Mega Dosing Iodine = Bad, Destroys Thyroid Tissue Permanently

[Cirion]

I suspect that iodine might be more dangerous to people with lots of PUFA in the system, since it prevents thyroid from using iodine. However, I am not quite sure what to look for to confirm or disprove that.

I believe there is truth to this. RP apparently notes that the reaction of iodine with PUFA may cause a spike in TSH. I think this one of the reasons that TSH is expected to increase, when starting an Iodine protocol. However, it seems like you'd have no choice but to fight through the initial discomfort until all the PUFA is eliminated if you ever wish to replenish Iodine stores. It may also explain why very high dosages are recommended when starting to detox - since most of the Iodine will be "wasted" (on PUFA, halides, heavy metals), if you aren't intaking a high enough dose, there won't be any left for your thyroid.

Ironically, as such, if your dose is not high enough, perhaps as much as 100% of the Iodine you take will be spent on detox, with 0% going to the thyroid.

When you consider that possibility, I could see how the combination of:

1.) Remove existing halides from the thyroid gland
2.) Not have any halides to replace the thyroid gland

Could easily make one hypothyroid. Yes, bromine is not good for the thyroid gland (results in a deranged variant of T4/T3), but a lack of ANY halide in the thyroid gland COULD be even worse.

I think this is now my working hypothesis as to how 2 of his patients got Iodine induced hypothyroid.

This could also explain the discrepancy as to how some scientific studies indict Iodine as being bad for the thyroid in submaximal doses (500mcg-1 mg or so), and yet other studies show Iodine as being helpful in large dosages (> 10 mg).

In that context, it's actually possible that both the studies indicting Iodine as being evil AND Dr. Brown could be BOTH correct. An interesting possibility. Sometimes its useful to think outside of the box, and consider that "Option number three" could be the answer, rather than the more "obvious" option one or two.

 

[burtlancast]

Even though chlorine is contained in both substances, the impact it has is completely different on the body.

Only one electron separates chlorine and chloride, and it makes all the difference between a highly poisonous warfare agent or an essential mineral.

As far as Mr Garrett Smith goes, he's just another biased individual who chose to disregard the mountain of scientific facts pointing to the safety and essentiality of high dose iodine, hoping his readers don't know any better.

 

[LeeLemonoil]

How could, biochemically, the proposed healt hazard of potassium iodide be explained? The potassium surely is not the alleged culprit? So Iodide it is?

 

[Cirion]

Only one electron separates chlorine and chloride, and it makes all the difference between a highly poisonous warfare agent or an essential mineral.

As far as Mr Garrett Smith goes, he's just another biased individual who chose to disregard the mountain of scientific facts pointing to the safety and essentiality of high dose iodine, hoping his readers don't know any better.

Just to be somewhat devils' advocate, not necessarily, or rather just a misunderstanding of analyzing potassium iodide alone and not understanding that it needs to be coupled with elemental iodine as well.

We see this a lot in the medical industry and studies. Too much linear thinking. Not enough outside the box thinking, to really dig deep and understand the complexities.

"Patient A consumed substance B. Patient A developed health problems. Therefore, substance B is bad."

Sometimes that is true sometimes it is not. Correlation =/= causation

 

[ecstatichamster]

How could, biochemically, the proposed healt hazard of potassium iodide be explained? The potassium surely is not the alleged culprit? So Iodide it is?

I think this is nonsense. Potassium iodide has a very safe history compared to elemental iodine.

 

[Captain_Coconut]

This is what Dr. Garrett Smith says about potassium iodide:

"Lugol's, Iodoral, SSKI, and under many other names...high-dose POTASSIUM IODIDE ruins thyroids, and this is well documented in the literature.

I am NOT saying iodINE is bad, I am saying that POTASSIUM IODIDE IS BAD. See for yourself below. This is not some crazy conspiracy, it's in the literature. Just because something may be helpful during nuclear fallout (ie. not dying from radiation toxicity damage to the thyroid), DOES NOT mean that it is something that is healthy to take in high doses on a daily basis!

Thyroid failure after potassium iodide treatment of diffuse toxic goiter. - PubMed - NCBI
"1. The treatment of Graves' Disease by Potassium Iodide (like thyroidectomy, radioiodine, and antithyroid drugs) is followed by rate failure of thyroid function.[...] 4. In certain patients, Potassium Iodide appears to be an effective means of controlling the hyperthyroidism of Graves' Disease."

Translation: Potassium iodide directly ruins (chemically damages) the thyroid.

