Ray Peat On Iodine

[Makrosky]

Ok, so many people is talking about iodine now. A user called visionsofstrenght over the old peatarian.com forum posted this, so I'm copying it here as well. Original thread (http://beesandbutterflies.org/52426/iod ... 426#q52426)

Here are the Peat references on iodine:

The Myth of Iodine Deficiency - Interview with Dr. Ray Peat

Is iodine supplementation safe and, if not, is there a safe amount of supplemental iodine?

Dr. Peat: “A dosage of 150 mcg (micrograms, not milligrams, e.g. ug not mg) is a safe amount of iodine. My current newsletter has some references describing the effect of even moderate iodine excess (even below a milligram per day) on the thyroid. An iodine deficiency can cause hypothyroidism (rare now), but so can an excess. Most goiters now are from estrogen-like effects, but they used to be from iodine deficiency. Chronic excess iodine tends to cause thyroiditis, regardless of the gland's size.
The amounts used by Abraham and Flechas are much larger than this – very toxic doses, enough to cause severe thyroid problems. “

Is the Iodine Test Kit (from Dr. Abraham) valid and does it reveal thyroid deficiency?

“Guy Abraham and his followers are iodine cultists; some of them claim that an iodine deficiency can be shown by the quick disappearance of a spot of iodine painted on the skin. Iodine is converted to colorless iodide by reductants, including vitamin C, glutathione, and thiosulphate.

The skin test of iodine deficiency is just completely brainless. Iodine is converted to colorless iodide by reductants, including vitamin C, glutathione, and thiosulphate. My current newsletter has some references describing the effect of even moderate iodine excess (even below a milligram per day) on the thyroid. An iodine deficiency can cause hypothyroidism, but so can an excess.

The Iodine Test Kit is just a way to sell more of (G. Abraham’s) iodine overdose pills. Those, malic acid, and gold are products of Optimox/Abraham. The test is completely irrational. It implies that the body should be saturated with iodine.

Is there a rational test for iodine overdose/deficiency?

Dr. Peat: “It could be done, but it isn't considered to have any health significance, since goiter is the only generally recognized effect of a deficiency. Hypothyroidism is strongly associated with breast disease, including cancer. John Myers probably started the talk about iodine receptors, which has led people to confuse oxidative damage with a physiological effect. As a general principle, it's good to figure that everything they say about iodine is false. Hypothyroid people get cancer, but iodine deficiency is an unusual cause of hypothyroidism, except in a few places, like the mountains of Mexico and China, and the Andes. John Myers seems to be the one that started the idea of an iodine receptor, thinking about the ability of sulfhydryl compounds (such as cysteine or glutathione) to reduce molecular iodine to iodide, but there's really no particular meaning to the idea of an iodine receptor. John Myers wasn't quite as flaky as the current crop of iodine crazies, but he didn't have any clear ideas, either. High iodine intake can suppress TSH, and since high TSH is pro-inflammatory, the iodine can have some protective anti-inflammatory actions, but in the long run, the thyroid suppression becomes a problem.”

Iodine toxicity References
Re the urinary iodine test, it’s one of the big cults going around lately, telling people they should be saturated with iodine. Iodine reacts easily with toxic PUFA (omega-3 and -6 oils) to make antithyroid molecules.

Science 1985 Oct 18;230(4723):325-7
Induction of autoimmune thyroiditis in chickens by dietary iodine.
Bagchi N, Brown TR, Urdanivia E, Sundick RS.
Clinical studies have suggested that excess dietary iodine promotes autoimmune thyroiditis; however, the lack of a suitable animal model has hampered investigation of the phenomenon. In this study, different amounts of potassium iodide were added to the diets of chicken strains known to be genetically susceptible to autoimmune thyroiditis. Administration of iodine during the first 10 weeks of life increased the incidence of the disease, as determined by histology and the measurement of autoantibodies to triiodothyronine, thyroxine, and thyroglobulin. Further support for the relation between iodine and
autoimmune thyroiditis was provided by an experiment in which iodine-deficient regimens decreased the incidence of thyroid autoantibodies in a highly susceptible strain. These results suggest that excessive consumption of iodine in the United States may be responsible for the increased incidence of autoimmune thyroiditis.

