This is a post with more advanced info on iodine. It’s not the right post for you, if you just need some basic info on supplementing with iodine. I have a post for beginners, that I actually think everybody taking iodine should read, Iodine for beginners. That is on how to supplement iodine safely, and special precautions in terms of the thyroid and thyroid antibodies.
I have a post on the iodine protocol as well, that is, the protocol for taking high doses of iodine, The iodine protocol
Abstract
This is long post, so I have put in some links. So that you can scroll to what might be of particular interest. This is a post I will probably revise and add to as time goes on. I haven’t included THAT much on iodine and cancer. But some. There are a lot of positive findings on iodine and cancer. But the post would just become too long. There is a lot of info on cancer in some of the studies I link to though.
Is iodine converted to iodide in the GI tract?
The differences between iodide(I-) and molecular iodine (I2) in the body
How does iodine enter the cells?
There is so much going on in the iodine field at present. After the world has been plagued with iodine phobia in the wake of the Wolff-Chaikoff effect (see below). Which doctors have totally misunderstood and exaggerated. Something that has given us serious health issues world wide.
But now there are so many interesting new findings. I will not pretend to cover it all, but want to present some new findings. I find some of it difficult to understand, but will do my best. You might find it easier. And please, if you know something I don’t, comment below! Or write me.
There are whole scientific communities concentrating on iodine, and some scientists now advocate for changing the recommendations for daily intake. I believe we will see a lot of changes going forward. And as so often, we patients are leading the way. We should not diminish our own role. People are reading so much now. We are figuring things out for ourselves, and many of us are far ahead of our doctors.
The Wolff-Chaikoff effect
Ever since Wolff and Chaikoff conducted their study in 1948 (1), where they injected rats with large doses of iodine, the world has bee iodine phobic. Before that, iodine was a much used remedy for many ailments and diseases.
What is this Wolff-Chaikoff effect? What the study says, is that when we take a large dose of iodine, the thyroid gets flooded and shuts down.
‘the acute WolffChaikoff effect,’’ and it is due to increased intrathyroid iodine concentrations, which inhibit the iodination of tyrosyl residues of thyroglobulin (Tg) by thyroperoxidase (TPO). After48 hours of I excess, the thyroid gland escapes from this effect by an adaptation that decreases the thyroid iodine trap, thereby decreasing the intrathyroid iodine concentration. (2)
But this effect only lasts for max 48 hours. Sometimes only 24 hours. And it is correct, one does see this, also in later studies. Like the one over (2).
Dr. Abraham and Dr. Brownstein say, this is not correct. And they have several criticisms of the old study. Valid criticisms, like that the mice being injected with large doses of iodine (yes, injected) did not have their thyroid levels tested. Which they didn’t. And that the mice didn’t become hypothyroid. Which is probably also right, because hormone production resumes after 48 hours. You find Dr. Abrahams critical article here.(3)
I personally also react to the fact that the rats were injected with large doses iodine, up to the equivalent of 500 mg for a human. There is a discussion in iodine groups, is iodine reduced to iodide in the GI tract before absorption. I will come back to that later. But it is certain, that most iodine is reduced to iodide. So for the body to have large amounts of iodine floating around in the blood, is at least NOT normal.
The rats were also injected with radioactive iodine. They claimed, the doses were too low to affect the thyroid. But I don’t trust what doctors say about radioactive iodine and the thyroid. Doctors make hyperthyroid patients hypothyroid every day with radioactive I.
Never the less, there is a Wolff-Chaikoff effect.
But how on earth could this transient effect cause the world to fear iodine?
I don’t understand this. How can this have been translated into, iodine cause hypothyroidism? When thyroid levels normalize after 48 hours? It’s really difficult to understand this. Considering the serious consequences this has had for millions of people. Myself included. Doctors often run in one direction, believing in medical myths without looking into these myths themselves. They are often very busy. I think all doctors should have one study day every month.
Of course, iodine does play a part in thyroid autoimmunity. But iodine deficiency is more damaging than excess, I would say. I write about iodine and thyroid antibodies under each antibody in my antibody series:
Antibodies, part 2, Anti-thyroglobulin
Antibodies, part 3, TSHR abs, TRAb
Large dose iodine does not make most people hypothyroid, because the thyroid “learns” how to protect itself from the iodide, and how to just absorb the amount of iodide it needs. But this does not mean that nobody becomes hypothyroid on large dose iodine; some people do become hypo. Some people become hyper thyroid. There is no high dose iodine affects everyone the same, and it is not good for everybody either. It plays a part in thyroid autoimmunity, both iodine deficiency and iodine excess. But moderate doses starting low and increasing is much safer in terms of thyroid autoimmunity. I have more on that in the beginner post. Lots of people who have been hypothyroid for years, have either a shrunken thyroid, or a very damaged thyroid. For them, iodine will not further damage their thyroid, they will always need to take thyroid hormones anyway.
It’s thyroid healthy people and those who are in the beginning stages of thyroid disease, that need to take precautions in terms of the thyroid when supplementing iodine.
Does all forms of iodine induce the W-C effect?
According to this study (2), it’s iodide (I-) that cause the W-C effect. Molecular iodine (I2) does NOT induce it according to them. It’s a very interesting study where they try to find the safest way to treat breast cancer patients with large dose iodine. Unfortunately, it’s not open access. It goes very deeply into how I- and I2 works on the thyroid and mammary glands.
a moderately high I2 supplement (0.05%) causes some of the characteristics of the ‘‘acute Wolff-Chaikoff effect’’; namely, it lowers expression of the
sodium=iodide symporter, pendrin, thyroperoxidase (TPO), and deiodinase type 1 in thyroid gland without diminishing circulating levels of thyroid hormone. (2)
and even though I2 supplementation is accompanied by a decrease in
thyroid NIS, PEN, TPO, and D1 expression, the serum concentrations of THs were not reduced by I2 treatment. The possibility that I2 could be incorporated into Tg and thereby generate THs independent of TPO action is supported by results obtained in MMI animals, whose basal concentrations of T4, T3, and TSH were normal. (2)
So what they say is very interesting, but it’s a speculation and not a fact. They speculate, that even though I2 has the same short term effects on the thyroid, I2 does not decrease TH levels like I-. They think it could be because I2 maybe goes straight to the TG (thyroglobulin) molecules and participate in the synthesis of TH hormones directly. It seems likely.
Is iodine converted to iodide in the GI tract?
We discuss this in the American The Iodine Protocol group. I have believed it is so, that iodine does get converted to iodide in the gut before absorption. Because that is the current paradigm. That is what most scientists think. But in the iodine groups, people find that different kinds of iodine affects them differently. So they wonder, can this be correct? It’s important in terms of what kind of iodine to supplement with.
Molecular iodine and water-soluble iodine salts release the iodide ion in contact with water. Thus, iodine occurs in water in the form of iodide (I-), which is largely oxidised to molecular iodine during water treatment. Molecular iodine as well as water-soluble iodine salts are rapidly converted into iodide in the gut following
ingestion and this is efficiently absorbed throughout the gastrointestinal tract. (4)
This is from a Danish publication on iodine in drinking water. It’s just to show, how it’s widely accepted, that iodine in it’s various forms are converted to iodide before absorption in the gut. Please don’t ask me what “treatment with water” means 
.