Feel free to look at the documented toxicity of potassium iodide here (see link for references):

POTASSIUM IODIDE

POTASSIUM IODIDE - National Library of Medicine HSDB Database

• /SIGNS AND SYMPTOMS/ In a small proportion of individuals given large doses of iodide for long periods ... thyroid gland shows hyperplasia & is depleted of stores of iodine. Thyroid hormone corrects hypothyroidism and causes goiter to subside ... /Iodide preparation/ [Note above that iodIDE depleted the thyroid's iodINE stores]
• /SIGNS AND SYMPTOMS/ Sudden withdrawal may precipitate thyroid storm.
• Since some individuals are markedly sensitive to iodides, potassium iodide should be used with caution when initially administered. Patients at risk for iodine-induced adverse effects include those with hypocomplementemic vasculitis and those with goiter or autoimmune thyroid disease.
• Potassium iodide may cause skin rash and thyroid suppression in infants.
• Potassium iodide is distributed into breast milk; use by nursing mothers may cause skin rash and thyroid suppression in the infant.
• Prolonged use may result in hypothyroidism, parotitis, iodism, and, particularly in postpubescent patients, acneiform skin lesions.
• Iodides readily cross the placenta[fetus] and may result in abnormal thyroid function and/or goiter in the neonate. [newborn]
• ...repeat administration of potassium iodide should be avoided in neonates (birth to 1 month of age) to minimize the risk of hypothyroidism during a period of critical brain development...
• USES: Iodides have been utilized to treat iodine disorders, hyperthyroidism, bacterial, fungal or protozoal infections, and also were traditionally as expectorants because of their stimulatory effects on bronchial secretions. Potassium iodide is indicated for use as a thyroid blocking agent following exposure to radioisotopes of iodine from a nuclear reactor accident. [does it not make sense that something used to suppress hyperthyroidism is also a thyroid "blocking" agent, and long-term use would cause HYPOthyroidism?]
• ADVERSE EFFECTS:
  COMMON: POTASSIUM IODIDE can cause stomach upset, diarrhea, nausea, vomiting, stomach pain, skin rash and salivary gland swelling or tenderness.
  LESS COMMON: POTASSIUM IODIDE can cause gastrointestinal bleeding, confusion, dysrhythmias, numbness, pain or weakness in hands or feet, unusual fatigue, weakness or heaviness of legs, fever, and edema of neck or throat. Thyroid adenoma, goiter, and myxedema are also possible side effects.
  RARE: Iodism is a rare occurrence with iodides; however, it may develop during prolonged treatment or with the use of high doses. Symptoms include burning of mouth, severe headache, metallic taste, soreness of teeth and gums, symptoms of head cold, irritation of the eyes with swelling of the eyelids, unusual increase in salivation, acneform skin lesions in the seborrheic areas, and rarely, severe skin eruptions.
• Chronic iodide therapy has produced goiters, hypothyroidism, and rarely hyperthyroidism.
• Monitor thyroid function in cases of severe overdose for decreased serum T4 levels and increased serum TSH levels.
• Discontinuation of the iodide source will usually result in restoration of normal thyroid function within several weeks.
• Mechanism of Action: In hyperthyroid patients, potassium iodide produces rapid remission of symptoms by inhibiting the release of thyroid hormone into the circulation. The effects of potassium iodide on the thyroid gland include reduction of vascularity, a firming of the glandular tissue, shrinkage of the size of individual cells, reaccumulation of colloid in the follicles, and increases in bound iodine.
• When administered prior to and following administration of radioactive isotopes and in radiation emergencies involving the release of radioactive iodine, potassium iodide protects the thyroid gland by blocking the thyroidal uptake of radioactive isotopes of iodine.[KEY CONCEPT already noted above...potassium iodide BLOCKS normal thyroid uptake of ALL iodINE, not just the radioactive stuff!!!]
  
• Potassium iodide is indicated in the treatment of hyperthyroidism.
• Potassium iodide is used concurrently with an antithyroid agent to induce thyroid involution prior to thyroidectomy. [involution means degeneration]
• Interactions: Potassium iodide increased the toxic effect in selenium poisoning. [whoa...if you are doing high-dose potassium iodide AND selenium supplementation for your thyroid, you might want to reconsider]
• In treatment of hyperthyroidism /Lugol's solution/

When there is iodINE easily available, and the toxicity research seems quite overwhelmingly BAD on potassium iodIDE, why would anyone continue taking this stuff? Saying "somebody wrote a book on it" is not an acceptable answer to defend poisoning yourself or others. I do have specific iodine recommendations for my Nutritional Restoration clients, and due to the massive misinformation about all types of iodine on the internet, combined with people's tendency to overdo things, my recommendations will not be presented here. See my signature below if you are interested in working with me.

