Riboflavin and Vitamin D

Asklipia

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Along the lines of the B12-B2 balance question I think the B2-D interaction could be as important.

I wonder in which way supplementation with vitamin D could create a riboflavin deficiency. This is something I had noticed on myself but could find no explanation for.

It has to do with supplementation tough, because it never happened to me sunbathing. So there must be some truth in the assertion that what you get with UVs is not what you get with a pill.

I was not able to get information on how cholecalciferol supplementation depletes riboflavin, but obviously it is available somewhere since Dog Person mentioned it and seems to have communicated with Rich privately on the subject.
The topic I think is important, given the number of people taking D3 supplements.
It could also be a way to find out in which way supplementation in D3 differs from sunbathing. A question I believe has been pondered with no answer yet.

All your ideas are welcome!
Thanks,
Asklipia
 

adreno

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I am interested is this also, but haven't been able to find any references explaining why D would deplete B2.

I can understand why vitamin C should be avoided though, as it increases iron absorption, which we do not want, if our livers are already overloaded.

Sunlight destroys riboflavin in foods, but I am not sure about the effects of riboflavin in the body.

This article claims that excess riboflavin is toxic when the body is exposed to sunlight:
http://www.smart-publications.com/articles/excess-vitamin-B2-riboflavin-can-be-toxic
 

justy

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I am interested is this also, but haven't been able to find any references explaining why D would deplete B2.

I can understand why vitamin C should be avoided though, as it increases iron absorption, which we do not want, if our livers are already overloaded.

Sunlight destroys riboflavin in foods, but I am not sure about the effects of riboflavin in the body.

This article claims that excess riboflavin is toxic when the body is exposed to sunlight:
http://www.smart-publications.com/articles/excess-vitamin-B2-riboflavin-can-be-toxic
Hi Adreno, i'm not sure where the idea comes from that our livers are overloaded with iron - i have seen this mentioned on a couple of threads but not sure what its all about. I actually have a big problem with little or no iron stores - a persistently very low ferritin. perhaps i have missed something (im not very scientifically minded) can you explain please?
Best wishes, Justy.
 

adreno

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Hi Adreno, i'm not sure where the idea comes from that our livers are overloaded with iron - i have seen this mentioned on a couple of threads but not sure what its all about. I actually have a big problem with little or no iron stores - a persistently very low ferritin. perhaps i have missed something (im not very scientifically minded) can you explain please?
Best wishes, Justy.
According to christine, we have low serum ferritin because iron is accumulated in our livers. This is because of a B2, and possibly manganese, deficiency.
 

justy

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According to christine, we have low serum ferritin because iron is accumulated in our livers. This is because of a B2, and possibly manganese, deficiency.
Yes, i know this is according to Christine, but i am interested to know where her inforamtion came from. To actually see a source or something like that. Why would iron accumulate in our livers and get stuck there and not be available to be utilised. By what mechanism does this happen? Can and has it been shown that a B2 and Manganese deficiency can cause this.? I'm happy if that is the case as i have had persisitently low Ferritin for years and also have very low Manganeses (from a blood lab test) Supplementing with Manganese has so far not helped me, although the research i have read suggests that supplementing with manganese can improve my low iron status (the research doesnt mention releasing stores form the liver though, but that managnese helps to make RBC in the bone marrow.
I just am looking for some clarity, rather than the word of one member (who may be correct, but i cant just take someones word for it who i dont know)
All the best, Justy.
 

Rand56

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According to Christine, it's not only low ferritin is the result of iron accumulating in our liver but also high ferritin. This is what she said....

"If you have a high ferritin it is reflective that you have very high stores of iron in the liver. Same can be true of a very low ferritin - which I had and was actually more serious than a high ferritin. The hair charts show that the liver is malfunctioning at manufacturing adquate amounts of the carrier protein (transferrin) for iron and the carrier proteins for copper (ceruloplasmin, hepcidin) and binding those minerals to them."

It's from post # 19 in this thread....

http://forums.phoenixrising.me/showthread.php?16901-B2-I-love-you!/page2
 

aprilk1869

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I've not had a chance to go through these properly but I'm posting them now for others to look at..

