Ray Peat: “The small amount of iodide added to salt has been reported in more than 70 studies to damage the thyroid gland, even increasing thyroid cancer”
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Re: [Peat: .. I have never recommended several milligram doses of iodide](and I have often pointed out the damage to the thyroid gland that even moderate iodide supplements can cause: [studies follow])
Post in thread 'Ray Peat Email Advice Depository'
https://lowtoxinforum.com/threads/ray-peat-email-advice-depository.1035/post-875358Q: Hello Dr. Peat
Over the years you've said so many fascinating things about IODIDE and bad things about IODINE that made me wonder if they are the same substances?
What should I eat or buy as a supplement in order to increase my IODIDE?
Much love
RP: Very large doses of potassium iodide used to be used for certain inflammations or infections, but its effects haven’t been understood. The small amount of iodide added to salt has been reported in more than 70 studies to damage the thyroid gland, even increasing thyroid cancer.
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Food Chem Toxicol. 2000 Sep;38(9):773-81.
Studies on the carcinogenicity of potassium iodide in F344 rats.
Takegawa K(1), Mitsumori K, Onodera H, Shimo T, Kitaura K, Yasuhara K, Hirose M,
Takahashi M.
(1)Division of Pathology, National Institute of Health Sciences, 1-18-1 Kamiyoga,
Setagaya-ku, 158-8501, Tokyo, Japan.
A chronic toxicity and carcinogenicity study, in which male and female F344/DuCrj
rats were given potassium iodide (KI) in the drinking water at concentrations of
0, 10, 100 or 1000 ppm for 104 weeks, and a two-stage carcinogenicity study of
application at 0 or 1000 ppm for 83 weeks following a single injection of
N-bis(2-hydroxypropyl)nitrosamine (DHPN), were conducted. In the former, squamous
cell carcinomas were induced in the salivary glands of the 1000 ppm group, but no
tumors were observed in the thyroid. In the two-stage carcinogenicity study,
thyroidal weights and the incidence of thyroid tumors derived from the follicular
epithelium were significantly increased in the DHPN+KI as compared with the DHPN
alone group. The results of our studies suggest that excess KI has a thyroid
tumor-promoting effect, but KI per se does not induce thyroid tumors in rats. In
the salivary gland, KI was suggested to have carcinogenic potential via an
epigenetic mechanism, only active at a high dose. -
Jpn J Cancer Res. 1998 Feb;89(2):105-9.
Induction of squamous cell carcinomas in the salivary glands of rats by potassium
iodide.
Takegawa K(1), Mitsumori K, Onodera H, Yasuhara K, Kitaura K, Shimo T, Takahashi
M.
(1)Division of Pathology, National Institute of Health Sciences, Tokyo.
In a 2-year carcinogenicity study of potassium iodide (KI) in F344/DuCrj rats,
squamous cell carcinomas (SCCs) were observed in the salivary glands of 4/40
males and 3/40 females receiving 1000 ppm KI in the drinking water. Ductular
proliferation with lobular atrophy was observed at high incidence in the
submandibular glands of the high-dose animals, and squamous metaplasia was
frequently evident within the proliferative ductules and the larger interlobular
ducts. A transition from metaplasia to SCC was apparent. The results suggest that
squamous metaplasia in proliferative ductules, occurring secondarily to lobular
impairment induced by KI, may develop into SCCs via a non-genotoxic,
proliferation-dependent mechanism. -
Endocrinology. 2000 Feb;141(2):598-605.
Iodide excess induces apoptosis in thyroid cells through a p53-independent
mechanism involving oxidative stress.
Vitale M(1), Di Matola T, D'Ascoli F, Salzano S, Bogazzi F, Fenzi G, Martino E,
Rossi G.