Hanging on to potassium iodIDE because "that's what they did in the past" is a pure example of the "Appeal to Tradition" fallacy.
Appeal to Tradition
"Tradition, once established, becomes a cultural thing, where people do it without thinking and defend it simply because it now is a part of the woodwork. Familiarity breeds both ignorance of the true value of something and a reluctance to give up the 'tried and true'."

It's time to stop poisoning your thyroid, folks. Simple changes can have amazing results.

“There is nothing more deceptive than an obvious fact.” ― Arthur Conan Doyle, The Boscombe Valley Mystery"
Why I NEVER recommend anyone use POTASSIUM iodide, a known anti-thyroid compound

This kind of bad evidence on potassium iodine may help to explain why the data on large doses of iodized oil does not show much in the way of negative side effects, e.g. spiked TSH or hypothyroid symptoms. Iodized oil provides only elemental iodine to the body.

 

[dbh25]

Ironically, as such, if your dose is not high enough, perhaps as much as 100% of the Iodine you take will be spent on detox, with 0% going to the thyroid.

What dose did you start with, and what dose did you ramp up to?

 

[Cirion]

I'm not yet entirely happy with my dosage. I might actually increase it again. It's hard to find Dr.'s to test these things for you, although I did finally locate one in my city. He does not accept insurance though so I've been procrastinating. Anyway I currently do 50 mg a day. The first day I had it, I accidentally had way more (something like 150-200mg) because I miscalculated the dose (oops). The first day I had it I felt amazing. So that's why I think maybe (for me) 50 mg is not enough. My selenium and B2/B3 just arrived today though so those should help as they are required co-nutrients.

 

[dbh25]

I'm not yet entirely happy with my dosage. I might actually increase it again. It's hard to find Dr.'s to test these things for you, although I did finally locate one in my city. He does not accept insurance though so I've been procrastinating. Anyway I currently do 50 mg a day. The first day I had it, I accidentally had way more (something like 150-200mg) because I miscalculated the dose (oops). The first day I had it I felt amazing. So that's why I think maybe (for me) 50 mg is not enough. My selenium and B2/B3 just arrived today though so those should help as they are required co-nutrients.

Thanks for the info.
I thought people usually started at lower doses and worked up to a higher dose like 50mg.

 

[Cirion]

Thanks for the info.
I thought people usually started at lower doses and worked up to a higher dose like 50mg.

Yeah usually. In my case I did not mean to take that much, like I said I miscalculated lol.

 

[Whichway?]

What form of iodine do you take?
Most of the supplements seem to have some/all iodine in the form of potassium iodide.

 

[Whichway?]

What form of iodine do you take?
Most of the supplements seem to have some/all iodine in the form of potassium iodide.

 

[Cirion]

I take Lugol's which is a mix of the two.

 

[Davinci]

In the more extreme examples, people have been known to cause hundreds or even thousands of cherry angiomas pop up in their skin (a sign of severe toxic halide poisoning, usually bromine but cherry angiomas can be caused by fluorine and chlorine as well).

@Cirion I have quite a number of cherry angiomas and have been trying to find out what is. Never found a good reference. I'm glad you mention it here but I've also heard of other explanations like excess estrogen. Are there any materials you have seen or suggest that goes into this in more depth?

 

[LeeLemonoil]

I‘ve developed around 15 tiny cherry anginomas in the course of maybe 10-12 month, in a time where I supplemented a lot of Magnesium. I feared prolactin was a culprit but I have never read anything compelling. If you have something to read about halides and CAnginomas pls share if you please

 

[LeeLemonoil]

Ok, quick websearch with cherry anginomas and halides brings up results, even case reports in pubmed.

Though the halides are likely not stored directly at the site of the CA, I will topically apply some Lugols on a CA site every few days and see what happens

 

[Davinci]

Ok, quick websearch with cherry anginomas and halides brings up results, even case reports in pubmed.

Though the halides are likely not stored directly at the site of the CA, I will topically apply some Lugols on a CA site every few days and see what happens

How do you apply Lugol's to your skin? Do you dilute it down with something? One time I tried, it was painful and it left a scar for weeks. I think I was using Lugol's 2% strength but I'm not sure.