So I was really amazed, when I discovered, that it was established already in 1990, that not all I2 gets converted to iodide in the gut. It was two guys called Thrall and Bull who figured this out through experimentation on rats. (5)
In this experiment, they looked at the effect on the thyroid of the rats being given either molecular iodine (12) or iodide:
One hundred six rat were randomly assigned to 11 treatment groups (9 animals/compound/dose and 16 control animals receiving distilled water). Rats were maintained on distilled water containing either I2 or I- (in the form of NaI) at dose levels of 1, 3. IO, 30, and 1OO mg of iodine/liter of drinking water for 1 week. At the end of one week all animals received a single oral dose of radioiodide (1251m) in 1 ml of water 1 hr prior to being killed. At which time thyroids were excised and radioactivity was determined using a LKB gamma counter (Model 1282).
Differences in the distribution of 125 I to the thyroid and skin depended on chemical
form. No significant differences in the distribution of l25 I between I- and I2 were observed in the remaining tissues collected, including
kidneys, spleen, liver, blood, salivary glands, small intestine, and large intestine
DISTRIBUTION OF IODINE AND IODIDE
TABLE 1
UPTAKE AND DISTRIBUTION OF”~I IN FED AND FASTED ANIMALS WITH TIME
Iodide (I- ) Iodine (I2)
Thyroid
Fasted ( 1 hr) 2.4 +/- 0.5” 1.8 +/-O.3
Fasted (2 hr) 5.6 +/- 0.5 3.1 +/- 0.3
Fed (2 hr) 5.7 +/- 0.5 4.3+/- 0.6
Skin
Fasted (2 hr) 20.5 +/- 1.1 17.5 +/- 2.2
Fed (2 hr) 15.9 +/- 1 .O 17.4 +/- 1.7
Stomach wall
Fasted (I hr) I .2 +/- 0. I 2.4 +/- 0.2
Fasted (2 hr) 4.5 +/- 1.3 6.8 +/- I.2
Fed (2 hr) 2.4 +/- 0.5 3.8 +/- 0.5
Stomach contents
Fasted ( I hr) 43.6 +/- 2.1 47.3 +/- 2.2
Fasted ( 2 hr) 14.5 +/- 1.9 17.4 +/- 1.8
Fed (2 hr) 24.7 +/- 3.1 38.4 +/- 4.3
Table 1. Thrall and Bull (5) Values are percentages of the administered dose +/-SEM of six animals.
I have had to simplify this table a bit. If you knew how much bother I have had with this table! OMG. But I wanted to include it, as this study will be difficult to access for most people.
As you can see, there was a larger absorption of I- than I2 in the thyroid. Also in the skin. And larger uptake of I2 to the stomach wall. The rats were divided in different groups, fed or fasted.
Rats were maintained on distilled water containing either Iz or I- (in the form of NaI) at dose levels of 1, 3. IO, 30, and !OO mg of iodine/liter of drinking water for 1 week. At the end of I week all animals
received a single oral dose of radioiodide (1251m) in I .O ml
of water 1 hr prior to being killed. at which time thyroids
were excised and radioactivity was determined using a
LKB gamma counter (Model 1282).
They were given enormous doses of iodine. 100 mg/L for a 300 gram animal in the max iodine group! A rat drinks app 10 ml/100 gram apparently. So a 300 gram rat would drink 30 mg! That would be equal to a dose of several thousand mgs for us. For me at 58 kg it would be 5800 mg. I really wonder at this. They write, 90 to 95% of the iodine was excreted. They analyzed both urine and feces. So did the rats absorb maybe 3 mg of iodine? I find that amazing. Just a side thought.
I guess this is evidence, that not all iodine is converted to iodide in the gut. That some I2 is absorbed as is, and floats around in the blood in that form. And that the thyroid absorb this form to a lesser degree. But iodide is also converted to iodine, not only in the thyroid, but also in other tissues in the body. See more below.
So that is an old study. It’s strange that the info hasn’t been more wildly accepted. The study has only 43 citations. If you are not aware, a citation is where a study is referenced in other people’s work, studies or articles. And 43 is very little over 30 years.
But many scientists are looking at this now. A group of Mexican scientists have several studies on the difference between iodide and molecular iodine (I2), and how they affect the body.
This group adhere to the “not all iodine is absorbed as iodide”. But then they say this (6) at the same time:
Iodide decay displays similar patterns in serum and urine samples of both groups (Figure 4), which translates into similar half-lives of free
iodide in serum and urine of animals treated with iodine (7.89 h and 7.76 h, respectively) or iodide
(8.27 h and 8.90 h, respectively). These results indicate that iodine ingestion and intestinal absorbance were similar for both chemical forms of iodine. In animals supplemented for 6 days, similar patterns for free iodide were found in serum and urine from control, I2-, and I–treated groups (Figure 5). In both sample types, the highest free iodide concentrations were in I2-treated
I find this very confusing. I am sorry if I bring confusion to you as well. I am doing my best to understand this. I find it quite difficult, and regret starting this post even 🤣 On the one hand, they say, some iodine is absorbed as iodine, and not iodide. On the other hand, they find the same levels of iodide in serum and urine of rats given either iodine (I2) or iodide (I-). And that the highest levels of free iodide was actually found in the rats given I2. They write in this study (8), that this is because there are more iodine atoms in I2 than in I-. I don’t know why they didn’t write that in the study (6) where they looked into that. I was really puzzled by it, and found this explanation later.
You see the graphs here:
Chemical differences between iodide, iodine and molecular iodine
This is a good explanation.
I find understanding the different forms of iodine quite difficult. Especially when we venture into nancent iodine, atomic iodine, detoxified iodine. I read so much confusing and misleading info on this subject, I won’t go into it before, or until, I feel I really understand it.
The differences between iodide(I-) and molecular iodine (I2) in the body
These scientists (6) not only look at the differences between iodide and molecular iodine, but have come up with ways to study it. Again, it involves the killing of rats. So not very nice reading. They are killed humanly though, put down like we put down our pets.
They are particularly interested in the anti-neoplastic (anti cancer) and anti-oxidant properties of I- and I2. They are referring to studies, showing that” iodide is more effective in restoring a goitrous thyroid to normal, whereas molecular iodine is more effective in diminishing benign or cancer pathologies of mammary and prostate gland.”
I go into this study in the Further reading section.
Further reading, Eskin's study from 1995, looking at how I- and I2 affect thyroid and breast
I will give an overview of this study. It is from 1995, by Eskin BA et al. It’s purpose is looking at how I- and I2 affects the thyroid and breast. (7)
This research describes the effects of short-term elemental iodine (I2) and iodide (I-) replacement on thyroid glands and mammary glands of iodine-deficient (ID) Sprague-Dawley female rats. Iodine deficiency causes atypical tissue and physiologic changes in both glands. Tissue histopathology and the endocrine metabolic parameters, such as serum TT4, tissue and body weights, and vaginal smears, are compared. A moderate reduction in thyroid size from the ID control (IDC) was noted with both I- and I2, whereas serum total thyroxine approached the normal control with both I- and I2, but was lower in IDC. Thyroid gland IDC hyperplasia was reduced modestly with I2, but eliminated with I-. Lobular hyperplasia of the mammary glands decreased with I2 and increased with I- when compared with the IDC; extraductal secretions remained the same as IDC with I2, but increased with I-; and periductal fibrosis was markedly reduced with I2, but remained severe with I-. Thus, orally administered I2 or I- in trace doses with similar iodine availability caused different histopathological and endocrine patterns in thyroid and mammary glands of ID rats. The significance of this is that replacement therapy with various forms of iodine are tissue-specific
This is the abstract. The gist is, that both I- and I2 restored thyroid levels to normal in iodine deficient rats. But only I- reduced goiters back to normal size. AND they saw, that iodine deficiency caused breast issues in virgin rats.
