Iron is essential for ability of thyroid hormone to function

[cs3000]

Study highlighting the importance of having good iron levels for peat approach to health. in the peat realm sometimes there's a tilted view against iron as if it's on the same level as a PUFA or something to be avoided, so can be overlooked. (overload toxicity isn't good + trying to fix deficiency can cause damage if approached wrong). but overall cellular energetics is #1 priority for health where iron has important roles

e.g Thyroid hormone is a big key for ensuring the right type of energy production. & if we have iron levels too low thyroid hormone wont work:
Cellular Iron Deficiency Disrupts Thyroid Hormone Regulated Gene Expression in Developing Hippocampal Neurons

Irons relation to thyroid isn't only about iron being needed for conversion of T4 -> T3,
lacking iron = functional hypothyroidism regardless of t3 levels because it causes cells to signal extra T3 export. they recognise lack of iron as less ability to produce energy well so extracellular T3 levels rise and prevents thyroid being used

neuronal-specific iron deficiency reduces thyroid hormone-regulated gene expression, indicative of a functionally abnormal thyroid hormone status, despite normal thyroid hormone availability.

increase in extracellular T3 concentration in iron-deficient neuron cultures suggesting decreased T3 import or increased export. SLC16A2 (Slc16a2/Mct8) has been shown to also function as a T3 exporter (42); thus, increased expression of Slc16a2 as a result of iron deficiency may instead be indicative of a cellular response to decrease the intracellular availability of T3, in order to match the decreased metabolic potential of available iron and prevent oxidative stress.

Since neuronal iron deficiency decreases Crym expression and increases Slc16a2 expression, this provides further support that low neuronal iron status may result in the cell increasing T3 efflux to reduce overall thyroid hormone function, including genomic and non genomic functions, including mitochondrial metabolism and cytos keletal dynamics required to grow developing neurons

in vivo https://www.sciencedirect.com/science/article/abs/pii/S0271531705802088 thyroid hormone binding by nuclear receptors tended to be lower in ID rats when compared to CN controls. These results suggest that the metabolism of T4 is altered in iron deficiency and that ID rats are functionally hypothyroid.

1 common reason for not getting a response to supplementing thyroid

 

[NewACC]

Study highlighting the importance of having good iron levels for peat approach to health. in the peat realm sometimes there's a tilted view against iron as if it's on the same level as a PUFA or something to be avoided, so can be overlooked. (overload toxicity isn't good + trying to fix deficiency can cause damage if approached wrong). but overall cellular energetics is #1 priority for health where iron has important roles

e.g Thyroid hormone is a big key for ensuring the right type of energy production. & if we have iron levels too low thyroid hormone wont work:
Cellular Iron Deficiency Disrupts Thyroid Hormone Regulated Gene Expression in Developing Hippocampal Neurons

Irons relation to thyroid isn't only about iron being needed for conversion of T4 -> T3,
lacking iron = functional hypothyroidism regardless of t3 levels because it causes cells to signal extra T3 export. they recognise lack of iron as less ability to produce energy well so extracellular T3 levels rise and prevents thyroid being used

in vivo https://www.sciencedirect.com/science/article/abs/pii/S0271531705802088 thyroid hormone binding by nuclear receptors tended to be lower in ID rats when compared to CN controls. These results suggest that the metabolism of T4 is altered in iron deficiency and that ID rats are functionally hypothyroid.

1 common reason for not getting a response to supplementing thyroid

all these studies are even more interesting if you consider that often people here neglect to eat red meat or do it rarely, as well as chicken liver due to the fictitious excess of PUFAs in it, which is probably the funniest misconception here on the forum, since chicken liver contains a VERY small amount of both fat and PUFAs in it, no more than 2g for a VERY large portion of chicken liver, something like 400-500g, which is probably even dangerous to eat due to the excess amount of protein and iron. Why am I writing all this? Well, to the point that Ray Peat's diet without a daily liver is a perfect example of a diet with sometimes critically low iron levels, so I think that the problem of low iron intake is really relevant for many Peat's dieters

 

[cs3000]

all these studies are even more interesting if you consider that often people here neglect to eat red meat or do it rarely, as well as chicken liver due to the fictitious excess of PUFAs in it
Ray Peat's diet without a daily liver is a perfect example of a diet with sometimes critically low iron levels, so I think that the problem of low iron intake is really relevant for many Peat's dieters

yeah, (even liver would still leave many on low intake i think when keeping vit a levels from it in balance)
and we already lose ~1.5mg iron naturally daily (1mg - 2.5mg range). women higher end because of menstruation but that's balanced by ~2x higher absorption rates.
& ppl only absorb a minority % of dietary iron. so most people who are on a not "high" dietary intake are constantly playing catchup and probably get hit metabolically or are on their way to. its the most common deficiency in the world.
Even in pregnancy where absorption goes up, a diet high in absorbable meat iron doesn't or barely covers the typical iron loss at first. maybe its different if someone's estrogen is so high it puts them in the 2nd - 3rd trimester level or have hemochromatosis but these are exceptions

As was also discussed previously, iron absorption from a diet of very high iron bioavailability has been estimated to be 0.4, 1.9, and 5.0 mg/d during the first, second, and third trimesters, respectively

so i think the overload problem is very unlikely to be a food problem. its slow as **** to raise when iron deficient im not even sure we can do it effectively through diet alone where riboflavin/folate isnt the problem. as an intake problem: through supplements, or dodgy industrial fortified forms, or very deficient in vitamin e or lacking copper so have low iron mobilization high in some cells like ray mentioned.