IODIDE - not - IODINE cure for many diseases? (With Ray qoutes)

[UG Krishnamurti]

RP: " 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."

RP: [ IODIDE ]: 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.

RP: 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.

RP: 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.

RP: 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.

Did anyone had experiences with iodide and how and where should one get iodide from?

@Hans @haidut Do you have any info? Much love guys.

 

[Dr. B]

RP: " 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."

RP: [ IODIDE ]: 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.

RP: 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.

RP: 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.

RP: 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.

Did anyone had experiences with iodide and how and where should one get iodide from?

@Hans @haidut Do you have any info? Much love guys.

potassium iodide sometimes sodium iodide supplements are available, iodized salt often has potassium iodide added but can have silica added too.

 

[Hugh Johnson]

"Lugol's iodine, also known as aqueous iodine and strong iodine solution, is a solution of potassium iodide with iodine in water."

Lugol's iodine - Wikipedia

en.wikipedia.org

 

[Inaut]

"Lugol's iodine, also known as aqueous iodine and strong iodine solution, is a solution of potassium iodide with iodine in water."

Lugol's iodine - Wikipedia

en.wikipedia.org

I’m seeing nothing but benefits with lugols. I’m using it topically.

 

[UG Krishnamurti]

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."

Spoiler: STUDIES HE SHARED

1. 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.

3. 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.

2. 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. [email protected]
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.


4. 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.


5. 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.


6. 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.


7. 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.


8. Am J Vet Res. 1973 Jan;34(1):65-70.
Experimentally induced iodide toxicosis in lambs.
McCauley EH, Linn JG, Goodrich RD.



9. 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.



10. 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.



11. 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: [email protected].
(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: [email protected].
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.



12. 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: [email protected].
(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.


13. 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?
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?
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.

 

[Dr. B]

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."

Spoiler: STUDIES HE SHARED

1. 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.

3. 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.

2. 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. [email protected]
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.


4. 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.


5. 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.


6. 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.


7. 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.


8. Am J Vet Res. 1973 Jan;34(1):65-70.
Experimentally induced iodide toxicosis in lambs.
McCauley EH, Linn JG, Goodrich RD.



9. 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.



10. 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.



11. 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: [email protected].
(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: [email protected].
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.



12. 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: [email protected].
(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.


13. 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?
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?
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.

iodized salt may be one of the big contributors to people getting issues from fast food and restaurant foods, in addition to fluoride in water, PUFA. iodized salt can contain silica too. some websites claim that cooking/heating can get rid of some of the iodide. in people susceptible to autoimmune reactions iodine or potassium iodide seems to trigger or inflame them somehow. it could also depend on things like glutathione, selenium, antioxidant intake from diet, supplements, etc. glutathione and i think selenium are involved in the enzyme that turns peroxide into water.
supplementing T3 or t4 might be able to negate the effects i dont think the animal glandular meat would have an effect on that.
have you tried using the iodide yet

 

[UG Krishnamurti]

have you tried using the iodide yet

never used iodine in any form except in table salt my whole life and in form of a atlanitc dulse for a period of 6 months...

 

[hierundjetzt]

I’m seeing nothing but benefits with lugols. I’m using it topically.

I am interested. Could you please expand how you use and for what you use it and also what benefits you have seen. Thx

 

[Jstar]

I take an iodide formula that is made from:

1 lemon
2 oz apple cider vinegar
1 heaping tsp camu camu
4-6 drops of Lugol’s Solution (2%)
water
orange juice
1 tsp sodium bicarbonate
1/2 tsp potassium bicarbonate

I use this amount to make 3 portions which I drink in the morning and at two other times in the day. Sometimes I add limonene, meth blue, and/or some magnesium chloride flakes.

Bill, from EarthClinic.com writes:
“If you want a cheap and cheerful way to orally supplement DHA then, as Ted from Bangkok recommends, all you need is Lugol’s iodine, Baking Soda (Arm & Hammer is fine to use), Ascorbic acid, and a glass of water. First add 1/4 tsp of ascorbic acid (1 gram) to the water. Then add 6 drops of LI. You will notice that the iodine in the water turns from brown to clear and that’s because the ascorbic acid is oxidized and converted to DHA while the molecular iodine is reduced to clear iodide. The last thing you add is the baking soda—add this until the fizzing stops. Now you have an oral solution of sodium ascorbate + iodide + DHA in ascorbate form.