Endocrinology. 2008 Jan;149(1):424-33. Epub 2007 Sep 20.
Oxidative stress in the thyroid gland: from harmlessness to hazard depending on the iodine content.
Poncin S, Gérard AC, Boucquey M, Senou M, Calderon PB, Knoops B, Lengelé B, Many
MC, Colin IM.
Unité de Morphologie Expérimentale (MOEX), Université catholique de Louvain,
UCL-5251, B-1200 Brussels, Belgium.
In basal conditions, thyroid epithelial cells produce moderate amounts of reactive oxygen species (ROS) that are physiologically required for thyroid hormone synthesis. They are not necessarily toxic because they are continuously detoxified either in the process of hormone synthesis or by endogenous antioxidant systems. Using a rat model of goiter formation and iodine-induced involution, we found that compared with control thyroids, the oxidative stress, assessed by the detection of 4-hydroxynonenal, was strongly enhanced both in hyperplastic and involuting glands. The level of antioxidant defenses (glutathione peroxidases and peroxiredoxins) was also up-regulated in both groups, although somewhat less in the latter. Of note, increased oxidative stress came along with an inflammatory reaction, but only in involuting glands, suggesting that although antioxidant systems can adequately buffer a heavy load of ROS in goiter, it is not necessarily the case in involuting glands. The effects of 15-deoxy-Delta(12,14)-prostaglandin J2 (15dPGJ2), an endogenous ligand of peroxisome proliferated-activated receptor gamma (PPARgamma) with antiinflammatory properties, were then investigated in involuting glands. This drug strongly reduced both 4-hydroxynonenal staining and the inflammatory reaction, indicating that it can block iodine-induced cytotoxicity. When experiments were carried out with the PPARgamma antagonist, bisphenol A diglycidyl ether, 15dPGJ2-induced effects remained unchanged, suggesting that these effects were not mediated by PPARgamma. In conclusion, thyroid epithelial cells are well adapted to endogenously produced ROS in basal and goitrous conditions. In iodine-induced goiter involution, the increased oxidative stress is accompanied by inflammation that can be blocked by 15dPGJ2 through PPARgamma-independent protective effects.

Hokkaido Igaku Zasshi 1994 May;69(3):614-26
[Screening for thyroid dysfunction in adults residing in Hokkaido Japan: in
relation to urinary iodide concentration and thyroid autoantibodies]
[Article in Japanese]
Konno N, Iizuka N, Kawasaki K, Taguchi H, Miura K, Taguchi S, Murakami S, Hagiwara K, Noda Y, Ukawa S.
Department of Internal Medicine, Hokkaido Central Hospital for Social Health Insurance, Sapporo, Japan.
The prevalence of thyroid dysfunction and its relation to thyroid autoantibodies (TAA) and urinary iodide concentration (UI) was studied in apparently healthy adults in Sapporo (n = 4110) (Sapporo group), and in five coastal areas of Hokkaido (n = 1061) (coastal group) which produce iodine-rich seaweed (kelp). The frequency of above normal urinary iodine (high UI) in the morning urinary samples of coastal group was 10.8%, significantly higher than that of Sapporo group (6.4%) (p < 0.001). Frequency of positive TAA in both groups were similar. In Sapporo group TAA was positive in 6.4% of males and 13.8% of females with an age-related increase. The overall prevalence of hyperthyroidism (TSH < 0.15 mU/L) in coastal group (0.6%) was similar to that in Sapporo group (1.1%), while that of hypothyroidism (TSH > 5.0 mU/L) in coastal group (3.8%) was significantly higher than that in Sapporo group (1.3%) (P < 0.001). The frequency of high UI correlated significantly with that of hypothyroidism with negative TAA (r = 0.829, P < 0.05), but not with positive TAA, or with that of hyperthyroidism. Hypothyroidism was more prevalent in TAA negative subjects with high UI than with normal UI. Moreover, serum TSH and thyroglobulin levels were higher and free T4 level was lower in former than in latter group. These results indicate that 1) the prevalence of TAA negative hypothyroidism in iodine sufficient areas may be associated with the amount of iodine ingested, 2) this hypothyroidism is more prevalent and marked in subjects consuming further excess amounts of iodine, and 3) excessive intake of iodine should be considered an etiology of hypothyroidism in addition to chronic thyroiditis in these areas.

Clin Endocrinol (Oxf) 1989 Oct;31(4):453-65
Thyroid autoimmunity in endemic goitre caused by excessive iodine intake.
Boyages SC, Bloot AM, Maberly GF, Eastman CJ, Li M, Qian QD, Liu DR, van der Gaag RD, Drexhage HA.
Department of Medicine, Westmead Hospital, Sydney, Australia.
The pathophysiology of endemic goitre caused by excessive iodine intake is not well defined. By interacting with the immune system, iodine excess may trigger the development of autoimmune thyroid disease such as lymphocytic Hashimoto's thyroiditis (LT). In an attempt to examine this further, we compared the presence of thyroid autoantibodies in 29 goitrous children, from an iodine excess area, and in 26 healthy children, from an iodine sufficient area, of north central China. Serum was tested for antimicrosomal (MAb), anti-thyroglobulin (TgAb), second colloid antigen antibodies (CA2-Ab) and TSH
binding inhibitory immunoglobulins (TBII). Affinity chromatographically purified IgG was tested for thyroid growth-stimulating activity (TGI) by two different methods: a sensitive cytochemical bioassay (CBA) using guinea-pig thyroid explants and a mitotic arrest assay (MAA) employing a continuous rat thyroid cell line (FRTL-5). We found no increased prevalence of LT in patients with endemic iodine goitre. The levels of MAb, TgAb and CA2-Ab did not differ significantly between the two groups of children. Further, TBII were not present in either group. Thyroid growth-stimulating immunoglobulins (TGI) were the major autoantibodies found in children with goitres caused by iodine excess. In the CBA, 12 of 20 (60%) goitrous children and 0 of 12 (0% P less than 0.05) healthy children were positive for TGI. Similar results were found in the MAA, and a good correlation between results of the CBA and MAA was found (P = 0.003). Maximal TGI activity in dose-response CBA showed a good relation with clinical goitre size (r = 0.63; P less than 0.05) indicating a possible pathophysiological role for these antibodies. We conclude that endemic iodine goitre is not associated with Hashimoto's lymphocytic thyroiditis. Nevertheless,
autoimmune growth factors such as TGI may play a primary role in the pathogenesis of thyroid growth in this condition.