And I- actually INCREASED the cell growth (hyperplasia) in mammary tissue, whereas I2 markedly reduced it. The same with fibrosis.
So Lugols’s may not be the best for breast disease. Maybe better to use a pure molecular iodine with no iodide. This is just a thought. I see lots of people using Lugol’s for their breasts. And iodide actually gets converted to iodine in our tissues. As you can see elsewhere in this article.
So this is further evidence, that iodide and molecular iodine play different roles in the body. And that not all iodine is converted to iodide in the gut. I am not including any tables from the study. They become so messed up when I try to copy them, and it takes to so long to tidy them up. I think very few are THAT interested.
That iodine deficiency plays a big role in breast cancer and prostate cancer, as well as in less serious fibroid conditions in breast and uterus is well known in scientific circles. And Dr. Brownstein wrote this ages ago in his iodine book. Still, doctors don’t know this.
This is an article by Aceves, Anguiano and Delgado from 2012. This is an open source article, packed with information on the anti cancer and anti oxidant properties of iodine. (8)
Among other things, they say this
considerable evidence indicates that iodine per se can ameliorate physiopathologies of several organs that take up iodine, primarily the thyroid, mammary, and prostate glands and potentially the pancreas, gastric, and nervous systems, and it may act as an antioxidant in the whole organism if this element is ingested at concentrations higher than 3 mg/day (17). Dose-response studies in humans demonstrated that iodine at concentrations of 1.5 mg/day or less had no effect, whereas concentrations of 3, 5, and 6 mg/day, mainly in the form of molecular iodine (I2), exhibited significant beneficial actions in benign pathologies (mastalgia or prostatic hyperplasia) and antineoplastic effects in early and advanced breast cancer (14–16,18,19). These studies included treatments lasting from 5 weeks up to 2 years, and at these concentrations they do not exert any secondary effect. Some of these studies also analyzed higher concentrations of iodine (9 and 12 mg/day) and showed that these doses resulted in the same benefits but caused transient hypothyroidism in 20% of the studied individuals, while also producing an assortment of minor side effects (upper respiratory tract infection [26%], headache [20%], sinusitis [12%], nausea [9.9%], acne [9.0%], back pain [9.0%], diarrhea [9.0%], dyspepsia [8.1%], rash [8.1%], and abdominal pain [6.3%]) which disappeared when the high iodine supplement is stopped (15).
The authors recommend new recommendations of 3 mg Iodine/day. And they say, that doses of 1,5 mg does not have an effect on cell proliferation (cancer), whereas 3 mg has. But the same authors recommend 1 mg/day in one of their other studies. Which is very confusing. I think maybe 1 mg is ok for antioxidant effects, but if you have cancer, you need to take 3 mg or more. They are talking about molecular iodine.
I am not going too deeply into the method they have developed. It involves ion chromatography. I won’t claim to totally understand it. But the point is, that they can measure iodide(I-) and iodine (I2) in both bodily fluids and tissues very accurately. These scientists in Mexico, all women, are very dedicated to the study of iodine and you can find many studies by them.
What I don’t like about them, is, that they say different things in their various studies without explanation. In this study (6) from 2015, they say that molecular iodine , and not iodide, has an antioxidant effect throughout the body. But only taken over time and in doses of at least 3 mg. But in this 2021 study (8), they say, one must take at least 1 mg. There is no referring back to the previous study. I have even contacted the main author of the 2021 article, Carmen Aceves, and asked her to clarify. But have received no reply.
I have gone back to the study they refer to (9). This is an open source study, that you can read free of charge. It’s very complex. But nowhere in the study do I find any info on dosage for antioxidant effect of I2. I am starting to believe, there is a certain sloppiness here. That one do find, that for anti cancer effects, one needs from 3 mg and over to see effects. But I don’t think they actually have findings on antioxidant effects that says a particular dose. But if you can find it, please leave a comment. I may have missed it.
This is a shame, as people doing iodine very much want to know, what doses are both safe and sufficient. And we also want to know, what iodine to take. These scientists say, molecular iodine is superior as an antioxidant and that it is also safer for the thyroid. But where do we get this molecular iodine, and is it necessary? Or is Lugol’s more than good enough? I think so. Only if I had breast cancer would I feel the need to use pure molecular iodine.
Lugol’s has both I- and I2. 60% I- and 40% I2. In 1 drop 2% Lugol’s, there is 2,5 mg iodine. That means, there is 1,50 mg iodide and 1 mg iodine.
Povidone iodine (and Covid)
I thought this was the only iodine that contains molecular iodine only. And many write this online. But there is actually also another product today, made by ioTech International. And Povidone actually contains little I2 and more other kind of iodines, see below. There is also nanscent iodine.
In the US Povidone goes under the brand name Betadine. In the US you can also get it as a mouth wash. I have not found this in Europe. I have bought Povidone Iodine Cuidaplus myself. That is the antiseptic solution containing alcohol. I am not taking it internally, but do put a few drops in a glass of water and gargle. I do this if I have been in a situation where I could have picked up something, i.e. Covid.
I see online, sites like Webmed is warning against this. They write, vaccine critics are gargling with Povidone. I guess they want to make it seem like some kind of delusion. But it’s not only vaccine critics that gargle with Povidone, Webmed. Smart people do it. And we know now, there are and will be, new Covid strains that the vaccine you have at the time, will not protect against. Betadine writes on their site, it does not work against Covid. Like the Covid virus is different from all other viruses, and nothing can work against that. And WebMed even claim, ingesting Povidone can be DANGEROUS. OMG!
BUT THEY ARE WRONG. Here is a new review article stating, that gargling with Povidone for 30 sec will inactivate the Covid virus to not detectable levels.(11) They write that there are no clinical trials on this, only in vitro. That is not trials with live beings, only lab trials.
But there is at least one study, also from 2021. (12) It’s an Indian study, where they looked at the effect of nasal irrigation or nasal spray with Povidone, not gargling. They had 159 Covid infected people, divided into 3 groups. Each group given either nasal irrigation (NI), nasal spray (NS) or salt water. They trialed out various strengths. They found, that both irrigation and spray worked very well, with irrigation being the best.
Adjusting the differences, we observed a statistically significant proportion of nasopharyngeal clearance with all strengths of PVP-I NI and PVP-I NS compared to the corresponding controls. Additionally, 0.5% NI was significantly better than 0.5% NS for viral clearance (p = 0.018)
In the review article over, they give directions for the necessary and safe concentrations of mouth gargling with Povidone. Of course, if you can get mouth wash that is probably the best.
PVP-I is safe for use in the oral and nasal cavities at concentrations up to 1.25% [21]. In the absence of any commercially available preparations for routine dental use during the COVID-19 pandemic, it is advised to dilute 10% PVP-I by 1:20 and mix 0.5cc of the diluted PVP-I solution with 9.5cc of sterile saline or sterile water for routine clinical use
I mean, I just put a few drops of the 10% in a glass of water and gargle. But anyway, this is what they say.