"Without getting too technical, when you mix together Lugol’s iodine and ascorbic acid with water in a glass and then add sodium bicarbonate until the fizzing stops, the molecular iodine component of lugols is converted to sodium iodide and the ascorbic acid is converted to dehydro-ascorbic acid (DHA). Put simply, the ascorbic acid is oxidized to DHA by molecular iodine and the molecular iodine is reduced to sodium iodide during the reaction. You can see this happening in the glass because the brown color of the molecular iodine in Lugol's slowly turns colorless (iodide is colorless).
"Iodide is extremely useful to the body—very beneficial to the thyroid and it is essential to the immune system.
"The dehydro-ascorbic acid (DHA) has exactly the same properties as ordinary ascorbic acid except except for one difference—DHA is able to penetrate the blood/brain barrier whereas ordinary ascorbic acid cannot. Normally ascorbic acid is dependent upon and converted to DHA by glutathione in your body. So taking ascorbic acid with Lugol’s iodine like this also helps to save the glutathione stores in your body for more essential tasks.
“This is okay if you are taking this solution for thyroid problems or for general health because most organs, mucus glands and endocrine system can uptake both the iodide and iodine forms, but if you are taking Lugol's specifically for a breast problem like fibrocystic disease or for uterine fibroids or BV for example, the iodide form will not be of much use because the breasts, cervix and prostate all uptake the iodine form only. Also, iodine is the component that is truly anti-microbial, so if you are taking Lugol's against intestinal candida, better to take drops of Lugol's on its own in a glass of water (containing both iodide and iodine).

 

[Dr. B]

I take an iodide formula that is made from:

1 lemon
2 oz apple cider vinegar
1 heaping tsp camu camu
4-6 drops of Lugol’s Solution (2%)
water
orange juice
1 tsp sodium bicarbonate
1/2 tsp potassium bicarbonate

I use this amount to make 3 portions which I drink in the morning and at two other times in the day. Sometimes I add limonene, meth blue, and/or some magnesium chloride flakes.

Bill, from EarthClinic.com writes:
“If you want a cheap and cheerful way to orally supplement DHA then, as Ted from Bangkok recommends, all you need is Lugol’s iodine, Baking Soda (Arm & Hammer is fine to use), Ascorbic acid, and a glass of water. First add 1/4 tsp of ascorbic acid (1 gram) to the water. Then add 6 drops of LI. You will notice that the iodine in the water turns from brown to clear and that’s because the ascorbic acid is oxidized and converted to DHA while the molecular iodine is reduced to clear iodide. The last thing you add is the baking soda—add this until the fizzing stops. Now you have an oral solution of sodium ascorbate + iodide + DHA in ascorbate form.

"Without getting too technical, when you mix together Lugol’s iodine and ascorbic acid with water in a glass and then add sodium bicarbonate until the fizzing stops, the molecular iodine component of lugols is converted to sodium iodide and the ascorbic acid is converted to dehydro-ascorbic acid (DHA). Put simply, the ascorbic acid is oxidized to DHA by molecular iodine and the molecular iodine is reduced to sodium iodide during the reaction. You can see this happening in the glass because the brown color of the molecular iodine in Lugol's slowly turns colorless (iodide is colorless).
"Iodide is extremely useful to the body—very beneficial to the thyroid and it is essential to the immune system.
"The dehydro-ascorbic acid (DHA) has exactly the same properties as ordinary ascorbic acid except except for one difference—DHA is able to penetrate the blood/brain barrier whereas ordinary ascorbic acid cannot. Normally ascorbic acid is dependent upon and converted to DHA by glutathione in your body. So taking ascorbic acid with Lugol’s iodine like this also helps to save the glutathione stores in your body for more essential tasks.
“This is okay if you are taking this solution for thyroid problems or for general health because most organs, mucus glands and endocrine system can uptake both the iodide and iodine forms, but if you are taking Lugol's specifically for a breast problem like fibrocystic disease or for uterine fibroids or BV for example, the iodide form will not be of much use because the breasts, cervix and prostate all uptake the iodine form only. Also, iodine is the component that is truly anti-microbial, so if you are taking Lugol's against intestinal candida, better to take drops of Lugol's on its own in a glass of water (containing both iodide and iodine).

i thought ascorbic acid boosts glutathione, even the ascorbic acid supplements?

