healthunlocked.com/thyroidu... ~ discussing " Selenium, Iodine and Iron–Essential Trace Elements for Thyroid Hormone Synthesis and Metabolism" by Josef Köhrle Berlin, Germany.
msdmanuals.com/en-gb/profes... /professional/endocrine-and-metabolic-disorders/thyroid-disorders/hyperthyroidism "Iodine in pharmacologic doses inhibits the release of T3 and T4 within hours and inhibits the organification of iodine, a transitory effect lasting from a few days to a week, after which inhibition usually ceases. Iodine is used for emergency management of thyroid storm, for hyperthyroid patients undergoing emergency nonthyroid surgery, and (because it also decreases the vascularity of the thyroid) for preoperative preparation of hyperthyroid patients undergoing thyroidectomy. Iodine generally is not used for routine treatment of hyperthyroidism. The usual dosage is 2 to 3 drops (100 to 150 mg) of a saturated potassium iodide solution orally 3 times a day or 4 times a day or sodium iodide in 1 L 0.9% saline solution 0.5 to 1 g IV given slowly once a day."
"Excessive Iodine Promotes Pyroptosis of Thyroid Follicular Epithelial Cells in Hashimoto's Thyroiditis Through the ROS-NF-κB-NLRP3 Pathway" ~ study which links Hashimotos with too much iodine “in vitro”
sciencedirect.com/science/a... .... Matthew Kim, Paul Ladenson, in Goldman's Cecil Medicine (Twenty Fourth Edition), 2012
"THYROID.
Thyroid Hormone Transport and Metabolism
"More than 80% of the T3 present in target tissues is derived from T4 through the action of deiodinase enzymes that convert T4 to both T3, which contributes to the pool of T3 in the circulation, and biologically inactive reverse T3. The activity of deiodinase may be inhibited by systemic illness; iodide-containing compounds, including amiodarone and radiocontrast agents; glucocorticoid therapy; and selenium deficiency. Type 2 deiodinase is present in the pituitary gland and brain. Type 3 deiodinase is present in the glial cells of the central nervous system. It deactivates thyroid hormone by inner ring monodeiodination, a process that converts T4 to inactive reverse T3 (rT3) and T3 to inactive diiodothyronine (T2). Type 3 deiodinase is also expressed in placenta, accounting for the increased thyroxine dose requirement in pregnant women."
If you are referring to the reference I made to Japanese intake of iodine Tatty, I read that on Dr Myhill's website somewhere but unfortunately I haven't been able to locate it again although it did stick in my pile of sawdust at the time as both goitres and bc interested me greatly. Perhaps you may have better luck in finding it as you have a pile of straw which must be superior to sawdust😁
There are several different kinds of iodine supplement. Some forms of iodine are disinfectants rather than supplements. Wikipedia has a long list of possible formulations.
There is a relationship between selenium and iodine. People struggling to tolerate any iodine at all may be low in selenium. SeasideSusie recommended this selenium supplement :
This paper has a section on "Amiodarone and Hypothyroidism". It's worth reading the whole section (copied below) if you're worried about iodine (my bolding) :
"Amiodarone is an iodine-rich benzofuranic compound that is used to manage cardiac arrhythmias.13 It contains about 37% iodine by weight,14 and a 200-mg dose exposes the patient to about 300 times the recommended daily allowance.15,16 Due to its lipophilic nature, it concentrates in several tissues and organs, including the thyroid gland. Its active dealkylated metabolite, desethylamiodarone, tends to have a half-life of about 57 days, thus effects can be long-lasting even after discontinuation.16 Amiodarone-induced thyroid dysfunction could be secondary to iodine load or intrinsic effects of amiodarone itself. The iodine load from amiodarone can result in amiodarone-induced hypothyroidism (AIH) by inhibiting the oxidation of iodine, known as the Wolff-Chaikoff effect.17 This is particularly the case in patients with underlying or preexisting thyroid disease such as goiter or autoimmune thyroid disease.
Amiodarone by itself can also affect deiodinase activity.In vivo, it inhibits deiodinase-1 activity and pituitary deiodinase-2 activity, resulting in high T4, high reverse T3, and low T3. This may spur an initial increase in TSH that often returns to baseline in 2 to 3 months. With long-term treatment, TSH usually normalizes with total and free T4 and reverse T3 levels that remain slightly elevated. Early AIH may be present in 10% to 20% of patients treated with amiodarone, whereas the incidence with long-term treatment is often lower, from 5% to 10%. AIH is noted to be more frequent in iodine-sufficient areas of the world,18 and the presence of thyroid autoantibodies is associated with an increased likelihood of developing AIH. There is also an understanding that amiodarone may hasten the pathogenesis of Hashimoto thyroiditis. Since AIH manifests as primary hypothyroidism, diagnosis is similar to primary hypothyroidism, as is treatment with levothyroxine replacement (Figure 2).16
I just wanted to point out that I kept reading "AIH" as "Autoimmune Hypothyroidism" - but it isn't - in this paper it is "Amiodarone-Induced Hypothyroidism"
The reference to the Wolff-Chaikoff effect drew me to this article on wikipedia.
My personal opinion is that I would want a different treatment than Amiodarone for cardiac arrhythmia, if one exists, rather than risk my hypothyroidism getting worse. There are other alternatives, according to this link in the British National Formulary (BNF), but I haven't investigated them.
There is another possible result of taking high doses of iodine, caused by something known as the Jod-Basedow phenomenon - iodine-induced hyperthyroidism.
So, when it comes to iodine it seems we toss a coin as to whether we become hyperthyroid or hypothyroid. I haven't done enough reading to work out if one can foretell the result of iodine intake on an individual.
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Peripheral Thyroid Hormone Conversion and Its Impact on TSH and Metabolic Activity: 