 

[LeeLemonoil]

I use a ~ lugol-like Solution but with 60% ethanol/water and 2mg each of iodine and PI in 100ml, so roughly 2% as well. It is a commercial skin desinfectant. It would sting, but causing scarring is unusual

 

[Amazoniac]

- [URL='https://doi.org/10.1016/B978-0-12-374135-6.X0001-5']Comprehensive Handbook of Iodine: Nutritional, Biochemical, Pathological and Therapeutic Aspects[/URL]

↳ Chapter 15: Iodine Speciation in Foodstuffs, Tissues, and Environmental Samples: Iodine Species and Analytical Method

"Different species of iodine are involved in the transport of iodine from air, soil and water to food, and from food to the human body. In water, most iodine occurs as iodide and iodate while, in some cases, the concentration of organic iodine may be high. In the air, iodine exists as particle associated iodine, inorganic gaseous iodine (I2, HIO), and organic gaseous iodine (CH3I, CH2I2, etc.). In the body of humans and other mammals, iodine is utilized by the thyroid gland for the biosynthesis of the thyroid hormones T4 and T3. Besides T3 and T4, iodine also exists as MIT, DIT, T3, and rT3, which are mainly bound with proteins in thyroid and other tissues, but function as free T3 and T4. In milk and urine, most iodine occurs as iodide, but some species of organic iodine were also found. In seaweed, iodine species varies widely with the species of seaweed. In brown seaweed, most of iodine exists as iodide; while in green seaweed, iodine is mainly bound to organic molecules, such as protein and polyphenol. Iodine species in fish are similar to that in the human body."

Speciation analysis of iodine in milk

"Brätter et al. (1998) developed an online method for the investigation of iodine species in human milk – SEC separation coupled with ICP-MS detection. They reported that 80% of iodine in human milk was present as iodide; besides iodide, another six high-molecular-weight iodine-containing molecules (5–300 kDa) were also observed. The total iodine in European breast milk samples was determined to be 95 +- 60 mcg/l. Michalke (2006) also investigated iodine species in breast milk. He reported that total iodine varied according to lactation state, beginning at 60 mg/l on the 2nd day (postpartum) reaching 100 mcg/l on the 3rd day, and decreasing to 80 mg/l (6th day) or 60 mg/l constantly from 9th to the 60th day. A prefractionation by centrifugation showed that iodine is associated with fat at approximately 30%, and 70% of the low-molecular-weight fraction. Speciation analysis of iodine in milk whey (pooled human milk) was carried out by SEC-ICP-MS and IC using a strong anion exchange column combined with ICP-MS. The SEC showed predominantly iodide with about 37 mcg/l, as well as two more iodine species with 1.5 and 1.0 mcg/l having retention times pointing to T4 and T3. IC-ICP-MS results indicated iodide to be the major iodine species in human milk. Leiterer et al. (2001) also used an IC coupled with ICP-MS for the speciation of iodine in human milk. They also observed that iodide is the main iodine species in milk, but in a few samples it also has traces of iodate and several unidentified, presumably organoiodine, compounds."

"Sanandez and Szpunar (1999) determined iodine species in milk and infant formulas using SEC-ICP-MS. Iodine species were quantitatively eluted with 30 mM Tris buffer within 40 minutes and detected by ICP MS with a detection limit of 1 mcg/l (as I). A systematic study of iodine speciation in milk samples of different animals (cow, goat), humans of different geographic origin (several European countries) and in infant formulas from different manufacturers was carried out. Whey obtained after centrifugation of fresh milk or reconstituted milk powders contained more than 95% of the iodine initially present in milk in all the samples investigated, with the exception of the infant formulas in which only 15–50% of the total iodine was found in the milk whey. An addition of sodium dodecyl sulfonate (SDS) considerably improved the recovery of iodine from these samples into the milk whey. Iodine was found to be present principally as iodide in all the samples except infant formulas. In the latter, more than half of the iodine was bound to a high molecular weight (>1000 kDa) organic molecules."

Speciation analysis of iodine in fish

"Simon et al. (2002), using LC-ICP-MS, investigated iodine speciation in whole-body homogenates of adult male and female zebrafish (Danio rerio) and tadpoles of the African clawed frog (Xenopus laevis) at two different developmental stages (NF58 and 61) according to Nieuwkoop and Faber. A Capcell-C18 column and a mobile phase comprising Tris-HCl and methanol were used for chromatographic separation. Iodide, MIT, DIT, T4, T3 and rT3 were observed in these samples. In addition, another five species of iodine were also identified in the samples."

Speciation analysis of iodine in seaweeds

"Due to the high concentration of iodine in marine vegetation, the chemical species of iodine in plants is mainly focused on seaweed. Hou et al. (1997b, 2000) developed a method for the determination of various chemical species of iodine in seaweed, such as water-soluble iodine, soluble organic iodine, iodide, iodate and protein-, pigmentpolyphenol-, or polysaccharide-bound iodine."

