How does low T4 affect B2 transport for those of us on T3 meds?

Gondwanaland

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I'm remembering a well-attended discussion on B2 and its ability to release copper from the liver. Do you remember that, Izzy?
I don't, but a couple of days ago I took my low dose B complex which contains two miligrams of B2 and a few hours later it went ALL down the toilet, my pee was very yellow. I think it means I am currently not able to utilize it

I re-read a few old posts recently and @Asklipia reported that taking Manganese with B2 prevented loss of B2 in the urine.

My concerns about Mn right now are

  • I might be intolerant to it right now - the last time I took it I had unpleasant joint issues (felt like joint weakening?)
  • I read that Mn blocks uric acid elimination (my serum uric acid is currently sky high)
 

Gondwanaland

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Cellulose! It's in so many pills. Last year the doc had me try compounded T3 in a slow-release formula. The slow-release agent was a combination of cellulose and MCC (micro-crystalline cellulose). The stuff went through me without releasing the T3, :rolleyes::lol:. I actually got more hypo symptoms on it, and a gut-ache.

But it antagonizes copper, too. Who knew?
I bet it is in my thyroid caps. I will have to check with the pharmacist. I will have to get a medical order to be able to change the excipients in my thyroid replacement :ill:
 

BadBadBear

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I take the following:
7.5mcg Cytomel every day
one-half of a 15mg Armour tablet once every FOUR days. This is equivalent to 1.125mcg T3 plus 12.5mcg T4

T4 has a much longer half-life than T3, about 7 days, so in my case with this small dose, it works out OK.
Ooh, I am going to try subbing out my PM half tab of T3 for half of an NDT tab every 4 days or so. I like that idea a lot! Maybe an occasional micro-dose will be well tolerated and helpful. :)
 

pattismith

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Well, this shows how good my memory is ;). I posted the above in 2015 when I was trying to find out whether T3 will do what T4 does in B2 conversion! Here is the quote I posted:

"Riboflavin is the precursor of FMN and FAD, which are implicated in energy metabolism and electron transfer pathways. The conversion of riboflavin into FMN and FAD is catalyzed by riboflavin kinase and FMN adenylyltransferase (EC 2.7.7.2) in the presence of ATP and Zn2+ (30). T3 enhances riboflavin kinase activity (10, 13). The low T3 concentrations observed in PEM might be responsible for a reduction in riboflavin kinase activity, which would give rise to an insufficient conversion of riboflavin into its cofactors. Zinc deficiency, which was described previously in severely malnourished children (31, 32), might also be implicated in the impairment of riboflavin conversion into its cofactors. Along with the thyroid hormone concentrations observed in groups S and C, estimation of energy and zinc intakes in severely malnourished children (group S) and moderately malnourished children (group C) might help explain the observed riboflavin concentrations in group S.
Concentrations of riboflavin and related organic acids in children with protein-energy malnutrition"

Note: PEM = Protein-energy malnutrition
Note: Zn2+ is a cofactor!
Note: in the presence of ATP (Gaaaaah :aghhh:, maybe that's what's limiting our conversion.)
Thank you so much for your investigations !