The new molecular I by io Technical
I fell over this information (14) I thought I would not read the study, as you can see, it’s on densitry.
Io Technical has patented a new molecular iodine formulation. It’s much stronger than Povidone. I didn’t know this, but there is actually not a lot of I2 in Povidone.
Povidine Iodine vs. Molecular Iodine
First, let’s distinguish between PVP-I and I2 so that we better understand these very similar sounding, but very different acting, germicidal agents. PVP-I is an aqueous solution of several different species of iodine (including iodide, iodate, triiodide, hypo-iodous acid and molecular iodine). The iodine in PVP-I is bound to a large organic molecule, polyvinylpyrrolidone which, being highly soluble in water, carries the different iodine species, which have varying degrees of solubility, into solution along with it. 10% PVP-I (common brand: Betadine) is used in hospitals, medical and dental offices worldwide. It contains over 30,000 ppm of total iodine. The iodine species present in the least amount is I2 which is present at only 1-3 ppm1. All of the other species of iodine present contribute to staining, toxicity and irritation, but are not biocidal. Out of the over 30,000 ppm of total iodine, the 1-3 ppm of I2 accounts for all of the antimicrobial activity of PVP.ioTech International, a Florida-based antimicrobial company, has developed and patented stable aqueous formulations of I2 which contain over 100 times the available I2 (compared to PVP-I) while limiting the other non-bioactive iodine species from 30,000ppm to just a few hundred ppm (Fig. 1). This dramatically increases efficacy while drastically minimizing overall toxicity. The need for polyvinylpyrrolidone is also eliminated in these formulations. ioTech’s I2 formulations are essentially clear and do not stain compared to PVP-I, even at 10 times the strength of PVP-I. (14)
As you can see, Povidone contains many forms of iodine, with very little I2. Whereas in ioTech , there is more molecular iodine and less of the other iodine forms.
It’s an open source article where you can read how they compare Povidone, ioTech and chlorhexidine. And ioTech and secondly Povidone are much more effective than the CHX. And safer:
A key benefit of iodine formulations is that, unlike CHX and other antimicrobial agents, iodine does not induce resistance development in targeted microorganisms
I won’t go more into this here. You can read the article. I will only include this table where they compare oral rinses. I apologize for it being a bit small.
From “Molecular iodine: Could This Be a Game Changer for Dentistry?”
Antioxidant effects of I2, I- and ascorbic acid
The Mexican scientists looked at how well molecular iodine, iodide and ascorbic acid worked as an antioxidant. (9) As you can see, I2 had a much higher antioxidant effect than iodide. And ascorbic acid. They say, it is 10 times stronger than ascorbic acid, 50 times stronger than iodide. You can have a look at the original article for details on HOW they tested this.
And even though ascorbic acid is also a powerful antioxidant, iodine may be a more important one. This here is a very interesting open source article. Lots of info on the evolutionary importance of iodine and much more. (10)
It’s by an Italian scientist named Venturi. He says
. For this reason, we have hypothesized an “evolutionary hierarchy” for the wide range of antioxidants, where the most ancient might be more essential than the “modern” ones in protecting developing stages of animal and human organisms
What he and his group are saying, is that iodine is a very old antioxidant on our planet. With “modern ones” he means, phyto antioxidants like vitamin C and others.
Iodine has been around since the planet was formed. It’s breathtaking to read this (10)
The iodine atom (symbol I, atomic mass 126.9, atomic number 53, 53 electrons, 53 protons, and 74 neutrons) is a component of “nuclear ash”. In fact, it derives from a process of nucleosynthesis that occurred more than 10 billion years ago in a star-supernova that exploded and dispersed its dust,
which formed our planet Earth about 5 billion years ago. The iodine atom is one of the richest in electrons of our body and is essential in the diet of all living animals. Iodine is scarce in the earth’s surface, because, over hundreds of millions of
years, it has been washed away by rain and glaciations and transported from the terrestrial crust to the sea, which is enriched in iodine in the form of iodide (I-) and iodates [1,2].
He writes this as well
Our group has suggested that iodine and selenium
played an important role in protecting fragile, polyunsaturated membrane lipids, proteins and DNA from oxidation, and for this reason, these elements are important in animal
development and in human brain evolution
So iodine has been important in the very development of life on this planet. When I look at iodine, I think of the sun. The energy of life.
HOW does iodine work as an antioxidant?
Oxidized iodine (the process that takes place in the thyroid, iodide to iodine) can act as an electron donor neutralizing reactive oxygen species (ROS), or attach to the double bonds of some polyunsaturated fatty acids in cell membranes, making them less reactive to ROS (reactive oxygen species). (8) ROS is the what we lay people call oxidants. It’s a very important player in the developement of cancer. In addition, it has been shown that iodine binds to lipids, such as arachidonic acid (AA), exerts apoptosis, and/or has differentiation effects on diverse epithelial cells. (8)
Apoptosis is the process of programmed cell death.
I can’t explain what “differentiation effects” means. I have tried to understand it, but have given up. They talk about it in connection to the epithelial cells of tumors.
The iodine released by deiodination of thyroxine has been shown to be an antioxidant agent and an inhibitor of lipoperoxidation. (What that means is, as our thyroid hormones are broken down, iodine atoms are being released, and these iodine atoms are antioxidants in the body. As you know, iodine stands for the greater weight of a thyroid hormone. The number on the hormone, signifies the number of iodine atoms. T4 has 4 iodine atoms, T3 has 3. The hormones are broken down into T2 and T1, and the iodine atoms are saved in the body, while the tyrosine (T) part of the hormone molecule, is being excreted).
Lipoperoxidation means the chain of reactions of oxidative degradation of lipids.
Iodine also has anti inflammatory effects:
These specific actions of iodine agree with reports describing the anti-inflammatory effects of marine algae, which, as noted above, contain the highest iodine concentration of living organism, and suppress the levels of proinflammatory messengers such as nitric oxide, prostaglandine-E2, and proinflammatory cytokines (tumor necrosis factor-α, interleukin-6, and interleukin- 1β) (9)
You can find much more info on this in the study ” The Extrathyronine Actions of Iodine as Antioxidant, Apoptotic, and Differentiation Factor in Various Tissues”. (9) And in “Molecular Iodine Has Extrathyroidal Effects as an Antioxidant, Differentiator, and Immunomodulator” (8).
They write:
Several studies suggest that iodine works by neutralizing ROS, or by acting as a free radical iodinating tyrosine, histidine, and double bonds of polyunsaturated fatty acids in cell membranes, making them less reactive to ROS [4,49]. However, the antioxidant effect of iodine could be more complex and include various mechanisms (Figure 2). In a model of prostatic hyperplasia, our group demonstrated that I2 supplements prevent testosterone-induced oxidative stress, decreasing lipoperoxidation but also inhibiting the activity of both nitric oxide synthase (NOS) and type 2 cyclooxygenase (Cox2). The I2 supplement also inhibit the formation of prostaglandins with equivalent intensity to that observed with Celecoxib (a specific Cox2 inhibitor). The effect on Cox2 inhibition can occur by deactivating the heme iron active site or as a competitor of its main substrate, arachidonic acid (AA)
These things are quite complicated, and I don’t understand it all. Dr. Brownstein has written about the antioxidant effects of iodine in his book “Iodine, why you need it”. It’s especially iodine’s effects against ROS that he highlights. I believe he was pretty early with this info, I am not sure when the first edition of his book was published. It’s on it’s fifth edition now, in 2022.
