamin D3 Intake on Ambulation, Muscular Pain and Bone Mineral Density in a Woman with Multiple Sclerosis: A 10-Year Longitudinal Case Report
Article Authors: Barbara M. van Amerongen, François Feron
2.1.3. Serum 1,25(OH)2D
The NR of 1,25(OH)2D is 50–180 pmol/L. Serum 1,25(OH)2D fluctuated between 55 and 255 pmol/L. On four out of nine occasions 1,25(OH)2D reached levels above 180 pmol/L, the URL.
From March to July 2009, the subject was supplemented four times a day with 333 mg elemental calcium (including magnesium, zinc and copper). The serum level of 1,25(OH)2D declined by 46% (from 119 to 55 pmol/L) (Table 1 and Figure 1b).
So, your high levels of calcitriol would be the result of low phosphorous levels, according to THE book of Vitamin D, Dietary Reference Intakes for Calcium and Vitamin D.Low serum phosphorus levels stimulate calcitriol synthesis, whereas high serum phosphorus levels inhibit it.
http://www.ncbi.nlm.nih.gov/books/NBK56061/
My phosphorus is normal. 3.1 mg/dL range 2.5-4.5. I just need to leave it alone for a while and retest to get a sense for what is really happening rather than torture myself with all this guessing. Vitamin d never did this to me before so I think things are in flux.Squeakycat wrote:So, your high levels of calcitriol would be the result of low phosphorous levels, according to THE book of Vitamin D, Dietary Reference Intakes for Calcium and Vitamin D.Low serum phosphorus levels stimulate calcitriol synthesis, whereas high serum phosphorus levels inhibit it.
http://www.ncbi.nlm.nih.gov/books/NBK56061/
On the other question, calcitriol is NOT stored in cells as suggested by the source you cited.
Most vitamin D is stored in adipose tissue and half of that is in the unaltered form, not even 25(OH)D3, the converted, storage form. The source of this information is quite old, but PubMed doesn't show any more current updates on this so I assume it is considered to be definitive.
Source URL: http://www.ncbi.nlm.nih.gov/pmc/article ... 76/?page=8
PMID: 4322721
DOI: 10.1172/JCI106538
Journal Title: Journal of Clinical Investigation
Journal Date: March 1971
Journal Issue: 3
Journal Volume: 50
Journal First Page: 679
Abstract URL: http://www.ncbi.nlm.nih.gov/pmc/article ... t=abstract
Article Title: Deposition in and release of vitamin D3 from body fat: evidence for a storage site in the rat
Article Authors: Saul J. Rosenstreich, Clayton Rich, Wade Volwiler
From her paper, it appears she continued Vitamin D supplementation, but added the others.Anonymoose wrote:Hi squeaky,
Thanks! I was trying that approach but with vitamin d too. I couldn't do 1200iu d, 400mg calcium, 400mg mag and some other nutrients like zinc without causing pain. Did she supplement the calcium combo while completely stopping d supps? 1,25OH is also supposed to shut down pth...I'm tempted to test that level too.
I think that quote meant that 1,25OH level is a better indication of vitamin d stores, not that 1,25OH is stored. I've read d3 is a better measure too though. I've also dug up a page that claims the high calcitriol to low d ratio seen in ms may be protective.
http://bacteriality.com/2009/08/10/iom/. It's not well supported...but neither are the theories pushing higher vitamin d levels (as far as I can tell).
I don't think the Blaney study on which the article you quote says that high calcitriol to D3 levels is protective. It simply says that calcitriol may be a better marker of active disease state on the theory that degradation of calcitriol is blocked by a bacterial infection:Anonymoose wrote:I've also dug up a page that claims the high calcitriol to low d ratio seen in ms may be protective.
http://bacteriality.com/2009/08/10/iom/. It's not well supported...but neither are the theories pushing higher vitamin d levels (as far as I can tell).
In the IOM Vitamin D and Calcium book cited earlier, there is a very striking chart that shows mortality rates decrease with increasing levels of 25(OH)D3 up to a point and then begin rising slightly, but still FAR below the mortality rate of low 25OH levels. There is no question that higher levels are better, but there may well be an upper limit above which there is less benefit. They were using this chart which is based on a collection of studies which they deemed valid to prove that high levels were a problem, even though that is NOT what the chart shows."Results showed a strong positive association between these autoimmune conditions and levels of 1,25-D >110 pmol/L. However, there was little association with vitamin D deficiency or the other inflammatory markers, meaning that the results challenge the assumption that serum levels of 25-D are a sensitive measure of the autoimmune disease state."