Genetic evidence that the human CYP2R1 enzyme is a key vitamin D 25-hydroxylase
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC419671/?tool=pmcentrez

Dual metabolic pathway of 25-hydroxyvitamin D3 catalyzed by human CYP24
http://www.ncbi.nlm.nih.gov/pubmed/11012668

A tricistronic human adrenodoxin reductase-adrenodoxin-cytochrome P450 27A1 vector system for substrate hydroxylation in Escherichia coli.
http://www.ncbi.nlm.nih.gov/pubmed/21621619

Mitochondrial CYP enzymes use adrenodoxin, a flavoprotein, and adrenodoxin reductase, an iron-sulfur protein (Ziegler et al., 1999), to transfer electrons whereas endoplasmic reticulum CYP enzymes use NADPH-cytochrome P450 reductase, a flavoprotein (Gutierrez et al., 2003)
http://webcache.googleusercontent.c...=3+&cd=3&hl=en&ct=clnk&gl=uk&client=firefox-a

Remember that flavoprotein is made from riboflavin.
 

adreno

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Great finds, april. I don't know much about how vitamin D is converted in the body, but I gather the studies show that riboflavin is needed for this process. It would be great if you could make a short summary, when you have time.
 

SaraM

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Vitamin D caused Vit A deficiency and gritty eyes. 25,000 iu A helped with the eyes within a few days. Vitamin A in multi was not enough. Did not do a blood test for A, but will do it soon. Muscle pain gets worse with D.
 

aprilk1869

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Metabolism of vitamin D: current status

HF DeLuca

There has been much progress in our understanding of the metabolism of vitamin D. It is now clear that vitamin D3 can be produced in the skin or ingested in the diet. It accumulates very rapidly in the liver where it undergoes 25-hydroxylation, yielding 25-OH-D3, the major circulating metabolite of the vitamin. 25-OH-D3 proceeds to the kidney where it undergoes one of two hydroxylations. If there is a biological need for calcium or for phosphate the kidney is stimulated to convert 25-OH-D3 to the 1,25-(OH)2-D3, a calcium and phosphate mobilizing hormone. If, however, the animal has sufficient supplies of calcium and phosphate, the l-hydroxylase is shut down and instead the 25-OH-D3 is converted to a 24,25-(OH)2D3. The role of the 24,25-(OH)2D3 remains unknown; it may be an intermediate in the inactivation-excretion mechanism. 1,25- (OH)2D3 proceeds to the intestine where it stimulates intestinal calcium transport and intestinal phosphate transport. It also stimulates bone calcium mobilization and probably has other effects yet to be discovered in such tissues as muscle. The 25-OH-D3-l-hydroxylase, which is located exclusively in renal mitochondria, has been shown to be a three component system involving a flavoprotein, an iron-sulfur protein (renal ferredoxin), and a cytochrome P-450. This system has been successfully solubilized, the components isolated, and reconstituted. The 24-hydroxylase, however, has not yet been thoroughly studied. 1,25-(OH)2D3 is necessary for the appearance of the 24- hydroxylase; parathyroid hormone represses 24-hydroxylation. It is possible that the 24-hydroxylase represents the major regulated enzyme, so that its presence or absence may determine whether 1,25-(OH)2D3 is produced. Two metabolic pathways for 1,25-(OH)2D3 are known, conversion by the 24-hydroxylase to 1,24,25-(OH)3D3, and conversion of 1,25- (OH)2D3 to an unknown substance. In the latter instance, there occurs loss of a side chain piece, including at least one of the 26 and 27 carbons. Whether 1,25-(OH)2D3 must be metabolized further before it carries out all of its functions has yet to be established. The primary excretion route of vitamin D3 is via the bile into the feces. Urinary excretion appears small in magnitude and no excretion products have yet been identified positively. Much remains to be learned concerning the metabolism and function of vitamin D and its metabolites. This should therefore, prove to be a fruitful area of investigation for many years to come, especially since 1,25-(OH)2D3, 25-OH-D3, and lalpha-OH-D3 have been shown to be effective in a number of metabolic bone disease states.

http://www.ajcn.org/content/29/11/1258.abstract
 

dannybex

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Hello, is there anyone here who can explain me what are vitamin B2 deficit symptoms?

I have very low blood vitamin D levels BUT I can't use supplement.
These are the symptoms I experience with 2000 U.I. of vitamin D3 (cholecalciferol):
-palpitation
-fasciculation throughout the body
-depersonalization at night
-overactive mind (thought that continue without my own control) at night
-tight chest and neck

Since I have also bad anxiety without b-complex and zinc, is there any link?