"[..]9–99% [?] of iodine in seaweed is water soluble. In addition, the percentage of water-soluble iodine is the highest in brown algae and lowest in green algae. In the water leachate of seaweed, iodine exists mainly as iodide, the percentage of organic iodine ranges from 5 to 40%, and the iodate is lower than 5% in all 30 species investigated. In biological macromolecules, iodine is mainly bound with proteins, polyphenol and pigments, but few is bound with polysaccharide."

"Anion-exchange chromatography coupled to ICP-MS confirmed that the most predominant inorganic iodine species present in [Wakame and Kombu] is iodide. Protein-bound iodinated species were hydrolyzed by enzymatic digestion using proteinase K. Analysis of the hydrolyzate using reversed-phase HPLC-ICP-MS revealed the presence of MIT and DIT in Wakame."

"In seaweed, iodine species vary widely with the species of seaweed. In brown seaweed, most iodine exists as iodide; while in green seaweed, iodine is mainly bound to organic molecules, such as proteins and polyphenol."


"It is known that iodide or iodate have a high bioavailability (> 95%) in humans and animals. However, iodine in the diet may combine with different components and exist as organic iodine, which may have a low uptake in the digestive tract."

"It was reported that the bioavailability of pure mineral iodine, such as potassium iodide, was 96.4% in normal humans, while that of pure organic iodine, such as monoiodotyrosine, was 80%. A higher bioavailability of iodine in the seaweeds Gracilaria verrucosa and Laminaria hyperborea (80–99%) was also observed (Aquaron et al., 2002). A similar high bioavailability of iodine in the diet was also reported by Jahreis et al. (2001). They investigated the uptake of iodine in 12 women and found that 89% of the iodine was excreted in the urine and 11% in the feces. However, Wahl et al. (1995) reported a very low uptake of iodine from a normal diet; they observed that only 16–18% of the alimentary iodine was excreted with the urine. This may indicate that the type of diet and the species of iodine in the foodstuff are very important with respect to the nutritional status of iodine."

"Acute toxicity of iodine to animals has resulted in death at levels of 200–500 mg/kg-day, while levels of iodine greater than 10 mg/day, due to the intake of iodine-containing drugs or as a result of accidental poisoning, were toxic to some humans (Backer and Hollowell (2000). Forty-eight individuals were reported to have adverse effects, including goiter, hypothyroidism and sensitivity reactions, from iodine levels less than or equal to 10 mg/day (IPCS, 1988). One study reported that long-term intakes greater than 18 mg/day increased the risk of goiter (Wolff, 1969), while others demonstrated that high iodine intake is associated with an increased risk of thyroid papillary cancer in humans (Franceschi, 1988; Lind et al., 1998). The WHO has set a PMTDI for iodine of 1 mg/day, which was based on the observation that an iodine intake of 1 mg/day or less is probably safe for the majority of the population, but may cause adverse effects in some individuals, e.g., people with thyroid disorders or those that are particularly sensitive to iodine (IPCS, 1988)."

"The observation of toxicity of iodine mainly focused on the iodide or iodate, which is normally present in iodized salt, milk, water and leachate of foodstuffs. However, the toxicity of some other species of iodine may be much higher than that of iodide and iodate. For the prevention of iodine deficiency disorders, iodized oil was used as an injection or administered orally in many countries: iodized oil is normally produced by binding iodine atoms to the polyunsaturated fatty acid in the oil (Zimmermann et al., 2000). After administration, it was supposed that iodine is released gradually as iodide to maintain a constant supply of iodine to the body. Experience in the past decades shows that the utilization of iodized oil is safe. However, acute poisoning of iodized oil to children who are orally administered was reported in China in 1998; this may be related to the species of iodine, which may be more toxic than iodide or iodate. Iodine has been used as an effective, simple, and cost-efficient means of water disinfection (Backer and Hollowell, 2000), in which the active disinfectant species are elemental iodine and hypoiodous acid. Doses of iodine below 1 mg/l kill bacteria within minutes. Elemental iodine and hypoiodous acid remain in the disinfected water, which may be toxic to humans."

"Iodide and iodate have a low toxicity and high bioavailability, whereas the toxicity of elemental iodine and periodate is high."​

- A Review of Spectrophotometric and Chromatographic Methods and Sample Preparation Procedures for Determination of Iodine in Miscellaneous Matrices​

↳ Chapter 26: Is Iodine an Antioxidant and Antiproliferative Agent for the Mammary and Prostate Glands?