How does iodine enter the cells?
Iodine can enter the cells in various ways. Dr. Brownstein writes about only the Sodium Iodide Symporter (NIS), and this is the only receptor I see people in iodine groups mention. But NIS is not the only channel into our cells.
The thyroid
Iodide enters the thyroid through the sodium iodide symporters. Iodide enters the thyroid follicular cells, and the iodide then enters the colloid through another receptor called pendrin. The colloid is where the oxidation happens, where the TPO enzyme assists in oxidating the iodide to iodine. The iodine then moves into the thyroglobulin molecule. This is where the thyroid hormones are made.(13) An electron is removed from the iodide atom, and you have an iodine atom.
From Dr. Brownstein’s book, “Iodine, why you need it, why you can’t live without it.
There are also other ways iodine enters cells. (8) These transporters are anoctamin 1 (ANO1), cystic fibrosis transmembrane conductance regulator (CFTR) and multivitamin transporter (SMVT). These are all able to take up iodide.
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 (8)
They write that “this diffusion system could be similar to what happens in marine algea , indicating that I2 absorption could be an evolutionary conserved system. ” and that “the thyroid, mammary gland and prostate can accumulate both kinds of iodine, which are captured by different mechanisms”. ( 8)
So many organs traps or absorb iodine. Though the thyroid is the main organ trapping I.
The salivary glands, gastric mucosa, lactating mammary gland, nubile mammary gland (non lactating mammary gland, traps I2), nervous system, choroid plexus (where the spinal fluid is produced), lacrimal gland ( the little gland producing the tear film), ciliary body of the eye(a part of the middle layer of the eye. It’s behind the iris, and includes the ring shaped muscle that changes the shape of the lens as the eye focuses. It also produce the clear fluid that fills the space between the cornea and the iris), thymus, skin, placenta, ovary, uterus, prostate and pancreas.
I was very excited to read the Mexican scientists had also discovered that even the pineal gland traps iodine. (6) It’s not a surprise of course, as Dr. Brownstein says, ALL glands in the body traps and use iodine. But nice to have verified.
Mammay glands and iodide/ molecular iodine
As I wrote in the abstract, I won’t go too much into cancer in this post. But I have to include some info on iodine and the breasts. There is a lot of info on this topic online, but I just want to point out, that scientists found, that the mammary glands only traps iodide via NIS when they are lactating and when the breast is cancerous. (15) This study from 2000 has nearly 600 citations, so it has been very influential.
These results indicate that the mammary gland sodium/iodide symporter may be an essential breast cancer marker and that radioiodide should be studied as a possible option in the diagnosis and treatment of breast cancer. (15)
But as you saw over, that does not mean that the mammary glands don’t utilize any iodine at other times. That the non lactating glands actually absorbs molecular iodine through diffusion. It seems it’s very important to get molecular iodine for breast health.
I think this is very important. And even more so the fact that iodide can proliferate cells in breast tumors. You find that info in the Further reading section on the Eskin study over.
…several pieces of data in the literature show that I- treatment does not exhibit the antiproliferative and apoptotic effects of I2 treatment in in vivo and in vitro cancer models (6)
This is not an open source study, but this is a direct quote. So molecular iodine is better in cancer treatment. But at the same time, these same scientists have conducted a study (16) on mammary cancer in rats (poor animals!) with KI (iodide), I2 and Lugol’s (KI and I2) and they found that all solutions had an anti cancer effect. But their results showed, that the iodide needed to be oxidized into I2 in the tissues to have this effect.
They found this out by inhibiting the PO enzyme. Which is the enzyme oxidating iodide into molecular iodine. They did find that both KI, I2 and Lugol’s can induce antineoplastic (anti cancer) actions in rats they had given mammary cancer. But if they inhibited the enzyme lactoperoxidase (LPO), which is present in mammary cancers, they saw no apoptotic effect of KI, iodide. They inhibited the enzyme with MMI, Methimazole. (16)This is an anti thyroid drug that inhibits the peroxidaze enzyme, and thereby inhibits the hormone production. This is why it’s used in hyperthyroid conditions.
So it looks like, iodide needs to be oxidized into iodine in order to kill cancer cells. The Mexican scientists claim, it is only thyroid and mammary tissues that have the ability to organify iodide. In the thyroid, the peroxidase enzyme is called TPO (thyroidperoxidaze) and in the breast, it’s called LPO (lactoperoxidaze).
I think if I had breast cancer, I would look to get molecular iodine. To be sure to get the maximum anticancer effects.
Iodine and the immune system
It’s exciting to see the role of iodine for our immune system.
In the Bilal study (17) they found that human leukocytes have both NIS and Pendrin on their surface, with the highest expression on monocytes and granulocytes. And when they treated leukocytes with Nal or Lugol’s, it induced increased protein production of both pro-and anti -inflammatory cytokines. So both good and bad.
In this same study, they looked at if iodide could be toxic to human leukocytes. They incubated leukocytes with Nal for 3 days. They found no significant changes in total cell count or viability (“life force”) with iodide treatment.
They also looked at “whether iodide could alter immunity related transcriptional events in human immune cells”. They immersed leukocytes in either iodide or in some control media (PBS). They found that “immune cells treated with iodide had significant changes in total 29 genes with 24 being upregulated”. You can read more in the study, it’s an open source study. I don’t know that much about the immune system to understand all the details. They did see increase in various cytokines.
Transcription is the process of making an RNA copy of a gene sequence.
They wanted to see, if other forms of iodine would also affect basal cytokine release, they immersed leukocytes in Lugol’s as well. That is, a mixture of KI and I2. In Lugol’s, they saw an even greater increase in protein release in IL6, IL10 and CXCL8. But it significantly reduced release of IFNγ . I don’t know what this means, but hopefully, you do😉
Bilal et al do not appear to have read the works of the Mexican researchers, who as we saw over, say that iodide gets converted to iodine (I2) in the tissues. And the more it gets converted, the more antioxidant it is. So the reason, Lugol’s caused an even bigger increase in protein release than iodide, is probably because, in that case, there was MORE I2 than with I- only.
In his article in” Hormone matters” (13), Bilal refers to an Italian study from 1985. It’s on T cell function in kids, healthy kids and kids with goiter. This is a study that it’s impossible to find anywhere. I have asked Bilal about this in a comment on the article. I asked if he himself had read the whole study, and actually SEEN the thyroid results for these children. He hadn’t been able to assess the study either. It’s very difficult to know if the author’s conclusions are accurate, when we don’t know for sure if the kids were euthyroid or not. Euthyroid means having good thyroid levels. It is my experience, that scientists do not generally know, WHAT are normal thyroid levels. If I had written that article, I would have mentioned this. I don’t just accept someone’s conclusion when I haven’t read the study. There is so much bad science.
The whole point of this study, is that despite normal thyroid levels, some of these kids with goiter have reduced immune response. And that after supplementing with iodine, the immune response is normalized. I am not saying, this is not the case. But before I see the thyroid levels with my own little blue, I have reservations. In most studies on the thyroid, people are hypothyroid without the scientists realizing. And IF the thyroid levels were too low before iodine, the iodine can have increased these levels. And this could be the reason for the improved immune response.