 

[Jam]

I have been taking anywhere from 150mg - 1gr of potassium iodide (as SSKI), per day for years, and can safely affirm that in my opinion, iodine is the most misunderstood, maligned, and suppressed beneficial substance in the history of medicine. In the same time, my wife and I have also ingested close to a liter of Lugol's. Both have their places.

 

[Shackles]

I have been taking anywhere from 150mg - 1gr of potassium iodide (as SSKI), per day for years, and can safely affirm that in my opinion, iodine is the most misunderstood, maligned, and suppressed beneficial substance in the history of medicine. In the same time, my wife and I have also ingested close to a liter of Lugol's. Both have their places.

What is so special about it, if I may ask? Reduction of Arthritis oder similar things? Less Plaque maybe even?

 

[Jam]

What is so special about it, if I may ask? Reduction of Arthritis oder similar things? Less Plaque maybe even?

These are the effects I've noticed so far, off the top of my head:
- (SSKI) Cured my arthritic shoulders, regained full movement
- (SSKI) Cured sciatica and general hip pain (very synergistic with d3)
- (SSKI) Removed a ganglion cyst on my right wrist
- (SSKI) Alleviates wife's endotoxin symptoms
- (SSKI) Made respiratory infections a thing of the past
- (SSKI) Greatly improved wife's asthma
- (SSKI + Lugol's) Cured multiple periodontal gum abscesses
- (SSKI) Increases energy levels, alleviates depression (wife)
- (Lugol's) Topically, resolves virtually any insect bite and annihilates ringworm.

 

[UG Krishnamurti]

These are the effects I've noticed so far, off the top of my head:
- (SSKI) Cured my arthritic shoulders, regained full movement
- (SSKI) Cured sciatica and general hip pain (very synergistic with d3)
- (SSKI) Removed a ganglion cyst on my right wrist
- (SSKI) Alleviates wife's endotoxin symptoms
- (SSKI) Made respiratory infections a thing of the past
- (SSKI) Greatly improved wife's asthma
- (SSKI + Lugol's) Cured multiple periodontal gum abscesses
- (SSKI) Increases energy levels, alleviates depression (wife)
- (Lugol's) Topically, resolves virtually any insect bite and annihilates ringworm.

So, basically all the benefits Peat mentioned in the quotes above
Before of course, he went on speaking against it.

What do you think are the mechanism in these studies in which it was shown that it can cause thyroid cancer?

 

[Jam]

So, basically all the benefits Peat mentioned in the quotes above
Before of course, he went on speaking against it.

What do you think are the mechanism in these studies in which it was shown that it can cause thyroid cancer?

Fraud.

 

[UG Krishnamurti]

Fraud.

Any research/information which could confirm your statement?

 

[CoconutEffect]

Very interested thread. @burtlancast , you had mentioned in a separate thread benefit to the pineal, also people reporting improved sleep and better circadian rhythms?

So we’re looking at SSKI orally and lugols topically from what can be gleaned thus far?

 

[UG Krishnamurti]

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."

Spoiler: STUDIES HE SHARED

1. 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.

3. 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.

2. 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. [email protected]
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.


4. 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.


5. 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.


6. 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.


7. 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.


8. Am J Vet Res. 1973 Jan;34(1):65-70.
Experimentally induced iodide toxicosis in lambs.
McCauley EH, Linn JG, Goodrich RD.



9. 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.



10. 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.



11. 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: [email protected].
(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: [email protected].
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.



12. 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: [email protected].
(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.


13. 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?
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?
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?

RP: Correcting elevated TSH lowers cholesterol and reduces vascular deterioration.

Spoiler: STUDY RP MENTIONED

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.

 

[Nebula]

I have been taking anywhere from 150mg - 1gr of potassium iodide (as SSKI), per day for years

Did you mean 150 mcg? My experience with supplemental iodine at 2mg per day was very bad and caused hypothyroidism I still haven’t recovered from years later. It’s puzzling how varied experiences with iodine are. A panacea for some, a disaster for others.

 

[UG Krishnamurti]

Did you mean 150 mcg? My experience with supplemental iodine at 2mg per day was very bad and caused hypothyroidism I still haven’t recovered from years later. It’s puzzling how varied experiences with iodine are. A panacea for some, a disaster for others

I agree that for almost all supplements.
D3 can be in the same category of supplements messing people up badly or providing relief.