(1)Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università
Federico II, Naples, Italy. mavitale@unina.it
Thyroid toxicity of iodide excess has been demonstrated in animals fed with an
iodide-rich diet; in vitro iodide is cytotoxic, inhibits cell growth, and induces
morphological changes in thyroid cells of some species. In this study, we
investigated the effect of iodide excess in an immortalized thyroid cell line
(TAD-2) in primary cultures of human thyroid cells and in cells of nonthyroid
origin. Iodide displayed a dose-dependent cytotoxicity in both TAD-2 and primary
thyroid cells, although at different concentrations, whereas it had no effect on
cells of nonthyroid origin. Thyroid cells treated with iodide excess underwent
apoptosis, as evidenced by morphological changes, plasma membrane
phosphatidylserine exposure, and DNA fragmentation. Apoptosis was unaffected by
protein synthesis inhibition, whereas inhibition of peroxidase enzymatic activity
by propylthiouracil completely blocked iodide cytotoxicity. During KI treatment,
reactive oxygen species were produced, and lipid peroxide levels increased
markedly. Inhibition of endogenous p53 activity did not affect the sensitivity of
TAD-2 cells to iodide, and Western blot analysis demonstrated that p53, Bcl-2,
Bcl-XL, and Bax protein expression did not change when cells were treated with
iodide. These data indicate that excess molecular iodide, generated by oxidation
of ionic iodine by endogenous peroxidases, induces apoptosis in thyroid cells
through a mechanism involving generation of free radicals. This type of apoptosis
is p53 independent, does not require protein synthesis, and is not induced by
modulation of Bcl-2, Bcl-XL, or Bax protein expression. -
Toxicol Pathol. 1994 Jan-Feb;22(1):23-8.
Effects of a six-week exposure to excess iodide on thyroid glands of growing and
nongrowing male Fischer-344 rats.
Kanno J(1), Nemoto T, Kasuga T, Hayashi Y.
(1)Department of Pathology, Faculty of Medicine, Tokyo Medical and Dental
University, Japan.
A 6-wk exposure to excess iodide intake (EII) via drinking water (260 mg
potassium iodide/L) demonstrated different effects on growing (4-wk old) and
nongrowing (45-wk old) male Fischer-344 rats. In growing rats, EII induced a
significant increase in thyroid weight, pituitary weight, serum
thyroid-stimulating hormone (TSH), and thyroxine (T4). The labeling index (LI) of
thyroid follicular cells was slightly increased, although not statistically
significant. Histologically, an increase in follicular cell height, an increase
in colloid accumulation, and evidence of colloid absorption were noted. The
effect of bovine TSH (bTSH) and protirelin tartrate (TRH-t) on LI was
significantly augmented by EII. In nongrowing rats, EII induced a significant
increase in thyroid weight and serum T4 but no increase in pituitary weight,
serum TSH, and the LI of follicular cells. Histologically, an increase in colloid
accumulation was found in small follicles. EII did not augment the effect of bTSH
and TRH-t on the LI of follicular cells. This study suggests that growing rats
are still susceptible to acute hypothyroidism even after 6 wk of continuous
exposure to excess iodide, whereas nongrowing rats are refractory within an
equivalent treatment period. -
Food Chem Toxicol. 1984 Dec;22(12):963-70.
Developmental toxicity and psychotoxicity of potassium iodide in rats: a case for
the inclusion of behaviour in toxicological assessment.
Vorhees CV, Butcher RE, Brunner RL.
Potassium iodide (KI) was fed to male and female rats before and during breeding,
to females only during gestation and lactation, and to their offspring after
weaning (day 21 after birth) through to day 90, at levels of 0, 0.025, 0.05 or
0.1% (w/w) of the diet. Dams in a fifth group (positive controls) were given 4
mg/kg ip of the anti-mitotic/cytotoxic drug 5-azacytidine on day 17 of gestation.