Endocrinol Metab Clin North Am 1987 Jun;16(2):327-42
Environmental factors affecting autoimmune thyroid disease.
Safran M, Paul TL, Roti E, Braverman LE.
Department of Medicine, University of Massachusetts Medical Center, Worcester.
A number of environmental factors affect the incidence and progression of autoimmune thyroid disease. Exposure to excess iodine, certain drugs, infectious agents and pollutants, and stress have all been implicated.

Acta Endocrinol (Copenh) 1978 Aug;88(4):703-12
A case of Hashimoto's thyroiditis with thyroid immunological abnormality manifested after habitual ingestion of seaweed.
Okamura K, Inoue K, Omae T.
An interesting case of iodide induced goitre with immunological abnormalities is described. The patient who was sensitive to synthetic penicillin had previously been treated for exudative pleuritis, congestive heart failure and acute renal failure. Following recovery, he began to ingest large amounts of seaweed after which he developed goitrous hypothyroidism. It was of interest that the serum level of gamma-globulin increased, and subsequently the antithyroid microsomal antibody became strongly positive, suggesting that thyroidal autoimmune processes had been precipitated. Biopsy of the thyroid gland revealed chronic thyroiditis, with evidence suggesting extreme stimulation by TSH. Hight thyroidal uptake of 131I, positive perchlorate discharge test and biochemical analysis of the thyroidal soluble protein showed severe impairment of hormone synthesis following continuous accumulation of excess iodide. While there is evidence suggesting that increased iodide may be an important factor in the initiation of Hashimoto's thyroiditis, this may result from the marked increased sensitivity of Hashimoto's gland to the effects of iodine. Thus an occult lesion could be unmasked in this manner. The mechanism by which iodide mediates this effect is not clear.

Presse Med 2002 Oct 26;31(35):1670-5
[Hypothyroidism related to excess iodine]
[Article in French]
Wemeau JL.
Clinique endocrinologique Marc Linquette CHRU de Lille USNA, 59037 Lille. [email protected]
WOLFF-CHAIKOFF'S EFFECT: The thyroid gland has a capacity to reduce thyroid hormone production in the presence of excess iodine by reducing the organification of the iodine. This Wolff-Chaikoff effect is observed after 48 hours and protects the organism from excessive synthesis of the thyroid hormones. This effect is usually temporary and within a few days thyroid hormone synthesis returns to normal through the so-called 'escape' phenomenon. However in a few normal individuals and in some susceptible patients, the escape does not occur. THE CONTEXT OF OCCURRENCE: Iodine-induced hypothyroidism is observed in fetuses, newborn, adults and in the elderly. It is observed in individuals without underlying overt thyroid disorder, and especially in patients with autoimmune thyroiditis or those previously treated for thyroid diseases (Graves' disease, subacute or pospartum thyroiditis, iatrogenic thyroid dysfunction...). FROM A CLINICAL AND PROGRESSIVE POINT OF VIEW: The hormone deficiency is of obvious clinical expression, or sometimes discreet and revealed by hormone exploration. It is usually temporary, regressing with a few days or weeks after iodine withdrawal. Nevertheless, some patients require transient hormone replacement therapy.

Thyroid 2001 May;11(5):427-36
Iodine and thyroid autoimmune disease in animal models.
Ruwhof C, Drexhage HA.
Department of Immunology, Erasmus University, Rotterdam.
Thyroid autoimmune diseases are complex, polygenic afflictions the penetrance of which is heavily dependent on various environmental influences. In their pathogenesis, an afferent stage (enhanced autoantigen presentation), a central stage (excessive expansion and maturation of autoreactive T and B cells), and an efferent stage (effects of autoreactive T cells and B cells on their targets) can be discerned. At each stage, a plethora of inborn, endogenous or exogenous factors is able to elicit the abnormalities characteristic of that stage, thus opening the gateway to thyroid autoimmunity. Iodine is an important exogenous modulating factor of the process. In general, iodine deficiency attenuates, while iodine excess accelerates autoimmune thyroiditis in autoimmune prone individuals. In nonautoimmune prone individuals, the effects of iodine are different. Here iodine deficiency precipitates a mild (physiological) form of thyroid autoimmune reactivity. Iodine excess stimulates thymus development. Iodine probably exerts these effects via interference in the various stages of the autoimmune process. In the afferent and efferent stage, iodine-induced alterations in thyrocyte metabolism and even necrosis most likely play a role.
By contrast, in the central phase, iodine has direct effects on thymus development, the development and function of various immune cells (T cells, B cells macrophages and dendritic cells) and the antigenicity of thyroglobulin.