Why do I mention this? I believe many iodine nerds read this article. I have a very critical comment on it in the next section. But don’t misunderstand me, I think there is a lot of good and interesting stuff in that article. BUT I have found some unfounded claims, that I find quite serious.
Can there be thyroid hormone production outside the thyroid?
Can thyroid hormones be made outside of the thyroid? M Y Bilal strongly suggests this in his article “The extrathyroidal Role of Iodine” in Hormone matters (13). Here comes my critique of his claims.
When I first read his claims, that human immune cells could potentially produce thyroid hormones, I was quite excited. Luckily, I read his own study from 2017 (17), which he builds his claims on. I find, that he misrepresents his own findings, and I will tell you how.
In the article he writes:
The classical view is that only the thyroid can do this, and indeed the thyroid bears the weight of making these hormones. However, it turns that immune cells can perform very similar functions to the thyroid. The same 2017 study showed that human immune cells could uptake the Thyroglobulin protein and then produce from it thyroxine (T4) and triiodothyronine (T3). These cells can also potentially make thyroglobulin and iodinate it using inorganic iodine – although organification of thyroglobulin by iodine has not yet been clearly shown experimentally outside of the thyroid. Nevertheless, the study shows that your thyroid is not the only place where thyroid hormones can be made!
One gets the impression, that the immune cells produce T4 and T3, right? That it is very likely, that they can perform the same function as the thyroid. But is this the case? No.
I got quite excited when I first read this. But then I read his own 2017 study that he is referring to. In the study it says:
leukocytes incubated with TG released substantial amounts of T4 and T3
The key word is release. Not produce.
What they did, was incubate leukocytes with thyroglobulin molecules. You remember, the thyroglobuline molecule is where thyroid hormones are produced and stored. So these TG molecules contained T4 and T3 molecules, and these were released in the leukocytes. The leukocytes did not produce anything.
I find the article misleading on this one topic. There is no real proof of production of thyroid hormones in immune cells. But Bilal says, this has already been proven. Please read his comment below, and my reply for further info. Is there even a release of hormones in immune cells in real life? In thyroid healthy people, there is supposed to be very little thyroglobulin in the blood. It’s when we have autoimmune thyroid disease, that TG leaks out. For the hormones to be released from the TG molecule at that time, is not a good thing. The person becomes hyper. In thyroid health, the thyroid hormones are released from TG inside the gland.
They did find something very interesting though, that the immune cells can convert T4 to T3. They incubated immune cells with T4 hormones. And could measure, T3 in the solution.
But there are no grounds for saying, that the immune cells can make thyroid hormones. There has to be peroxidase enzyme for there to be thyroid hormone production. Not only does the enzyme oxidate iodide, it attaches iodine atoms to the tyrosine inside the thyroglobulin molecule, called iodination. This iodination creates MIT and DIT ( T1 and T2). These are then attached to each other to create T3 and T4. This process is also facilitated by TPO.
So even if the immune cell got I2 directly, with no need for oxidation, there had to be peroxidase in order to make T3 and T4. You can read more about this process and the TPO enzyme here.
Do the immune cells have the PO enzyme? I don’t think so. The Mexican scientists say:
, it is well established that, with exception of the thyroid and lactating mammary gland, other tissues that take up iodine do not have the enzymatic system to oxidize and organify I-, resulting in its
transitory uptake and release within minutes or hours (16)
The PO enzyme is present in many other tissues besides the thyroid- and mammary glands. In various forms. (18,19) But according to this, these tissues still lack the ability to oxidize and organify iodide. So the thought that an immune cell should be able to do this, seems strange to me.
It might be, that one does find thyroid hormone production outside the thyroid at some point. I don’t know. But no one has found such production so far. At least, I haven’t seen such proof. I have read an article where they claim to have proven, immune cells produce T3. A study Bilal reference in his 2017 study. I don’t think the claims they make hold up though. Have a look at my reply to Bilal’s comment . That study isn’t open source though, so most people can’t read more than the abstract. I have read the whole thing .
We must wait and see. If they find peroxidase and MIT and DIT inside immune cells, I will believe, immune cells can produce thyroid hormones. Would be a bit strange, if millions or billions of immune cells make thyroid hormones. Considering the wave of hypothyroid disease sweeping the world.
Bilal has made a comment on this post. He thinks I don’t understand his 2017 paper, and that I haven’t read it thoroughly. You can read his comment below, as well as my reply.
In that comment, he claims that his and other groups have shown that immune cells can produce T3. In his 2017 study, he refers to this study (20). It’s not open source, but I have read the whole thing. They plied immune cells with TSH in a higher concentration than what’s normal. They found an increase in T3. They conclude, immune cells produce T3. This is what I call bad science. There is no discussion, of what could be the cause of the increase. I believe this was a question of conversion of T4 to T3.
They didn’t apparently think to look for peroxidase or MIT and DIT or TG. I describe the thyroid hormones production process including MIT and DIT on this post.
If they had proved that immune cells produce T3, that would be a sensation. So to just off handedly claim, that they do just on these flimsy grounds, that’s surprising, to say the least.
Bilal himself has shown, that immune cells can convert T4 to T3. He plied immune cells with T4, and could later detect T3. (19) Most likely, that’s what happened in the study over.
Extrathyroidal thyroid hormone production in other tissues?
Bilal is also referring to this study, which I think has more potential of proving extrathyroidal hormone production. There is no talk of hormone production in immune cells, they measured T4 and T3 in some vital tissues in rats after thyroidectomy (T groups). At various times after the surgery. (21) It is not open source. It’s a very old study, from 1981. I would say they were ahead of their time. The study has some shortcomings though.
What they did was removing the thyroid from female rats. Then they slaughtered them at 15 days, 2 months and 4 months. They compared them to healthy controls, that they also slaughtered at the same time intervals. They caution though, that the vital organs that they looked at, like the liver and kidneys are smaller in the thyroidectomy groups. So when they compare percentages, the amounts in the T groups are actually lower than what the numbers say. But they were surprised by the T4 and T3 levels in liver, kidneys, brain, heart and muscle as time went by. The plasma levels of T4 and T3 went down to under 5% of controls at the 15 day mark. They discuss themselves, they should have slaughtered already at 2 days, to see how fast the plasma levels dropped. Most of the T rats died at 6 months, from myxedema coma. The few who didn’t die, were killed at that point. So it’s not like one can live for a long time without a thyroid. But the mice lived longer than one maybe would have believed.
Concentrations of T3 and T4 in tissues are shown in Fig. 2LAs already summarized in Table 1, by 15 days
after T the concentrations of T3 and T4 in plasma had fallen to values below 5% of those of controls. The concentrations of T3 and T4 also decreased in all the tissues.studied. However, they were still clearly detectable in most tissues up to 4 months after T. The rate of decrease both of T4 and T3 was slower than expected from plasma data. This becomes more evident when the mean tissue T3 or T4 concentrations are expressed as percentages of the values found in intact animals: in all the tissues
studied, T3 or T4 concentrations were clearly above 5% of the control value, in contrast with the plasma data.