All offspring were reared by their natural dams and were evaluated blind with
respect to treatment in a battery of standardized behavioural tests between 3 and
90 days of age. KI produced no significant reductions in parental body weight or
food consumption, though it significantly reduced litter size and increased
offspring mortality at the highest dose, and decreased weight gain at the two
highest doses throughout the first 90 days after birth. Functionally, KI delayed
auditory startle at the two highest doses, delayed olfactory orientation to the
home-cage scent at the middle dose and decreased female running-wheel activity at
all dose levels. In rats killed on day 90 after birth KI reduced brain and body
weight at a dose of 0.1% of the diet, and reduced body but not brain weight at a
dose of 0.05% of the diet. No significant effect was found on absolute or
relative thyroid weight at 90 days of age. Several additional behavioural effects
were observed in the low-dose KI group, but because these effects were not
dose-dependent, they were not regarded as reliable. 5-Azacytidine produced
evidence of substantially greater developmental toxicity than KI. It was
concluded that KI produced evidence of developmental toxicity consistent with a
picture of impaired thyroid function. The inclusion of tests of functional
development added useful evidence to the overall picture of KI developmental
toxicity. -
J Allergy Clin Immunol. 1980 Sep;66(3):177-8.
A time to abandon the use of iodides in the management of pulmonary diseases.
Hendeles L, Weinberger M. -
Endocrinol Jpn. 1975 Oct;22(5):389-97.
The effect of iodide administration on hog thyroid gland and the composition of
thyroglobulin and 27-S iodoprotein.
Tarutani O, Kondo T, Horiguchi-Sho K.
The effect of excess iodide on hog thyroid gland has been examined with regard to
the change in the chemical composition of thyroglobulin and in the accumulation
of 27-S iodoprotein by the in vivo treatment of hogs with iodide for various
lengths of time. The iodine content of thyroglobulin was either unchanged by
short term administration of excess iodide, or somewhat lowered. However, the
iodine content as well as the total amount of thyroglobulin increased in the
glands enlarged by prolonged treatment with iodide. The iodine highest reached
1.17% of the protein on an average. On the other hand, 27-S iodoprotein decreased
and finally disappeared after the chronic treatment. Monoiodotyrosine and
diiodotyrosine increased in parallel with the increase in the iodine content
(0.15 to 1.17%) caused by the iodide treatment, while thyroxine increased but
reached a plateau at the level of three residues per mole of thyroglobulin, and
no change was observed even in the proteins with the higher iodine content than
0.75%. Proteolytic activity measured by amino acid release from the thyroid
protein was depressed by the chronic treatment. On the other hand, the amount of
iodocompound released by the autoproteolysis, which may reflect hormone
secretion, increased, possibly because of the marked increase in the iodine
content of thyroglobulin. -
Am J Vet Res. 1973 Jan;34(1):65-70.
Experimentally induced iodide toxicosis in lambs.
McCauley EH, Linn JG, Goodrich RD. -
Toxicol Appl Pharmacol. 1966 Mar;8(2):185-92.
The toxicology of potassium and sodium iodates. 3. Acute and subacute oral
toxicity of potassium iodate in dogs.
Webster SH, Stohlman EF, Highman B. -
Clin Toxicol (Phila). 2013 Jul;51(6):521. doi: 10.3109/15563650.2013.804549. Epub
2013 May 23.
Regional centers: added value to poison center surveillance.
Durigon M, Kosatsky T.
Comment on
Clin Toxicol (Phila). 2013 Jan;51(1):41-6. -
Environ Toxicol Pharmacol. 2014 Jul;38(1):332-40. doi:
10.1016/j.etap.2014.06.008. Epub 2014 Jun 27.
The effects and underlying mechanism of excessive iodide on excessive
fluoride-induced thyroid cytotoxicity.
Liu H(1), Zeng Q(2), Cui Y(2), Yu L(3), Zhao L(2), Hou C(2), Zhang S(4), Zhang
L(2), Fu G(2), Liu Y(3), Jiang C(4), Chen X(4), Wang A(5).
(1)Tianjin Centers for Disease Control and Prevention, 6 Huayue Road, Hedong
District, Tianjin 300011, PR China; School of Public Health, Tianjin Medical
University, 22 Qi Xiang Tai Road, Heping District, Tianjin 300070, PR China.
Electronic address: liuhongliang@cdctj.gov.cn.
(2)Tianjin Centers for Disease Control and Prevention, 6 Huayue Road, Hedong
District, Tianjin 300011, PR China.