Clin Immunol Immunopathol 1996 Dec;81(3):287-92
Iodine-induced autoimmune thyroiditis in NOD-H-2h4 mice.
Rasooly L, Burek CL, Rose NR.
Department of Molecular Microbiology and Immunology, School of Hygiene and Public Health, Johns Hopkins University, Baltimore, Maryland 21205, USA.
Excess iodine ingestion has been implicated in induction and exacerbation of autoimmune thyroiditis in human populations and animal models. We studied the time course and sex-related differences in iodine-induced autoimmune thyroiditis in NOD-H-2h4 mice. This strain, derived from a cross of NOD with B10.A(4R), spontaneously develops autoimmune thyroiditis but not diabetes. NOD-H-2h4 mice were given either plain water or water with 0.05% iodine for 8 weeks. Approximately 54% of female and 70% of male iodine-treated mice developed thyroid lesions, whereas only 1 of 20 control animals had thyroiditis at this
time. Levels of serum thyroxin (T4) were similar in the treatment and control groups. Thyroglobulin-specific antibodies were present in the iodine-treated group after 8 weeks of treatment but antibodies to thyroid peroxidase were not apparent in the serum of any of the animals. Levels of thyroglobulin antibodies
increased throughout the 8-week iodine ingestion period; however, no correlation was seen between the levels of total thyroglobulin antibodies and the degree of thyroid infiltration at the time of autopsy. The thyroglobulin antibodies consisted primarily of IgG2a, IgG2b, and IgM antibodies with no detectable IgA,
IgG1, or IgG3 thyroglobulin-specific antibodies. The presence of IgG2b thyroglobulin-specific antibodies correlated well with the presence of thyroid lesions.

Verh Dtsch Ges Pathol 1996;80:297-301
[Spontaneous Hashimoto-like thyroiditis in cats]
[Article in German]
Schumm-Draeger PM, Langer F, Caspar G, Rippegather K, Herrmann G, Fortmeyer HP, Usadel KH, Hubner K.
Medizinische Klinik I, Johann Wolfgang Goethe-Universitat, Frankfurt/M.
A breeding line of domestic cats spontaneously developing symptoms of hypothyroidism between the 40th and 60th day of life (fur changes, loss of appetite, growth retardation), elevated levels of antibodies against microsomal structures and thyroglobulin, and lymphocytic thyroid infiltration has been recently established at our facility. Aim of our studies was to examine the effect of high iodine ingestion or prophylactic thyroid hormone therapy on functional and morphological characteristics of this Hashimoto-like thyroiditis in cat. From birth to day 80 of life cats were treated with iodine (n = 9; 0.1 mg/l) or thyroxin (n = 13; 2.0 micrograms/ kg/d) respectively. Untreated animals served as controls (n = 12). Cat-serum was tested for thyroid function (TT3, TT4). After 8 weeks the thyroid tissue was submitted to routine histological processing (H&E) and the inflammatory activity was scored. Additionally immunohistological staining was performed for MIB-1, IgG, IgM and MHCII expression. Both untreated hypothyroid (UHC) as well as iodine-treated (IC) cats revealed a significantly higher degree of thyroid inflammation and higher levels of IgM as the thyroxin-substituted animals (TC). Epithelial proliferation decreased significantly in the IC and TC groups as compared to the untreated controls. No significant differences regarding IgG production and HLAII expression were detectable. Early thyroid hormone therapy significantly
decreases both incidence and activity of autoimmune thyroiditis in cats as measured by inflammatory infiltration, IgM production and epithelial proliferation. Animals with excess iodide intake, however, show an aggravation of the autoimmune inflammatory activity.

Autoimmunity 1995;20(3):201-6
Excess iodine induces the expression of thyroid solid cell nests in lymphocytic thyroiditis-prone BB/W rats.
Zhu YP, Bilous M, Boyages SC.
Department of Clinical Endocrinology, Westmead Hospital, Sydney, Australia. Previous epidemiological studies have suggested that lymphocytic thyroiditis and/or an increased iodine intake may be risk factors for the development of thyroid cancer. We previously reported that excess iodine accelerated the development of thyroid lymphocytic infiltration (LI) in the autoimmune BB/W rat model. We also found that excess iodine increased thyroid cell proliferation in a disordered manner. The present study was designed to further explore these observations and to address the question as to whether excess iodine under certain conditions predisposes the thyroid gland to neoplasia. To test this hypothesis, the lymphocytic thyroiditis-prone BB/W rat was exposed to excess iodine in drinking water. Ten BB/W rats at 4 weeks of age were given iodine water (NaI 0.05%) for 10 weeks, whilst another 10 BB/W rats were given tap water and served as controls. Eighteen normal Wistar rats were also divided into excess iodine and control groups, served as a comparison to the BB/W rats. We found that an excess iodine intake accelerated the development of LI in the BB/W rat. Severe LI was usually accompanied by prominent thyroid cell proliferation, evident as numerous microfollicles and cell masses, not forming normal thyroid follicles. Numerous lymphocytes and plasma cells often encroached on these areas of increased cellular proliferation. The surprising feature, and a possible indicator of activated thyroid cell proliferation, was the high incidence of thyroid solid cell nest-like lesions (SCN) in the iodine treated BB/W rats.(ABSTRACT TRUNCATED AT 250 WORDS)

 

[montmorency]

FWIW, Abraham, Flechas and Brownstein do not go by the iodine patch test.

