Mega Dosing Iodine = Bad, Destroys Thyroid Tissue Permanently

Amazoniac

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- Potassium iodide - Wikipedia

"Potassium iodide can be conveniently prepared as a saturated solution, abbreviated SSKI. This method of delivering potassium iodide does not require a method to weigh out the potassium iodide so it can be used in an emergency situation. KI crystals are simply added to water until no more KI will dissolve and instead sits at the bottom of the container. With pure water, the concentration of KI in the solution depends only on the temperature. Potassium iodide is highly soluble in water so SSKI is a concentrated source of KI. At 20 degrees Celsius the solubility of KI is 140-148 grams per 100 grams of water. Because the volumes of KI and water are approximately additive, the resulting SSKI solution will contain about 1.00 gram (1000 mg) KI per milliliter (mL) of solution. This is 100% weight/volume (note units of mass concentration) of KI (one gram KI per mL solution), which is possible because SSKI is significantly more dense than pure water—about 1.67 g/mL. Because KI is about 76.4% iodide by weight, SSKI contains about 764 mg iodide per mL. This concentration of iodide allows the calculation of the iodide dose per drop, if one knows the number of drops per milliliter. For SSKI, a solution more viscous than water, there are assumed to be 15 drops per mL; the iodide dose is therefore approximately 51 mg per drop. It is conventionally rounded to 50 mg per drop."​

Check this out:

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Source: the internet.

- United States temperature extremes | Simpedia

- air water temperature relationship | Google Search
 

Dr. B

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Sorry, I can't present much info at the moment, beyond mere conjecture and anecdotal evidence, which I don't have access to at the moment. But, as with selenium, it appears that iodine supplementation requires vitamin d sufficiency in order to safeguard, and potentially also heal, the thyroid in people with auto-immune conditions.
would vitamin d alone heal the thyroid, or does it need to be combined with supplemental iodine
 

Jam

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would vitamin d alone heal the thyroid, or does it need to be combined with supplemental iodine
That probably depends on the kind and amount of damage. If there is iodine deficiency, or if the body is overloaded with toxic halogens such as bromine or flouride, iodine supplementation would be required, for example.
 

Amazoniac

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With lugols, i get severe hypo smptomps with less than half-drop. 2-3mg was enought to make me feel bad, low heart beat and cold. Selenium doesnt change this.
But when I mix it with acorbic acid, and iodine oxidizes to iodide and loses its color, I get positive benefits, better skin and mood the next day, no hypo symptoms at all.

Anyone with similar experience?

(..and yes i know there are both iodine and iodide in lugols)
Elite, that's curious.
- Mega Dosing Iodine = Bad, Destroys Thyroid Tissue Permanently

In Lugol's solution, the ratio of iodide to molecular iodine is about 1.5:1 or 3:2. For a 2.5 mg dose (as in a drop of the 2% solution), we have 1.5 mg (3/5) of iodide and 1 mg (2/5) of molecular iodine. Are you superstitious? If so, the 5% solution didn't work, 2% neither, perhaps 1% is what aligns best with you.

Regardless of the fate of molecular iodine, the iodide that gets to the thyroid is going to be toasted with hydrogen peroxide.

- Iodine and thyroid hormones | Epidemiology of Thyroid Disorders

"Iodide inside the thyroid aids in reactions leading to synthesis of active thyroid hormones. The first reaction is when iodide is oxidated and incorporated into MIT and DIT, which are hormonally inactive iodotyrosines. This process is called organification. Iodide is usually oxidized quickly and appears immediately in organic combination with thyroglobulin. Iodination, which leads to the formation of iodotyrosines, takes place in thyroglobulin but not in free amino acids. The heme-containing protein thyroid peroxidase (TPO) mediates oxidation of thyroidal iodide. This requires hydrogen peroxide (H2O2) that is generated by the dual oxidase (DUOX1 and DUOX2) enzymes that require calcium. The TPO protein has a membrane-spanning region close to the carboxy-terminus. It is positioned in the apical membranes of thyroid cells with residues 1-844 within the follicular lumen where iodination takes place (see Fig. 3.1)."

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- Assessment of existing correlation between in vivo and in vitro models of calcium induced thyroid disorder (appears shady in skimming)

- Structural and functional aspects of thyroid peroxidase

"The first step in the process of thyroid hormone synthesis is the binding of iodine to tyrosine residues in Tg, which yields MIT and DIT residues. This process occurs at the apical membrane of thyrocytes, facing the colloid. Iodide must be oxidized into an iodinating form. The identity of the iodinating species has been extensively debated, and this issue has not yet been settled [86–92]. One of the ideas put forward is that oxidation may produce both free iodine and tyrosine radicals, but both may bind to TPO, giving MIT, which then separates from the enzyme. The heme iron in native TPO is in the ferric form (FeIII) as in lactoperoxidase. H2O2 is thought to oxidize the free enzyme, entailing the loss of two electrons and leading to the formation of compound I consisting of an FeIV-porphyrin-cation radical containing an oxoferryl heme [93]. Iodide binds to compound I, is oxidized and gives compound II, and then reacts with a Tg tyrosine residue. The newly formed I• and Tyr•-Tg free radicals interact, resulting in the formation of MIT–Tg, and the enzyme reverts to its free state. A further reaction between free iodine radicals and MIT gives DIT. Numerous experimental studies have suggested that TPO reduction occurs directly via a two-electron reaction, in which compound I is directly reduced to the native enzyme [84,88,92,94,95]. The second suggestion, which was based on studies on rapid spectral absorption changes, is that TPO–I+ may be the iodination intermediate and that the preferential pathway will be via the oxidation of TPO by H2O2 followed by two-electron oxidation of I− into I+, which then reacts with a tyrosine residue [83,84,88]. The third proposal put forward is that oxidized TPO and I− may produce hypoiodite (OI−), which also involves a two-electron reaction [89]."​

- Thyroid peroxidase | GenomeNet [Reactions (KEGG)]

So, it yields (molecular) iodine or other oxidized species anyway.