(3)School of Public Health, Tianjin Medical University, 22 Qi Xiang Tai Road,
Heping District, Tianjin 300070, PR China.
(4)Department of Environmental Health and MOE Key Lab of Environment and Health,
School of Public Health, Tongji Medical College, Huazhong University of Science
and Technology, 13 Hangkong Road, Hubei, Wuhan 430030, PR China.
(5)Department of Environmental Health and MOE Key Lab of Environment and Health,
School of Public Health, Tongji Medical College, Huazhong University of Science
and Technology, 13 Hangkong Road, Hubei, Wuhan 430030, PR China. Electronic
address: wangaiguo@mails.tjmu.edu.cn.
In many regions, excessive fluoride and excessive iodide coexist in groundwater,
which may lead to biphasic hazards to human thyroid. To explore fluoride-induced
thyroid cytotoxicity and the mechanism underlying the effects of excessive iodide
on fluoride-induced cytotoxicity, a thyroid cell line (Nthy-ori 3-1) was exposed
to excessive fluoride and/or excessive iodide. Cell viability, lactate
dehydrogenase (LDH) leakage, reactive oxygen species (ROS) formation, apoptosis,
and the expression levels of inositol-requiring enzyme 1 (IRE1) pathway-related
molecules were detected. Fluoride and/or iodide decreased cell viability and
increased LDH leakage and apoptosis. ROS, the expression levels of
glucose-regulated protein 78 (GRP78), IRE1, C/EBP homologous protein (CHOP), and
spliced X-box-binding protein-1 (sXBP-1) were enhanced by fluoride or the
combination of the two elements. Collectively, excessive fluoride and excessive
iodide have detrimental influences on human thyroid cells. Furthermore, an
antagonistic interaction between fluoride and excessive iodide exists, and
cytotoxicity may be related to IRE1 pathway-induced apoptosis.
Copyright
2014. Published by Elsevier B.V. -
Chemosphere. 2015 Feb;120:299-304. doi: 10.1016/j.chemosphere.2014.07.011. Epub
2014 Aug 24.
Toxicity of tetramethylammonium hydroxide to aquatic organisms and its
synergistic action with potassium iodide.
Mori IC(1), Arias-Barreiro CR(2), Koutsaftis A(2), Ogo A(2), Kawano T(3),
Yoshizuka K(3), Inayat-Hussain SH(4), Aoyama I(2).
(1)Institute of Plant Science and Resources, Okayama University, Kurashiki
710-0046, Japan. Electronic address: imori@okayama-u.ac.jp.
(2)Institute of Plant Science and Resources, Okayama University, Kurashiki
710-0046, Japan.
(3)School of International Environmental Science, The University of Kitakyushu,
Kitakyushu 808-0135, Japan.
(4)Faculty of Health Sciences, Univerisiti Kebangsaan Malaysia, Kuala Lumpur,
Malaysia.
The aquatic ecotoxicity of chemicals involved in the manufacturing process of
thin film transistor liquid crystal displays was assessed with a battery of four
selected acute toxicity bioassays. We focused on tetramethylammonium hydroxide
(TMAH, CAS No. 75-59-2), a widely utilized etchant. The toxicity of TMAH was low
when tested in the 72 h-algal growth inhibition test (Pseudokirchneriellia
subcapitata, EC50=360 mg L(-1)) and the Microtox
test (Vibrio fischeri, IC50=6.4
g L(-1)). In contrast, the 24h-microcrustacean immobilization and the 96 h-fish
mortality tests showed relatively higher toxicity (Daphnia magna, EC50=32 mg
L(-1) and Oryzias latipes, LC50=154 mg L(-1)). Isobologram and mixture toxicity
index analyses revealed apparent synergism of the mixture of TMAH and potassium
iodide when examined with the D. magna immobilization test. The synergistic
action was unique to iodide over other halide salts i.e. fluoride, chloride and
bromide. Quaternary ammonium ions with longer alkyl chains such as
tetraethylammonium and tetrabutylammonium were more toxic than TMAH in the D.
magna immobilization test.
