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
1 common reason for not getting a response to supplementing thyroid
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.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
1 common reason for not getting a response to supplementing thyroid
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