Good to see some more research on these issues. I suspect a lot of the standard picture of selenium and iodine with respect to thyroid wellness requires much verification and a fair bit of revision.
The continuing problem is identifying what needs to be done - and how to achieve appropriate levels of all the nutrients together - without excesses of some.
Obviously needs care in translation from mice to men. [1]
[1] Used for mild humour - not literally.
Nutrients . 2021 Oct 25;13(11):3773.
doi: 10.3390/nu13113773.
The Nutritional Supply of Iodine and Selenium Affects Thyroid Hormone Axis Related Endpoints in Mice
Selenium and iodine are the two central trace elements for the homeostasis of thyroid hormones but additional trace elements such as iron, zinc, and copper are also involved. To compare the primary effects of inadequate intake of selenium and iodine on the thyroid gland, as well as the target organs of thyroid hormones such as liver and kidney, mice were subjected to an eight-week dietary intervention with low versus adequate selenium and iodine supply. Analysis of trace element levels in serum, liver, and kidney demonstrated a successful intervention. Markers of the selenium status were unaffected by the iodine supply. The thyroid gland was able to maintain serum thyroxine levels even under selenium-deficient conditions, despite reduced selenoprotein expression in liver and kidney, including deiodinase type 1. Thyroid hormone target genes responded to the altered selenium and iodine supply, whereas the iron, zinc, and copper homeostasis remained unaffected. There was a notable interaction between thyroid hormones and copper, which requires further clarification. Overall, the effects of an altered selenium and iodine supply were pronounced in thyroid hormone target tissues, but not in the thyroid gland.
Thanks for posting So would this suggest supplementing with selenium and perhaps copper too? I know we get iodine in thyroxine so presumably not necessary?
I don't think you can take this paper as supporting any copper supplementation - just raising questions. Aside from anything else, mice really are different.
this seems to be saying that selenium deficiency reduces dio1 activity in liver and kidney , but doesn't reduce dio1 activity in thyroid tissue. (because the thyroid takes the selenium that is available first, if it is in short supply)
Confirming that having enough selenium is very important for T4 to T3 conversion in those who have absent (defunct ?) thyroid gland
from "discussion"
" The liver and to some extent also the kidney play crucial roles in the peripheral metabolism of TH, but also for selenium distribution and excretion.
Approximately 30 to 40% of the extrathyroidal T3 production originates from these two organs [52].
In this context, however, another characteristic emerges. Whereas the supply of selenium to the thyroid, like to the brain or testis, is maintained, the selenium content in the liver and kidney decreases faster in the case of persistently low selenium supply, according to the organ hierarchy of selenium [53].
The liver is thereby classified as more susceptible to selenium deficiency compared to the kidney [54]. Although the selenium content per mg of tissue is higher in the kidney, the difference in selenium content between adequately and deficient animals was much more pronounced in the liver (Figure 2C,D).
This was also reflected by a stronger decrease in Gpx (16.6- vs. 3.0-fold) and Txnrd activities (2.8- vs. 1.6-fold) in liver compared to the kidney.
In general, the deiodinases are high in the hierarchy of selenoproteins [12,55].
Accordingly, thyroidal Dio1 activity was maintained independent of the selenium supply (Figure 1C). In the liver and kidney, Dio1 activity was reduced in selenium-deficient mice (Figure 3A,B). As Dio1 mRNA levels were not affected this is most probably a translational effect due to limited selenium availability and is in accordance with literature describing the organ-specific effects of severe selenium deficiency [56]. "
I won't have time to read this as I need to prioritise my work (including sorting out the heating at home!). I'm suspicious of experiments in rodents as they often induce deficiency levels that we don't see in humans, at least in the developed world. Years ago I saw a paper that looked at selenium and iodine deficiency in central Africa. Given the low levels of iodine there were remarkably few cases of cretinism. This was due to the concurrent selenium deficiency which by reducing deiodinase conserved T4 which was able to cross the placenta and keep the babies reasonably euthyroid. I've tried to find this paper a few times with no luck.
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Has anyone managed thyroid hormone replacement related raised blood sugar levels successfully?
Blood Test for vits (and thyroid)