Source URL: http://www.ncbi.nlm.nih.gov/pubmed/19758177
PMID: 19758177
DOI: http://dx.doi.org/10.1111/j.1749-6632.2009.04875.x
Journal Title: Annals of the New York Academy of Sciences
Journal Date: Sep 2009
Journal Volume: 1173
Journal First Page: 384-90
Abstract URL: http://www.ncbi.nlm.nih.gov/pubmed/1975 ... t=abstract
Article Title: Vitamin D metabolites as clinical markers in autoimmune and chronic disease.
Article Authors: Greg P Blaney,Paul J Albert,Amy D Proal
It follows that any substance that slows the innate immune response will decrease this battle between man and microbe, causing the patient to feel better. The more the immune response is slowed, the greater the decrease in inflammation and inflammatory markers. But while such measures can make the patient appear as if they are getting better for years, ultimately the bacteria causing their disease are able to spread much more easily and exacerbate the disease state over the long-term.
Our molecular and clinical data shows that 25-D, like the pathogens we describe above, binds the Vitamin D Receptor and slows its activity.[1] Since the VDR largely controls the innate immune response, increasing 25-D levels could easily display the pattern of immunosuppression described above. This begs the question – is 25-D a miracle curative substance or simply an excellent palliative?
We have found that when 1,25-D is high, the vitamin D feedback pathways naturally downregulate levels of 25-D. This means that what is now viewed as “deficiency” could simply be a result of the chronic disease process. Under such circumstances, allowing people to create extra 25-D by raising the DRI is not only useless but harmful.
Well, that's what I tried and it didn't work! LolSqueakycat wrote:From her paper, it appears she continued Vitamin D supplementation, but added the others.Anonymoose wrote:Hi squeaky,
Thanks! I was trying that approach but with vitamin d too. I couldn't do 1200iu d, 400mg calcium, 400mg mag and some other nutrients like zinc without causing pain. Did she supplement the calcium combo while completely stopping d supps? 1,25OH is also supposed to shut down pth...I'm tempted to test that level too.
I think that quote meant that 1,25OH level is a better indication of vitamin d stores, not that 1,25OH is stored. I've read d3 is a better measure too though. I've also dug up a page that claims the high calcitriol to low d ratio seen in ms may be protective.
http://bacteriality.com/2009/08/10/iom/. It's not well supported...but neither are the theories pushing higher vitamin d levels (as far as I can tell).
Hard to read the quote in any other way: "However, vitamin D 25-hydroxy levels do not indicate the amount of vitamin D stored in your bodys tissues. Vitamin D, 1, 25-hydroxy is a better indicator of stored vitamin D . . ."
Both vitamin D3 and calcitriol suppress PTH in large doses. This is why calcitriol is used to manage calcium levels in kidney failure.
Right. Blaney was a joint study with Amy Proal, but your reference is to the Marshall hypothesis that it is all bacterial, we just can't see the bacteria and vitamin D supplementation is harmful in the long run.Anonymoose wrote:I wasn't speaking of the Blaney study. I was referring to the ideas of the authors of the page.It follows that any substance that slows the innate immune response will decrease this battle between man and microbe, causing the patient to feel better. The more the immune response is slowed, the greater the decrease in inflammation and inflammatory markers. But while such measures can make the patient appear as if they are getting better for years, ultimately the bacteria causing their disease are able to spread much more easily and exacerbate the disease state over the long-term.
Our molecular and clinical data shows that 25-D, like the pathogens we describe above, binds the Vitamin D Receptor and slows its activity.[1] Since the VDR largely controls the innate immune response, increasing 25-D levels could easily display the pattern of immunosuppression described above. This begs the question – is 25-D a miracle curative substance or simply an excellent palliative?We have found that when 1,25-D is high, the vitamin D feedback pathways naturally downregulate levels of 25-D. This means that what is now viewed as “deficiency” could simply be a result of the chronic disease process. Under such circumstances, allowing people to create extra 25-D by raising the DRI is not only useless but harmful.
This inflammatory response is being induced by the cells attacked by the bacteria. For that to happen, calcitriol has to be able to act through VDRs to initiate the pro-inflammatory response. That tells me the VDRs are actually working or there would be no inflammatory response.Emerging molecular evidence suggests that symptomatic improvements among those administered vitamin D is the result of 25-D's ability to temper bacterial-induced inflammation by slowing VDR activity. While this results in short-term palliation, persistent pathogens that may influence disease progression, proliferate over the long-term.