"Most of the investigations regarding the status of iodine in humans and animals have been focused on the role of iodine in thyroid function. Relatively little attention has been given to its extrathyroidal roles. Recently [2009], some groups have postulated that iodide may have an ancestral antioxidant function in all iodide-concentrating cells, from primitive algae to more recent vertebrates (Cann et al., 2000; Venturi, 2001; Smyth, 2003). In these cells, iodide acts as an electron donor in the presence of H2O2 and peroxidase; the resulting iodine atom is a free radical that readily iodinates tyrosine, histidine and certain specific lipids. In fact, iodine can attach to double bonds of some polyunsaturated fatty acids in cellular membranes, making them less reactive with oxygen radicals (Cocchi and Venturi, 2000). Moreover, it has been demonstrated that iodine distribution in the organism depends on the chemical form of iodine ingested (Thrall and Bull, 1990), and that molecular iodine (I2) is not reduced to iodide (I-) before it is absorbed systemically from the gastrointestinal tract (Thrall et al., 1992). Indeed, in iodine deficiency conditions, I- appears to be more efficient than I2 in restoring the thyroid gland to normal from a goitrous state, whereas I2 is distinctly more effective in diminishing mammary dysplasia and atypia secondary to iodine deficiency (Eskin et al., 1995; Ghent et al., 1993; Kessler, 2004)."

"The importance of I2 as an oxidized chemical form of iodine agrees with our recent demonstration (Alfaro-Hernandez, 2004) that the addition of I2, but not potassium iodide (KI), to mammary gland homogenates from virgin rats significantly decreases lipoperoxidation measured by the thiobarbituric acid reaction and expressed as malondialdehyde. The inability of I- to decrease lipoperoxidation may be explained by the absence of lactoperoxidase (LPO) in mammary glands from virgin rats, which is only present during pregnancy and lactation (Strum, 1978). LPO is a homolog of thyroperoxidase (TPO); both enzymes are able to oxidize I- in order to bind iodine covalently to proteins or lipids."

"[..]we hypothesize that iodine generated by LPO activity is bound to an abundant and specific protein (e.g., thyroglobulin in the thyroid and casein in lactating mammary gland), whereas I2 or another oxidized form of iodine, obtained by deiodination or in the diet, binds to lipids and/or other membrane or nuclear components, and acts as an antioxidant and/or antiproliferative agent (Aceves et al., 2005). This notion is supported by our finding that in the tumoral mammary cell line MCF-7, I2 but not I- supplement, is accompanied by antiproliferative effects and the appearance of iodinated proteins and lipids (Arroyo-Helguera et al., 2006)."

"In rat mammary carcinomas induced by 7,12 dimethylbenz[a]anthrancene (DMBA), supplementation with Lugol’s solution (mixture of I- and I2) exerts a suppressive effect on the development and size of the neoplasias (Kato et al., 1994). This suppressive effect is enhanced when the Lugol treatment is combined with progesterone (medroxyprogesterone acetate). The suppressed tumors were found to have significantly higher iodine content than unsuppressed tumors, with uptake was apparently enhanced by progesterone (Funahashi et al., 1996). The enhancement of iodine uptake by progesterone has been observed in other hormone-dependent tissues, including the uterus and the ovary (Brown-Grant and Rogers, 1972). Data generated in our laboratory (García-Solís et al., 2005) have shown that chronic administration of I2 exhibits a potent protective effect (70%) against mammary cancer induced by the carcinogen N-methyl-N-nitrosourea (MNU). This effect is exerted only by I2, not by KI or T4. The cancellation of I2 treatment is accompanied by the development of latent mammary cancers that do not progress to overt cancers, suggesting that I2 acts by decreasing carcinogenesis at the promotion level (Figure 26.3). Moreover, this protective effect of I2 was accompanied by a significant reduction in lipoperoxidation and an increase in catalase activity (Table 26.2). These findings are important in relation to the notion that reactive oxygen species (ROS), such as single oxygen (O2), superoxide anions (O2 − ), hydrogen peroxide (H2O2) and hydroxyl radicals (OH), are interrelated in the etiology of cancer (Moraes et al., 1990; Cook et al., 2004). Human tumor cells produce a substantial amount of H2O2 (Szatrowski and Nathan, 1991). ROS have a wide range of cellular and molecular effects resulting in mutagenicity, cytotoxicity and changes in gene expression. G–C base pairs in CpG dinucleotide sequences are a common site for point mutations in p53 tumor suppressor gene closely related to breast cancer (Lane, 1994). Cellular genes are usually converted into oncogenes, particularly ras family oncogenes in codons 12 and 13. It has been demonstrated that these G–C sites are the main targets of oxidative damage (Bos, 1988). In this respect, our data suggest that the antioxidant effect of I2 could operate by two mechanisms: (1) I2 competes with ROS for various cellular components, or it neutralizes OH radicals by the formation of hypoiodous acid (HOI); and/or (2) I2 acts indirectly to increase the expression or activity of antioxidant enzymatic machinery."