"The distribution and action of iodine in organisms depend on the chemical form of iodine that is ingested. For example, molecular iodine (I2) is not reduced to iodide (I−) in the blood before being absorbed in the gastrointestinal tract [11], induces differential effects [12], and its capture is 40% lower in the thyroid [13]. In fact, under conditions of iodine deficiency, I− appears to be more efficient than I2 in restoring the thyroid gland to normality in goiter stages, while I2 is more effective in decreasing mammary alterations secondary to iodine deficiency [14]."

"Although the main uptake of iodine takes place in the thyroid, many other organs take it up (Figure 1), including the salivary glands, gastric mucosa, lactating mammary gland, nervous system, choroid plexus, ciliary body of the eye, lacrimal gland, thymus, skin, placenta, ovary, uterus, prostate, and pancreas, and they can maintain or lose this ability in pathological conditions [1]. The I− transport system in many of these extrathyroidal tissues involves the expression of the sodium iodide symporter (NIS) and/or the anion exchanger Pendrin (PDS/SLC26A4). Recent studies have also demonstrated the direct participation of other transporters including anoctamin 1 (ANO1), cystic fibrosis transmembrane conductance regulator (CFTR) and sodium multivitamin transporter (SMVT) that are capable to take up I− [1]. On the other hand, various studies have shown that I2 is captured by an independent mechanism of NIS, PDS, Na+ and ATP, but it is saturable and depends on protein synthesis, suggesting a facilitated diffusion system [34]. This mechanism is similar to the one described in marine algae [35], indicating that I2 absorption could be an evolutionary conserved system. Indeed, we demonstrated that the thyroid, mammary gland, and prostate can accumulate both types of iodine, which are captured by different mechanisms. The thyroid, lactating mammary gland, and prostate exhibit a significant uptake of I−, which is internalized by NIS (inhibited by KClO4). Molecular iodine is taken up by these tissues, but also by others like the nubile mammary gland, and NIS does not participate in its internalization [36]. These findings agree with the notion that I2 contributes to maintaining the integrity of these organs."​

Molecular iodine might behave more randomly, but if it attacks unsaturated fats, the products should be less harmful. What you report seems consistent with an effect in the thyroid, but I don't know how it deals with such iodine form. In case it's necessary to obtain iodide, maybe it leads to a local and futile consumption of antioxidants (glutathione?) that could've been spared for later use when dealing with hydrogen peroxide.
 

Peater

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More accurately, PUFA is dangerous if it is allowed to oxidize, but neutral or possibly beneficial if it is able to bond to Iodine (as previously discussed, it becomes Iodostearic acid). In either case it is technically not "PUFA" anymore. When I think of the word PUFA I think of the oil before it has either oxidized or bonded to Iodine.

Iodostearic acid could (I need to read the papers on it) provide some benefit that regular stearic acid does not such as "brain health" (the proposed benefits from Omega-3 oils that people claim).

It's something I don't pretend to be even close to knowledgeable about. Just kinda thinking out loud.

I just thought of another reason PUFA could be bad. We all know how Bromine, Flourine, and Chlorine can bond to the thyroid gland by now right?

What if Bromine, Flourine, or Chlorine bonds to PUFA???

This makes me think of brominated vegetable oil in stuff like Mountain Dew which even the mainstream says it bad.

It's a shame @Cirion and @Captain_Coconut does not seem to visit any more, I found this thread absolutely fascinating. I'd speculated about saturating PUFA with iodine myself, after reading about the iodine test. I wonder if MCT from coconut oil would help drive it out of cells, as well as good old Vitamin E.

@burtlancast you still about mate?
 

Dr. B

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This makes me think of brominated vegetable oil in stuff like Mountain Dew which even the mainstream says it bad.

It's a shame @Cirion and @Captain_Coconut does not seem to visit any more, I found this thread absolutely fascinating. I'd speculated about saturating PUFA with iodine myself, after reading about the iodine test. I wonder if MCT from coconut oil would help drive it out of cells, as well as good old Vitamin E.

@burtlancast you still about mate?

If iodine does saturate pufa, i dont think taking iodine supplements will saturate the pufa in the body. If that were the case there should be minimal cases of side effects from iodine supplements. Isnt that what vitamin E is meant to do, to saturate PUFA inside the body. Many people have totally different effects from vitamin E vs iodine, the only similarity i think is if you take megadoses of either it can cause skin issues.

Also does that mean the fish with PUFA dont have enough iodine in them, since the high fat fish will often have lots of PUFA.
 

Peater

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Just a thought...this thread has mentioned the 'iodination' (Is that a word?) of PUFAs but as was quite rightly pointed out, you would need to ingest a huge amount.

But...what about topically applied directly? Strong Lugol's solution or the iodinated oil someone mentioned, the oil would be a carrier just like in Progest-E.
 
EMF Mitigation - Flush Niacin - Big 5 Minerals

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