Despite the more rapid t^ of disappearance from plasma of T3 than of T4 (9), the decrease of T3 concentration in tissues is slower than for T4. Concentrations of T3 and T4 become more similar after T, even for liver and kidney, where there are large differences in intact rats. The data pertaining to T3 and T4 concentration might lead us to overestimate the actual amounts of T3 and T4 found in T rats, because the weight of many organs is reduced in such animals (Table 2). Figure 3 shows total T3 and T4 contents of the liver, kidney, brain, and heart. These organ contents represent a smaller percentage of those of intact rats than might appear from concentration data. We observed that 6 months after T several severely
hypothyroid rats died within a few days. The five remaining animals of the group were killed. No gross changes in the appearance of the liver, kidney, lungs, or brain were evident at autopsy. The T3 and T4 concentrations were determined in tissue and plasma extracts. T3 and T4 were hardly detectable in most samples using the same tissue equivalents for the RIA as employed for the groups shown in Fig. 2: the concentrations of T3 and T4 in liver, kidney, and brain were below 5% of those of intact rats, except for T3 in kidney (10%). The total organ contents of T3 and T4 had decreased to values below 5% of normal in all the tissues studied.
They conclude like this
In Conclusion, thyroid hormones are present in tissues for long periods after T despite virtual absence from
blood and signs of severe hypothyroidism, and hence T
animals are not living in the absence of these hormones. The thyroid hormones found in such animals might arise from thyroid remnants, extrathyroidal synthesis, or ingested food.
There are a lot of good tables and graphs in the study. I just can’t manage to copy them, I would have to manually make diagrams. And that takes more time than I want to spend. But this is the reason why I include this much text from the study.
We can’t know for sure that there was extrathyroidal hormone production in these vital organs. But it could be. What is certain though, this cannot replace the thyroid’s production, and the rats died. At the time of dying, the T4 and T3 levels in the organs were under 5% of those of the controls. Except for the kidneys with 10%. SO IF THERE WAS EXTRATHYROIDAL PRODUCTION, THIS WAS TEMPORARY. A big weakness of this study, is that they excluded all the rats that had put on weight after 15 days. So the rats that showed the most hypo symptoms, were excluded. I don’t understand the rationale for this. They should have been included. The fact that some rats become overweight fast and others didn’t would suggest that there are big individual differences. This should have been explored.
Of course, this is animal abuse. The rats suffered. But it is a very interesting study. Such a shame that they didn’t make the most of it by looking more closely at individual differences and that they excluded the rats who became hypothyroid fastest.
Iodine, a finite resource
Just a final thought, and an appeal to you who take very high doses of iodine. As you saw over, iodine is a very limited resource. As well as being the foundation for life. Is it ok to use so much more than your share of this element?
I don’t think these super high doses are healthy either. I think it’s a very big strain on the kidneys. Stephanie Buist also speaks out against them. But my main concern is the depletion of our iodine resources. They are already low. So I hope you will consider that. Are these mega doses necessary? I think not. I see people using over 50 mg a day, some people as much as 400 mg. I don’t think it has a function. Try, and see, if you cannot do with less. We, and other beings, should be able to live on the planet also in the future.
References
- J. Wolff & J.I. Chaikoff. Plasma inorganic iodide as a homeostatic regulator of thyroid function. https://doi.org/10.1016/S0021-9258(19)52781-8. https://www.jbc.org/article/S0021-9258(19)52781-8/fulltext
- B. Anguiano,* P. Garcıa-Solı´s,* G. Delgado, and C. Velasco. Uptake and Gene Expression with Antitumoral Doses of Iodine in Thyroid and Mammary Gland: Evidence That Chronic Administration Has No Harmful Effects. DOI: 10.1089/thy.2007.0122 Link
- G.E. Abraham. The Wolff-Chaikoff Effect: Crying Wolf? https://www.optimox.com/iodine-study-4
- Iodine, inorganic
and soluble salts, https://www2.mst.dk/Udgiv/publications/214/01/978-87-93026-87-2.pdf - K.D.Thrall & D.J. Bull. Differences in the distribution of iodine and iodide in the Sprague-Dawley rat. doi: 10.1016/0272-0590(90)90164-f. https://pubmed.ncbi.nlm.nih.gov/2373302/
- G. Delgado et al.Total iodine quantification in fluids and tissues from iodine- or iodide-supplemented rats by ion chromatography following microwave-assisted digestion. DOI: 10.1089/thy.2014.0290. https://pubmed.ncbi.nlm.nih.gov/25668583/
- Ba. Eskin et al. Different tissue responses for iodine and iodide in rat thyroid and mammary glands. https://link.springer.com/article/10.1007%2FBF02788999
- C. Aceves et al. Molecular Iodine Has Extrathyroidal Effects as an Antioxidant, Differentiator, and Immunomodulator. doi: 10.3390/ijms22031228. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7865438/
- C. Aceves et al. The Extrathyronine Actions of Iodine as Antioxidant, Apoptotic, and Differentiation Factor in Various Tissues. 10.1089/thy.2012.0579. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3752513/
- S. Venturi. Evolutionary Significance of Iodine. Current Chemical Biology, 2011, 5, 000-000. https://www.ign.org/cm_data/2011_Venturi_Evolutionary_Significance_of_Iodine.pdf
- A. Chopra et al. Can povidone iodine gargle/mouthrinse inactivate SARS-CoV-2 and decrease the risk of nosocomial and community transmission during the COVID-19 pandemic? An evidence-bas. ed update. doi:0.1016/j.jdsr.2021.03.001. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7959263/
- M.K.Arefin et al. Virucidal effect of povidone iodine on COVID-19 in the nasopharynx: an open-label randomized clinical trial. DOI: 10.1007/s12070-021-02616-7. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8130786/
- M. Bilal. The Extrathyroidal Role of Iodine. https://www.hormonesmatter.com/extrathyroidal-role-of-iodine/
- Herb Moskowitz et al. Molecular Iodine: Could This Be a Game Changer for Dentistry? https://www.oralhealthgroup.com/features/molecular-iodine-could-this-be-a-game-changer-for-dentistry/
- U H Tazeby et al. The mammary gland iodide transporter is expressed during lactation and in breast cancer. DOI: 10.1038/78630. https://pubmed.ncbi.nlm.nih.gov/10932223/
- O. Soriano et al. Antineoplastic effect of iodine and iodide in dimethylbenz[a]anthracene-induced mammary tumors: association between lactoperoxidase and estrogen-adduct production. DOI.org/10.1530/ERC-11-0065. https://erc.bioscientifica.com/view/journals/erc/18/4/529.xml
- M Y Bilal. A Role for Iodide and Thyroglobulin in Modulating the Function of Human Immune Cells. doi.org/10.3389/fimmu.2017.01573. https://www.frontiersin.org/articles/10.3389/fimmu.2017.01573/full
- M Bhattacharjee et al. Critical role of an endogenous gastric peroxidase in controlling oxidative damage in H. pylori-mediated and nonmediated gastric ulcer. doi.org/10.1016/S0891-5849(02)00757-8. https://www.sciencedirect.com/science/article/abs/pii/S0891584902007578?via%3Dihub
- AA Khan. Biochemical and Pathological Studies on Peroxidases –An Updated Review. doi: 10.5539/gjhs.v6n5p87. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4825458/
- G. Csaba and É. Pállinger. Thyrotropic hormone (TSH) regulation of triiodothyronine (T3)
concentration in immune cells. DOI 10.1007/s00011-008-8076-8 - M J Obregon et al. Presence of L-Thyroxine and 3,5,3′-Triiodo-L-thyronine in Tissues from Thyroidectomized Rats*. Doi: 10.1210/endo-109-3-908.
