Does Anyone Know How Iodine Is Involved In Methylation, Please?
- Thread starter Jigsaw
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PeterPositive
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I don't think iodine plays a direct role in the methylation cycle.
However there might be a link with hypothyroidism which can slow down methylation:
https://www.ncbi.nlm.nih.gov/pubmed/10646653
https://www.ncbi.nlm.nih.gov/pubmed/15554351
However there might be a link with hypothyroidism which can slow down methylation:
https://www.ncbi.nlm.nih.gov/pubmed/10646653
https://www.ncbi.nlm.nih.gov/pubmed/15554351
Well, yes, iodine is needed in quantity by the thyroid gland, so hypothyroidism can be caused by lack of iodine, and hypothyroid slows down ALL processes.
I was looking for something that links iodine and B12 specifically, and methylation generally.
I'm on T3 in vast quantity, so hypo-t shouldn't, in theory, be an issue for me, though I suspect it still is (temp still sub-normal amongst other things).
I was looking for something that links iodine and B12 specifically, and methylation generally.
I'm on T3 in vast quantity, so hypo-t shouldn't, in theory, be an issue for me, though I suspect it still is (temp still sub-normal amongst other things).
Indirectly, it can be involved by its relationship to thyroid function.
T4 (thyroxine 4) is needed to convert riboflavin to the active form FAD and FAD is an important cofactor for MTHFR. Low FAD can slow the MTHFR enzyme.
So low iodine can lead to lower functioning thyroid which means lower T4, followed by low FAD which results in decreased activity of MTHFR.
T4 (thyroxine 4) is needed to convert riboflavin to the active form FAD and FAD is an important cofactor for MTHFR. Low FAD can slow the MTHFR enzyme.
So low iodine can lead to lower functioning thyroid which means lower T4, followed by low FAD which results in decreased activity of MTHFR.
@zelda
Hi Zelda, thanks for that
Well, that would certainly explain my inability to convert riboflavin to FMN or FAD - I'm on 100mcg T3 and consequently both my TSH and T4 are practically zero. I take FMN. Riboflavin makes me extremely nauseous.
Mind you, it always has done, and up til 2000, I was still making good amounts of it, just wasn't converting it to T3.
I'm now up to 52.5mg Lugol's. As soon as I hit 50mg, I was able to reduce my T3 by 10mcg, and my hydrocortisone by 10mg - both very big deals for me.
So if I get my thyroid making T4 again by being able to reduce my T3 via iodine therapy, I *should* be able to convert riboflavin. That would be nice
Any thoughts as to non-T4 reasons why I have never been able to convert riboflavin to FMN or FAD?
Thanks again,
J
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Not sure, but here is some good information on riboflavin.
http://lpi.oregonstate.edu/mic/vitamins/riboflavin
There are also some enzymes involved in riboflavin transport, just like for B12 and/or folate (and other B vitamins). Those could be slowed for various reasons although I am not sure they are related to activation necessarily.
Thanks, Zelda!
Ha!
"The conversion of riboflavin into FAD and FMN is impaired in hypothyroidism and adrenal insufficiency (3, 4)"
I'm hypothyroid and adrenally insufficient. Both conditions took over 15 years to get dx'd.
I've been on supra-physiological doses of T3, ditto hydrocortisone, since c.2005 (T3 went from 20mcg to 80mcg) and 2007 when the breast cancer landed (hydro up to 160mg/d at one point, currently 80-100mg, and T3 100mcg), but am still far from well.
Funny how my endo Prof is ignorant of this. And literally every so-called thyroid specialist I've seen, ditto every doctor, consultant, etc. (Sigh.)
Thanks for that, @zelda
. Another piece of my personal puzzle