Abraham especially rubbishes the so-called Wolff-Chaikoff effect.

Well, since Ray has let them have both barrels, I think it's only fair to hear the other side:

BTW, the dosage of 150 mcg was established way back as that necessary to prevent overt goitre, and nothing else.. Does Ray seriously believe that iodine is not used in the rest of the body? David Derry, among others talks about this, and very interesting it is too.
It doesn't take that big of a daily dose to saturate the thyroid, but when that is achieved further doses are then available for the rest of the body, e.g. breasts, ovaries, prostate...lots of places. It's in nasal mucus, for example, so if you have a cold and runny nose, you are losing iodine all the time.

Anyway, here are some views from the other side of the trenches:

http://www.optimox.com/pics/Iodine/pdfs/IOD14.pdf
http://www.optimox.com/pics/Iodine/pdfs/IOD15.pdf
http://www.optimox.com/pics/Iodine/pdfs/IOD16.pdf

(The only thing that worries me about Abraham is that he's obviously a member of the god-squad and he lets it interfere with his scientific views).
(no offence...)

I'm a little surprised that Ray takes those studies he cites at face value. After all, he's pretty cynical about medical studies and medical literature in general, so why isn't he at least skeptical about those? Perhaps because they confirm his pre-existing views. After all, after the "Wolff-Chaikoff Effect" was "discovered", it seems that then it was normal to assume that "excess" iodine inhibited thyroid function. This became the received wisdom like "cholesterol causes heart disease" or "saturated fat causes heart disease", and nobody questioned it. Therefore studies would tend to be designed to support this now normal belief (and quite probably, people who wanted to do genuinely open-minded studies that could go either way would not get funding or not get published.

And lastly, unlike the usual Ray, he does not define a physiological mechanism which demonstrates exactly why "excess" iodine causes hypothyroid (or Hashi's, or both). Since iodine supplementation in any quantity has been so unpopular for so long, you'd think someone could have discovered exactly why this happened by now, if indeed it was happening.

Edit: I notice that quite a few of those studies are animal studies, one is a human n=1 study of a man eating loads of seaweed (not measured) - the "iodine Doctors" do not recommend seaweed, the other human test seem to depend on lab tests (and isn't Ray always telling us that traditional doctors (like Broda Barnes) went more by the actual human symptoms, which are not mentioned there. The Wolff-Chaikoff one, I'll leave to Abraham to refute.

As for this:

Endocrinol Metab Clin North Am 1987 Jun;16(2):327-42
Environmental factors affecting autoimmune thyroid disease.
Safran M, Paul TL, Roti E, Braverman LE.
Department of Medicine, University of Massachusetts Medical Center, Worcester.
A number of environmental factors affect the incidence and progression of autoimmune thyroid disease. Exposure to excess iodine, certain drugs, infectious agents and pollutants, and stress have all been implicated.

WTF?

And they all mention "excess iodine" as if this were some cabalistic or sacred number revealed from on high, instead of a number to be determined by experiment. If you previously define "excess" as, say, more than 1mg per day, then the answer to the question "how do you know that what X is taking is excess?" the answer will always be "well, because it's more than 1mg per day, stupid!".

Oh, of course.

Colour-supplement science.

 

[Giraffe]

post 101107 FWIW, Abraham, Flechas and Brownstein do not go by the iodine patch test.

An evaluation of Abraham's iodine test kid

In conclusion, modifications need be made to the iodine loading test before it is used to determine whole body iodine sufficiency or a need for supplemental iodine. Currently the iodine loading test does not provide a realistic assessment of an individual's whole body iodine sufficiency or deficiency due to flaws in the methodology and the use of an arbitrary excretion cutoff point. Extending the iodine loading test's collection period past 24 hours and including analysis of iodine in feces would provide a better picture of iodine retention after consumption of 50 mg iodine/iodide.

post 101107Abraham especially rubbishes the so-called Wolff-Chaikoff effect.

If you want to spoil your day, read Abraham's rant on the Wolff-Chaikoff effect.

 

[ilovewriting]

Ray Peat writes extensively about how important iodine is to mitochondrial function, prevention of inflammation and even endotoxins, and did so decades before Abraham and Brownstein began their reckless promotion of their product.

The mechanism of unsafe overdosing on iodine seems to be that the combination of iodide with unsaturated fatty acids suppresses the thyroid.

From Nutrition for Women (1993), Page 17:

Because iodate is used as a "dough conditioner" (to make bread water-heavy), the American eater often gets ten times more iodine than is recommended. Combined with unsaturated oils, as organic iodides, excess iodine can powerfully inhibit the thyroid.

and on Page 50:

The American Dietetic Association warns about overdosing with kelp, because of the iodide; but the Japanese eat various iodide-rich seaweeds without the thyroid problems the A.D.A. says might occur on the kelp-lecithin-vinegar B6 diet. In the U.S. people who eat bakery bread receive about 10 times more than the RDA of iodine. Iodides are known to benefit arteriosclerosis, with visible improvement occurring in blood vessels in the retina (see Physicians Desk Reference, iodides). In old age, the walls of blood vessels tend to become hardened with calcium. In at least some tissues, it is known that calcification begins in degenerating mitochondria, and mitochondria tend to deteriorate in aging tissue. Nutrients such as iodine, vitamin E, magnesium and vitamin B2 are especially important for maintaining the function of the mitochondria, which produce most of our energy.