Copyright 2014 Elsevier Ltd. All rights reserved. -
J Invest Dermatol. 1981 May;76(5):381-3.
Sterile cutaneous pustules: a manifestation of primary irritancy? Identification
of contact pustulogens.
Wahlberg JE, Maibach HI.
An animal model (the rabbit) was used to define which of 8 chemicals caused
pustule formation on topical application. Large occlusive chambers (diameter 12
mm), petrolatum as the vehicle and wrapping contributed to efficient occlusion
and pustulation. Sodium lauryl sulfate and mecuric chloride gave reproducible
results and clear dose-responses indicating that this pustulation is an
expression of primary irritancy. Ammonium fluoride pustulation was not
reproducible; croton oil pustules were more difficult to evaluate due to
simultaneous erythema and edema. Sodium arsentate, nickel sulfate and potassium
iodide pustules developed at sites where the skin barriers had been damaged by a
stab injury. Benzalkonium chloride caused yellow staining and edema but not
pustules. Because of lack of epidemiologic data, we do not know how frequently
similar findings occur in man.
Q: If I understand correctly you've changed your mind based on this new data?
"Among the factors that probably have a role in preventing cataracts: Thyroid, progesterone, pregnenolone, vitamin E, iodide, pyruvate. Increasing the carbon dioxide lowers the cell’s pH, and tends to resist swelling. Palmitic acid (a saturated fat that can be synthesized by our tissues) is normally oxidized by the lens. Calcium blockers experimentally prevent cataracts, suggesting that magnesium and thyroid (which also act to exclude calcium from cells) would have the same effect."
"The sea cucumber has been used to study the physical properties of connective tissue, and it has been found that certain salts tend to soften the connective tissues, but that iodide doesn't. The well-established use of iodide to resolve granulomas, even when it doesn't eliminate the infectious agent, might suggest that it is protecting against something which is disrupting the connective tissue structure. The only publications I have seen that presented clear evidence of the disappearance of arteriosclerosis involved treatment with iodides. In the retina, blood vessels can be seen to return to their normal appearance following a course of iodide treatment. Besides its possible direct effects on the mucins, iodide might help to eliminate calcium from the walls of blood vessels, since calcium iodide is very soluble."
"Besides its possible direct effects on the mucins, iodide might help to eliminate calcium from the walls of blood vessels, since calcium iodide is very soluble."
"Endotoxin, produced by bacteria, mainly in the intestine, disrupts energy production, and promotes maladaptive inflammation. The wide spectrum of benefit that iodide has, especially in diseases with an inflammatory component, suggests first that it protects tissue by blocking free radical damage, but it also suggests the possibility that it might specifically protect against endotoxin."
"One of the best-known free radical scavenging substances that has been widely used as a drug is iodide. It has been used to treat asthma, parasites, syphilis, cancer, Graves’ disease, periodontal disease, and arteriosclerosis. Diseases that produce tissue overgrowth associated with inflammation--granulomas--have been treated with iodides, and although the iodide doesn’t necessarily kill the germ, it does help to break down and remove the granuloma. Leprosy and syphilis were among the diseases involving granulomas* that were treated in this way. In the case of tuberculosis, it has been suggested that iodides combine with unsaturated fatty acids which inhibit proteolytic enzymes, and thus allow for the removal of the abnormal tissue."
Do you think supplementing thyroid while using iodide would prevent the damaging effect?
Ever since I stopped eating iodized salt (for 3 months now) and moving to pickled salt I think I've experienced more symptoms of calcification and hardening of the arteries and blood vessels than before. Would you say that it could be because of removing iodine?
Is iodide the same as Iodine or is it different and what would be the safest way to consume it if one decides to use it?
Thank you.
RP: The treatments generally involve local injection of large amounts into the tumor. Iodine is the oxidized form, iodide is the ionized form that appears in the presense of cysteine, vitamin C, and other reductants.