Here is the iodine FB group I belong to. The admins are open to new science and there is room for discussion :
Hello, this is Dr. Bilal. I want to first thank you and appreciate your research and in-depth analysis! We certainly need more of this. I enjoyed reading your blog.
However, I do want to say that in your conclusions about my articles, you have missed some of the important points that I made which led you to believe that I am making “wild” conclusions. The points you missed actually answer many of your concerns. Here are some examples:
1. You mention “I have even asked Bilal about this in a comment on the article. but I never got an answer. ”I’ve actually responded to your comment on HormonesMatter within the same day…
2. About the immune cells making hormones… I clearly say in the HM article AND the study what I exactly mean. That immune cells CANNOT make thyroid hormones just by giving them iodine, but instead they require Thyroglobulin – I even have a figure/image on this. In essence, immune cells can perform thyroid related functions (i.e. breaking down TG into T4 and T3). Here is a quote from the HM article “the same 2017 study showed that human immune cells could uptake the Thyroglobulin protein and then produce from it thyroxine (T4) and triiodothyronine (T3). ”
If you look at the 2017 closer you will find detailed explanation – I did not make more claims than what the data shows. The 2017 study contains plenty of information about this extrathyroidal T4/T3 effect, even by other groups. An example quote “Under our experimental settings, we could not detect any increase of T4 or T3 when the cells were incubated with 1 mM of NaI for 72 h in complete media ”
I understand your skepticism about extrathyroidal hormones, but I am going to have to disagree here because of our data and other groupss data. Do they make hormones better than the thyroid? No, but they certainly can make it in the presence of thyroglobulin. Again, this was made very clear in the write-ups. You need to understand that creation of thyroid hormones is a multi process, the first is oxidation of iodine, and then release of the hormones by the thyroid. The immune cells can perform all of these steps with the exception of oxidation of iodine (hasn’t been proofed yet).
You also mention “One gets the impression, that the immune cells produce T4 and T3, right?”… You only get this impression if you misread the paper! the quotes are direct and clear. Please read my 2017 article’s detailed discussion on this topic.
3. You mention “Bilal et al do not appear to have read the works of the Mexican researchers”. We do understand that iodide is converted to iodine (this is mentioned in the introduction of the study and the article!). And we have mentioned about the IFNy effect between NaI and Lugol’s as such “The subtle differences between NaI and Lugol’s can be explained by the distinct iodine-derivatives between the two treatments.”
4. You mention “The key word is release. Not produce. ”. This is all semantics and mere opinion. Immune cells uptake thyroglobulin and then “release” hormones. The thyroid does the same exact thing. Again see my point above, we CLEARLY say what does and doesn’t happen.
5. You mention “It might be, that one does find thyroid hormone production outside the thyroid at some point.” If your read the paper discussion and intro section you will see that this has already been shown by other groups. What our article did was to show that immune cells can perform similar functions to the thyroid – by breaking down Thyroglobulin.
By the way, did you know that immune cells produce TSH and have TSH receptors…?
Unfortunately it seems that your own conclusions about what we have represented seem to be vague and, I don’t think you have looked my article or paper in detail, but I do respect the analysis.
Hi Mahmood Bilal!
First of all, I apologize for the not replying comment. I will correct that on the post later. I don’t understand what happened, as I went back and looked for your reply. Again, sorry. I have replied to your reply now.
I can assure you, that I have read both your article and study several times. I am quite thorough when I write my posts. That does not mean, I cannot misunderstand or misinterpret. But I am not sure I have done this here. I haven’t reread them now, I don’t have the time. But when I look at the parts I have highlighted, I find, that you use the word “release” in the study and “produce” in the article. Which is what I criticize. I think “produce” is misleading. I think that what the immune cell has done is what happens also in the gut, it has broken down the thyroglobulin protein, and the hormones stored are released. Many immune cells contain serine proteases. I add this info for the readers, you know this obviously. And better than me. I take TG every day, in my NDT. The TG is broken down by protease in my gut, and T4 and T3 released. Would you say, the protease enzyme PRODUCED the hormones? I would not.
I have read the Csaba and Pallinger study you refer to. If this is the study you claim proves that immune cells produce T3, I don’t think it proves that. They ply immune cells with TSH and find an increase in the T3 level. They conclude, the cell has produced the T3. I call this sloppy science. This would be revolutionary findings, but there is no discussion. They just draw that conclusion. Not a word about deodinase. Which I think is what happened. T4 being converted to T3. If there was hormone production, they would have found peroxidase and thyroglobulin. If there was T3 produced, they must have found some of these. And MIT and DIT. The thyroid first produce MIT and DIT, and then combine the two into T3. T4 is 2 DIT molecules combined. For the readers, you can find this process described here, Antibodies, part 1, Anti-TPO If they didn’t even look for any of these, and still just concluded, the immune cell produced hormone, I find that sloppy.
Both the organification of iodide and the combining of MIT and DIT are dependent on peroxidase. Is it so difficult to detect peroxidase? They detect it in the thyroid and mammal glands, so why not in immune cells? If it is there?
Can thyroid hormones be produced outside the thyroglobulin molecule? TG is not only the storage site for hormones, it’s where the hormones are produced. I don’t know.
You say, it’s mere semantics. I don’t agree. I think words are important, and that science needs to be precise. For me produce means make. Releasing something that is already made, is not making. I get the impression, you think peroxidase will soon be detected in immune cells when you write “yet”. We will see.
I don’t think it has been proven that immune cells produce thyroid hormones. I believe there must be both peroxidase and thyroglobulin present. Neither of which has been detected, as far as I can see.
I just don’t understand how come so many are hypothyroid if there is thyroid hormone production in millions, not to say, billions of immune cells. Seems very strange to me. I will be the first to admit I was mistaken once it is proven. I try to leave my ego out of my learning about the thyroid and the body in general. I try to have a scientific mind, always open to new data. I see myself as a forever student, sharing what I learn with my fellow patients. In the hope that what I write will improve someone’s life. As a cand.psychol, I am well versed in reading and interpreting scientific literature though. I have a lot of training in statistics and methodology.
By the way, you write in your 2017 study, that the thyroid releases relatively low amounts of T3. I know this is what all endoes say, but it’s not correct. The truth is, it’s very individual how much T3 the gland produces. It was detected already in 1990, by Pilo et al, here. In their study, they saw that it varied between 6,5% and as much as 42% in individuals. You find a diagram of this on this post, under T4 medicine, Optimal thyroid levels It was Tania Sona Smith at Thyroid patients Canada who made me aware of this. And she has made that diagram.
I think it is so great, that there is so much science going on on iodine now. I think there is a lot of great info in your study. It is so important, that scientists and doctors realize, how important iodine is. Hopefully this crazy fear of iodine will end soon. Most doctors still believe, the thyroid is the only organ utilizing iodine. So your work is very important. I do think my critique holds up though. We will just have to disagree. I will add to the post, that you have written a reply here in comments. Then people can decide for themselves.
You say my own conclusions are vague. Well, I am not really in a position to conclude. I am looking at the science and conveying what I think about it. My conclusion at this time is, that I don’t think thyroid hormone production in immune cells have been proven. When they detect peroxidase and MIT and DIT inside immune cells, I will believe it.
I am not saying, that there cannot be extrathyroidal thyroid hormone production. But i haven’t seen it proven, that there is such production in immune cells. So far.
Thanks again for contacting me. I look forward to reading your future research.
All the best, Liv