"[An] important effect of iodine on the thyroid is its ability to diminish the hypervascularity and hyperplasic characteristics of the diffuse goiter in Graves’ disease. This phenomenon is widely used to facilitate surgical therapy of this disorder, and although its molecular mechanism is uncertain, it has been postulated that iodine might be oxidized to a more reactive form that binds to organic components which, in turn, interfere with metabolic or molecular processes necessary for the maintenance of hyperplasia (Mutaku et al., 2002; Pisarev and Gartner, 2000). Vitale et al. (2000) showed that an excess of KI induces apoptosis in cultured thyroid cells, but if TPO activity is blocked with propylthiouracil, the apoptotic effect of KI is eliminated. Furthermore, Zhang et al. (2003), using lung cancer cells transfected with NIS or NIS/TPO, observed that only in NIS/TPO-transfected cells does KI excess induce apoptosis, indicating that I- from KI needs to be oxidized to have a cytotoxic effect."

"The postulated mechanism by which iodine induces apoptosis is via the formation of specific iodinated arachidonic acid (AA) derivatives, such as 6-iodolactone (6-IL) or iodohexadecanal (Dugrillon et al., 1990; Pisarev et al., 1994; Langer et al., 2003)."

"Our data (Figure 26.4) show that I2 administration significantly decreases the cellular proliferative rate in a tumor cell line from mammary (MCF-7) or prostate (LNCaP) gland, but not in normal cells (fibroblast NIH3T3), suggesting that tumoral cells contain specific components that can be iodinated and then can exert an antiproliferative effect. Similarly, the increase in DNA content induced by sex hormones in the prostate hyperplasia model is prevented with I2 supplementation, without any harmful effect observed in control tissue (Figure 26.5). Although the specific iodocomponent has not yet been characterized, several studies have reported elevated prostaglandin levels in breast and prostate cancer, but not in normal glands (Tan et al., 1974; Bennett et al., 1977; Rolland et al., 1980; Pham et al., 2004). Prostaglandins are produced from AA by the enzyme cyclooxygenase, indicating the presence of high levels of AA in breast and prostate tumors. It is possible that these high levels of AA, and the iodolipids formed from them, may explain the specific effect of I2 in tumoral cells."

"With regard to the mammary gland, studies in our laboratory have shown that chronic administration of I2, but not I-, has a potent antineoplasic effect at the promotional level of mammary cancer without altering p53 expression (García-Solís et al., 2005)."

"In conclusion, it is possible that iodine in vertebrates acts in the following different ways:
- as an antioxidant by competing with free radicals for membrane lipids, proteins and DNA, or by increasing the expression or activity of antioxidant enzymes to help stabilize the cells. This antioxidant action can be exerted through oxidized iodine species (I*) obtained in the diet or by local deiodination;
- as inducers, through PPAR receptors, of antiproliferative and apoptotic mechanisms after incorporation into iodolipids; and
- as a constitutive part of thyroid hormones."

"As we and other authors have demonstrated, a chronic I2 diet supplement is not accompanied by any harmful secondary effects on the health of humans or animals (body weight, thyroid economy, reproductive cycle). Thus, we propose that I2 supplementation should be considered for use in clinical trials of breast and prostate cancer therapies."

@Obi-wan - You were after controlled stress, this might be an option.​

- Iodine or Iodide? A Laboratory Evaluation of the Content of Powdered Iodine Supplements
- Formation of molecular iodine during oxidation of iodide by the peroxidase/H2O2 system: Implications for antithyroid therapy

 

[LeeLemonoil]

Thanks a lot for the many references Amazoniac.
It seems that Iodide as in PI is also a viable form of supplemental bioavailable iodine.
Interesting that iodine in fish is similar to physiological iodines in humans. I really begin to think that Fish‘s purported health benefits in the mainstream is not complete without the consideration of iodine ... maybe Omega3s form iodolipids that are preferable to O3s unconjugated

 

[Cirion]

I find it interesting, that in nature, pro-nutrients and anti-nutrients usually balance themselves. I still want to learn more about the effects of Iodine on PUFA's. I plan to read some of the articles many of you have linked here, over the weekend when I have time.

Ray peat seems to think this reaction is bad ("Equivalent to anti-thyroid effects").

Jack kruse seems to think this reaction is good ("Protective on the PUFA, makes the PUFA a beneficial fat, by avoiding oxidation damage").

I am not sure who is correct. I can't see how in-activating a PUFA can be a bad thing though?