An excess of iodine from bread or kelp is much more likely to interfere with the thyroid when the diet contains a large amount of unsaturated fat, such as safflower or soy oil, because these combine with iodine to form substances which inhibit the thyroid. These oils in themselves suppress the thyroid, and this might be a factor in the premature aging and increased cancer rate which have been observed in people who use larger amounts of those oils.

And this:

Email. From Cini Staughn: I continue to see folks on health forums obviously being harmed by iodine
therapy, especially we autoimmune thyroid folks - and yet the advice they are often given is just take more. Or to do salt flushes for detox. It's all rather frightening and I hope this high iodine fad passes at some time. I've been outspoken on thyroid forums regarding the need for caution in using Abraham/Brownstein's high dose iodine protocol, in particular for AITD (Hasimoto’s Thyroiditis). I was even banned from Iodine yahoo forum when I criticized Dr. Brownstein for not even testing TSI antibodies when his Hashi's folks had problems, etc. (so far some of the most adverse reactions have been by those with TSI antibodies). The moderator is a patient of his. I heard you are also a critic of the Brownstein iodine protocol...and refute some of the displacing bromide/fluoride claims. I'm just writing to say that we critics sure could use some more ammunition. Time for you to write an article? I have AITD myself...and am so tired of seeing my fellow AITD folks getting harmed by high dose iodine. Is someone making a mint off of Iodoral? Anyway, just wanted to express my thoughts...it's time for the high iodine fad to pass away before more AITD folks are harmed.

From Dr. Ray Peat: I can send you quite a bit of information about the toxic effects of even a relatively small excess amount of iodine, even a milligram. Considering the huge amount of publicity, I would suppose that they are making a lot of money on it.

 

[Parsifal]

That's great and very interesting! Thanks ilovewriting :).

 

[Elie]

Regarding iodine in bread - My understanding is that iodine was replaced with bromine a long time ago, potassium bromate, more specifically.
I had read that Iodine is important for the structural integrity of breast tissue and other reproductive organs. 3000mcg was shown in a study to improve fibrocystic breasts, although I got good feedback regarding a significant reduction in cysts (upon palpation) at approx 170mcg a day from kelp extract.
From what I read 150mcg to a few hundred mcgs of iodine per day, especially for women seem both safe and beneficial. Also in pregnancy iodine requirements rise to 250mcg and adequate intake may help both the fetus (brain development and cognitive function) and mother (to help prevent or reduce hypothyroid related symptoms) postpartum.

 

[HDD]

A friend of mine has been seeing a doctor for six months regarding low thyroid function. She has blood work done regularly. Both her doctor and her naturopath have recommended iodine supplementation. She has been supplementing 12.5 mg for the past six months and her recent labwork still shows low in iodine, 31.7 (ref. 40-92) Her naturopth told her that her thyroid medication blocks iodine.

Besides bloodwork, her naturopath had her do an iodine loading test. She ingested Iodorol and then measured output.

I have sent her what Ray Peat says about iodine deficiency so she asked me to inquire here about her continued low serum iodine while supplementing.

Anyone know why supplementing is not improving her numbers?

 

[Luna]

Regarding iodine in bread - My understanding is that iodine was replaced with bromine a long time ago, potassium bromate, more specifically.

Indeed, potassium bromate is used in bread, however some countries have now banned it as it may be a potential carcinogen.

As a wikipedia search yields this:

Regulation[edit]
Potassium bromate is classified as a category 2B carcinogen (possibly carcinogenic to humans) by the International Agency for Research on Cancer (IARC).[4]

Potassium bromate has been banned from use in food products in the European Union, Argentina, Brazil,[5] Canada, Nigeria, South Korea, Peru and some other countries. It was banned in Sri Lanka in 2001,[6] China in 2005,[citation needed] and India on 20 June 2016.[7]

In the United States of America, it has not been banned. The FDA sanctioned the use of bromate before the Delaney clause of the Food, Drug, and Cosmetic Act—which bans potentially carcinogenic substances— went into effect in 1958. But since 1991 the FDA has urged bakers to voluntarily stop using it. In California a warning label is required when bromated flour is used.[8]

Japanese baked goods manufacturers stopped using potassium bromate voluntarily in 1980; however, Yamazaki Baking resumed its use in 2005, claiming they had new production methods to reduce the amount of the chemical which remained in the final product.[9]

I had read that Iodine is important for the structural integrity of breast tissue and other reproductive organs.

Given that you mentioned, Iodine is used in breast tissues,
I wonder if the Bromine from Potassium Bromine, is occupying the place of Iodine in the breast tissues, when breads are replaced of Iodine with Potassium Bromine.