Q: I'm very interested in it's uses in atherosclerosis
You've said" The only publications I have seen that presented clear evidence of the disappearance of arteriosclerosis involved treatment with iodides."
Is there any way that you can remember how it was used and what was the doses for that specific problem?
Also, would you say that increasing thyroid hormone while using potassium iodide would reduce the possible damaging effect?Much love
RP: Correcting elevated TSH lowers cholesterol and reduces vascular deterioration.
Hypothyroidism and Atherosclerosis
Anne R. Cappola, Paul W. Ladenson
The Journal of Clinical Endocrinology & Metabolism, Volume 88, Issue 6, 1 June 2003, Pages 2438–2444,
Cardiovascular Endocrinology: Special Features
“There was edema of the skin… much serous effusion in the pericardium… the heart was large… the arteries were everywhere thickened, the larger ones atheromatous.” (1)
[Dr. William Smith Greenfield, 1878]
This autopsy finding of diffuse atherosclerosis in a 58-yr-old woman was published as an appendix to William Ord’s classical description of the syndrome of myxedema. Soon thereafter, the hypothesis of a causal relationship between hypothyroidism and atherosclerosis was first raised in 1883 by E. Theodor Kocher (2), who noted that arteriosclerosis commonly occurred after thyroid extirpation. Since the time of the first associations between these two common disorders, hypothyroidism and atherosclerosis have subsequently been linked by a body of clinical case reports, epidemiological studies, and biochemical observations. The hypothesis of a relationship has subsequently been tested in case-control and cohort studies. Important associations have been identified among hypercholesterolemia, hypertension, and certain newer risk factors for atherosclerosis in individuals with overt hypothyroidism and, in some cases, subclinical hypothyroidism. There have also been clinical observations and trials describing the consequences of treating hypothyroidism in patients with ischemic heart disease and of revascularizing patients with ischemic heart disease who are hypothyroid. These studies are the subject of this commentary. -
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@16characterstwas said in Ray Peat: “The small amount of iodide added to salt has been reported in more than 70 studies to damage the thyroid gland, even increasing thyroid cancer”:
The small amount of iodide added to salt has been reported in more than 70 studies to damage the thyroid gland, even increasing thyroid cancer
Table salt
Iodine is typically in the form of potassium iodide (KI), usually (the most common form), or potassium iodate (KIO3), in regions with warmer, more humid climates, as it is more stable than potassium iodide. 3 months after packing, the lost could be 50 % (evaporated) if the store conditions were not optimal.
DOI: 10.1080/10256010208033316
=> So, you’ve got I- with table salt. Not a mix with I2. Iodide added in table sodium (I-) can be oxidized to iodine (I2), which can then sublimate (turn directly into a gas) or react with other substances, leading to iodine loss. Do not store in a metal can (reactive).Comment:
- table salt (chloride sodium) is not the right kind. We need 2 forms.
- Excess iodine is deleterious
Say that or nothing is the same. Compare with HD SFA. All excesses are bad.
Contradiction: a small amount in the salt and the the results of the studies with a high level. If the level is not adapted to the needs, you've got a Wolff-Chaikoff effect ... The NIS symporters must be accustomed (progressivity). Selenium is required before supplementation ...
No need to repeat here what I've already posted elsewhere if you don't listen to 
Edit: I don't recommend table salt, obviously. I prefer a titrated form, between 150-250 mcg, at the beginning of the process. I use kelp.
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theres multiple posts on the reddit sub about experiencing problems by removing iodized salt from diet.
i used to use pickling salt, it’s idiotic to cook and season with except in soups where it totally dissolves. i actually got some sort of stomach issue that lasted weeks before it resolved from accidently swallowing a bunch of undissolved kosher salt crystas in my coffee. i actually almost threw up a couple times drinking the super concentrated undissolved pickling salt crystals in my milk too
i went back to iodized saltsearch the reddit sub. theres one user that says they/them are allergic to seafood and that xer got suicidal after two months off iodized salt and it instantly resolved in two minutes after taking a bit of iodized salt in the middle of the night when xer was on auto pilot as if their body knew they needed it