My remembrance of chemistry is limited. From what I do recall, some of the bonds in PUFA are somewhat weak, and thus can be oxidized (oxygen forming a bond with the fat), which is the definition of oxidation right? As such, if Iodine has a chance to form a bond with the fat first, wouldn't this "block" oxidation (block oxygen from having a chance to form a bond) and thus avoid the damaging effects of PUFA? Or does RP think that this Iodine bonded PUFA is just as damaging (or even more) than oxidated PUFA?

Could it be - that once again, both people who say PUFA are bad and people who say PUFA are good are BOTH correct? Aka, "door number three"? I don't think we can ignore the fact that the latest study seemed to have shown that african americans had, what was it, 77% reduced incidence of heart attacks or something due to fish oil intake? We must keep an open mind if we truly want to learn how to live optimally.

PUFA is bad IF : Overall body fat is high, SFA is low, Iodine is low (most americans) - most people, thus PUFA damages most people. Because most people fall under this camp, I could see how RP would be whole-heartedly against PUFA. I could probably agree that someone healthy may not need more than a few mg of Iodine to maintain. And even if you're healthy, I could agree that you don't need or want a lot of PUFA in your diet, simply because there are better options (SFA's). Any PUFA's you may "need" for your "brain health" would be very small and probably could be achieved with one or two simple servings of fish now and then, and many discussions on these forums have showed that you have to try very hard to get true "EFA deficiency" anyway if there is indeed a PUFA "requirement".

PUFA is neutral or even good IF : SFA is high, Iodine is high (not many people) - not many people, thus only select research shows PUFA is "good". This could also explain how some studies may show whole fish can be healthy like say trout or salmon, but the fish oil from a supplement is detrimental. Fish oil from a supplement wouldn't have any of the vitamin E or iodine you get from the whole fish, thus all you get is an oil which is easily oxidated and damaging. BTW for what its worth, usually when I eat trout and heavily salt and butter it... I feel really good after, and generally raises my body temp a lot especially if it is coupled with a starch like sweet potato that is also heavily salted / buttered. I think the key is to have PUFA's with some SFA and salt at the very least (and ideally also sugar). It could be that one of the biggest advantages of getting "Iodine Saturated" is to make your body basically invincible to PUFA's. You would have so much Iodine in the body, that any PUFA that you happened to ingest would instantly bond with the plethora of Iodine floating around and not have a chance to get oxidized. This could be one of the reasons why just about every one of Dr. Brown's patients feels better when they become iodine saturated, not just because of better thyroid function. Regardless, PUFA may be best avoided until you lose your body fat, at which time occasional PUFA intake from fish may be beneficial. Hard to say for sure if the net benefit from fish (if indeed there is one) is worth the risk until you've lost your bodyfat (excess PUFA) stores.

I am thinking that people not only iodine deficient, but bromine toxic, and heavy in PUFA (again, most people) would have a much higher need of iodine than someone who is not overweight, not toxic with bromines, and has an okay iodine level. We have to keep in mind too, that not only nowadays are we exposed to more bromine than any generation before us, we are also exposed to more EMF than any generation before us. I think EMF's are not talked about enough. I have reason to suspect that higher levels of EMF exposure also require more Iodine, though the exact mechanism behind it I'm not 100% sure of yet other than you probably need to ensure apoptosis of the EMF poisoned cells otherwise they may form cancerous tumors over time.

I believe I recall an older post by Haidut that basically said, unhealthy people tend to have higher Iodine in the bloodstream than healthy people. He tried to extrapolate this to suggest that to be healthier, you want lower levels of Iodine. I personally believe this to be a fallacy, much like how people in the medical industry say - unhealthy people have high sodium in the blood, high cholesterol, therefore to make them healthy we should remove the sodium and the cholesterol. It is in fact the high sodium, the high cholesterol (and potentially high iodine) that is keeping things from going further down hill in their health, and lowering sodium, cholesterol, and, I believe, Iodine, would serve to deteriorate their health further. This may also be one of the reasons why unhealthy people often tend to be hypothyroid. Maybe the body steals Iodine from the thyroid gland, and uses it for "damage control" (neutralizing the PUFA's). Because the body stole all the Iodine from the thyroid gland, you could have a situation where the body is "saturated in Iodine", and yet the thyroid gland is empty - thus hypothyroid. You could take this train of thought further to say hey look, Iodine causes hypothyroid - because the body is saturated in Iodine, you're intaking a healthy amount of Iodine (1 mg), and yet, still hypothyroid. But, if all of this Iodine is being used for damage control (inactivating PUFA's) and not for the thyroid, this could begin to explain why low-dose Iodine may "cause Hypothyroid" while mega-doses on the order of 50-100 mg may "cure hypothyroid".

I admit I pose a lot of ranting / hypothesis / conjecture but I'm trying to think how to answer all the unanswered questions here.