It is interesting to point out that in Japan, cancer rates are lower, and iodine intake is higher as per @Kasper 's quote of Funahashi's et al article, in another forum:

Japanese researchers have found that
iodine suppresses tumor growth in experimental animals
and they have demonstrated that seaweed, that is high
in iodine, induces apoptosis in human breast cancer cells
(Funahashi, H., Imaj, T., Tanaka, Y., et al, Suppressive Effect of
Iodine on DMBA-Induced Breast Tumor Growth in the Rat,
Journal of Surgical Oncology, 61:209-213, 1996, Funahashi,

Also, this is not the only argument those doctors who lead which they call, the iodine revival.


Iodine, is it needed in other tissues other than thyroid?

 

[uchihaMadara]

Deiodinase type I (D1)
D1 converts inactive T4 to active T3 throughout the body. D1 activity is also lower in females making women more prone to tissue hypothyroidism, with resultant depression, fatigue, fibromyalgia, chronic fatigue syndrome, and obesity despite having normal TSH levels. D1 but not D2 is suppressed and down-regulated (decreasing T4 to T3 conversion) in response to physiologic and emotional stress; depression; dieting; weight gain and leptin resistance; insulin resistance, obesity and diabetes; inflammation from autoimmune disease or systemic illness; chronic fatigue syndrome and fibromyalgia; chronic pain; and exposure to toxins and plastics.

Deiodinase type II (D2)
Pituitary T3 levels are determined by D2 activity, which is 1000 times more efficient at converting T4 to T3 than the D1 enzyme present in the rest of the body. D2 also has an opposite response from that of D1 to physiologic and emotional stress, depression, both dieting and weight gain, PMS, diabetes, leptin resistance, chronic fatigue syndrome, fibromyalgia, inflammation, autoimmune disease, and systemic illness. D2 is stimulated and up-regulated (increased activity) in response to such conditions, increasing intra-pituitary T4 to T3 conversion while the rest of body suffers from diminished levels of active T3. This causes the TSH to remain normal despite the fact that there is significant cellular hypothyroidism present in the rest of the body.

Deiodinase type III (D3)
The pituitary is the only tissue that does not contain D3, which converts T4 to reverse T3 and competes with D1 that converts T4 to T3. Reverse T3 is a competitive inhibitor of T3, blocking T3 from binding to its receptor and blocking T3 effect, reduces metabolism, suppresses D1 and T4 to T3 conversion, and blocks T4 and T3 uptake into the cell, all reducing intracellular T3 levels and thyroid activity.​

The research implies lower metabolism in women, most likely attributed with estrogen in circulation. Most of us know Ray's view on estrogen in the body, but this directly correlates with hypometabolic states others have been trying to grasp. If cells have low deiodinase I activity, T4 does not convert to T3. If deiodinase III is high, r-T3 blocks T3 action, if any, and induces hypometabolism. Taking excess iodine may suppress the thyroid, but I would at least hope that someone researches the necessary cofactors prior to excess supplementation. However, tissue T4 to T3 conversion is an often overlooked topic. I would advise to consider the factors potentially blocking thyroid function such as differing deiodinase activity as excess iodine/iodide may be excreted out of circulation via kidneys. I'm aware of iodine storage in other tissues than the thyroid as well. However, if the cells cannot utilize the thyroid hormones properly, there is little point in consuming excess iodine/iodide in hopes of saturating tissues and improving metabolism.

Source: diodinases (includes 283 references)

 

[papaya]

Deiodinase type I (D1)
D1 converts inactive T4 to active T3 throughout the body. D1 activity is also lower in females making women more prone to tissue hypothyroidism, with resultant depression, fatigue, fibromyalgia, chronic fatigue syndrome, and obesity despite having normal TSH levels. D1 but not D2 is suppressed and down-regulated (decreasing T4 to T3 conversion) in response to physiologic and emotional stress; depression; dieting; weight gain and leptin resistance; insulin resistance, obesity and diabetes; inflammation from autoimmune disease or systemic illness; chronic fatigue syndrome and fibromyalgia; chronic pain; and exposure to toxins and plastics.

Deiodinase type II (D2)
Pituitary T3 levels are determined by D2 activity, which is 1000 times more efficient at converting T4 to T3 than the D1 enzyme present in the rest of the body. D2 also has an opposite response from that of D1 to physiologic and emotional stress, depression, both dieting and weight gain, PMS, diabetes, leptin resistance, chronic fatigue syndrome, fibromyalgia, inflammation, autoimmune disease, and systemic illness. D2 is stimulated and up-regulated (increased activity) in response to such conditions, increasing intra-pituitary T4 to T3 conversion while the rest of body suffers from diminished levels of active T3. This causes the TSH to remain normal despite the fact that there is significant cellular hypothyroidism present in the rest of the body.

Deiodinase type III (D3)
The pituitary is the only tissue that does not contain D3, which converts T4 to reverse T3 and competes with D1 that converts T4 to T3. Reverse T3 is a competitive inhibitor of T3, blocking T3 from binding to its receptor and blocking T3 effect, reduces metabolism, suppresses D1 and T4 to T3 conversion, and blocks T4 and T3 uptake into the cell, all reducing intracellular T3 levels and thyroid activity.​

The research implies lower metabolism in women, most likely attributed with estrogen in circulation. Most of us know Ray's view on estrogen in the body, but this directly correlates with hypometabolic states others have been trying to grasp. If cells have low deiodinase I activity, T4 does not convert to T3. If deiodinase III is high, r-T3 blocks T3 action, if any, and induces hypometabolism. Taking excess iodine may suppress the thyroid, but I would at least hope that someone researches the necessary cofactors prior to excess supplementation. However, tissue T4 to T3 conversion is an often overlooked topic. I would advise to consider the factors potentially blocking thyroid function such as differing deiodinase activity as excess iodine/iodide may be excreted out of circulation via kidneys. I'm aware of iodine storage in other tissues than the thyroid as well. However, if the cells cannot utilize the thyroid hormones properly, there is little point in consuming excess iodine/iodide in hopes of saturating tissues and improving metabolism.

Source: diodinases (includes 283 references)

this is very interesting info. are there supplements u can take to change deiodinase levels?

 

[Fractality]

What about using iodine (Lugol's) as a mouth rinse? Would that risk overdose?

 

[Mauritio]

Iodine is the only thing that helps me sleep. It doesnt knock me out or anything rather it feels pretty natural. Can somebody try to explain that ?
I do not get the same effect from T3/T4 (Tyromix) ,so I wonder what it converts to ?!

 

[burtlancast]

Iodine is the only thing that helps me sleep. It doesnt knock me out or anything rather it feels pretty natural. Can somebody try to explain that ?
I do not get the same effect from T3/T4 (Tyromix) ,so I wonder what it converts to ?!

The pineal gland isn't protected by the blood brain barrier: it will accumulate halides like fluoride and bromide, as well as heavy metals like mercury. It's actually the organ who accumulates the most fluoride. And thus won't be able to secrete melatonin as it should.

Iodine detoxifies the pineal gland and allows it to secrete normally melatonin. It will inactivate the mercury and replace the fluoride and bromide.

 

[Mauritio]

The pineal gland isn't protected by the blood brain barrier: it will accumulate halides like fluoride and bromide, as well as heavy metals like mercury. It's actually the organ who accumulates the most fluoride. And thus won't be able to secrete melatonin as it should.

Iodine detoxifies the pineal gland and allows it to secrete normally melatonin. It will inactivate the mercury and replace the fluoride and bromide.

Let's suppose that is the mechanism behind it. Do you think it really decalcifies/detoxes my pineal gland and returns melatonin production to normal in matter of minutes ? Because that is how fast i feel the effects.

 

[burtlancast]

Let's suppose that is the mechanism behind it. Do you think it really decalcifies/detoxes my pineal gland and returns melatonin production to normal in matter of minutes ? Because that is how fast i feel the effects.

There are a few testimonies on the web on iodine's helpful effects on sleep quality, notably from life-long sufferers of delayed sleep phase syndrome who miraculously return to a normal sleep cycle.

Iodine detoxifies bromine by a factor of 20 in a matter of hours; and bromine is known to disturb both sleep and daytime activities.

Maybe it also enhances thyroid hormone production.

It's a very complex subject, but i'm pretty sure it's effects on halides is central to it's beneficial effect on sleep quality.

 

[Mauritio]

There are a few testimonies on the web on iodine's helpful effects on sleep quality, notably from life-long sufferers of delayed sleep phase syndrome who miraculously return to a normal sleep cycle.

Iodine detoxifies bromine by a factor of 20 in a matter of hours; and bromine is known to disturb both sleep and daytime activities.

Maybe it also enhances thyroid hormone production.

It's a very complex subject, but i'm pretty sure it's effects on halides is central to it's beneficial effect on sleep quality.

Okay interesting!

 

[Spartan300]

@Mauritio how are you using Iodine for sleep - Lugols & how much?

 

[Cirion]

The pineal gland isn't protected by the blood brain barrier: it will accumulate halides like fluoride and bromide, as well as heavy metals like mercury. It's actually the organ who accumulates the most fluoride. And thus won't be able to secrete melatonin as it should.

Iodine detoxifies the pineal gland and allows it to secrete normally melatonin. It will inactivate the mercury and replace the fluoride and bromide.

My understanding from reading Nathan Hatch's book is that melatonin is actually not a beneficial hormone. Yes it helps you sleep, but it helps you sleep through the "stress" pathway (i.e., not restful sleep). What we want is high GABA - this is the "pro-metabolic", "restful" sleep indicating hormone. GABA seems difficult to get high in, which is probably why I never feel rested lol.

I'm sure it also doesn't help that I am probably still high in Bromine since I haven't been mega dosing Iodine very long yet.

 

[Dave Clark]

Speaking of GABA, they say the drug picamilon crosses the BBB and breaks down into GABA and niacin, which is why it has relaxing/sedating qualities. Has anyone here used picamilon to help with sleep issues? I used it years ago for during-the-day use to relax myself, and it had nice effects, but never used it before bedtime.

 

[Mauritio]

@Mauritio how are you using Iodine for sleep - Lugols & how much?

Just one or two drops orally right before bed...