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]
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FYI
Post in thread 'Ray Peat Email Advice Depository'
https://lowtoxinforum.com/threads/ray-peat-email-advice-depository.1035/post-655068Q: Mr Peat im wondering if your recommendations regarding supplementation of iodine are the same as for iodide? Many people are aware of your comments regarding IodINE supplementation, but some people are claiming your comments apply only to Iodine and that you believe there are benefits to supplementing large, several milligram doses of IODIDE like potassium iodide. the logic being used is these people claim chlorine is bad chloride is essential, and similarly they claim you believe only iodine is bad whereas you like supplementing with iodide
A: No, 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:
Endocr Pathol. 2002 Fall;13(3):175-81.
Thyroid cancer and thyroiditis in Salta, Argentina: a 40-yr study in relation to iodine prophylaxis.
Harach HR, Escalante DA, Day ES.
Services of Pathology, Dr A Oñativia Endocrinology and Metabolism Hospital,
Salta, Argentina. rubenharach@ciudad.com.ar
The natural history of thyroid cancer and thyroiditis in relation to iodine
prophylaxis in the region of Salta, Argentina, where goiter is common was
investigated over a time span of 40 yr. For analysis of thyroid cancer, the
specimens were divided into two periods. The first 15 yr (59 cases), including 5
yr before prophylaxis, was compared with the second 25 yr (182 cases), a period
well after salt iodination. Papillary carcinomas formed the largest group of
tumors in both periods, with a significant increase in their proportion in the
second period (44 vs 60%, chi(2): p < 0.05), while the percentage of follicular
and undifferentiated carcinomas decreased and medullary carcinoma remained about
the same. The ratio of papillary to follicular carcinoma rose from 1.7:1 in the
first period to 3.1:1 in the second. Four thyroid lymphomas of non-Hodgkin's
B-cell type occurred in the second period in females over age 50. A severe
lymphoid thyroiditis was present in the two cases with assessable background
thyroid tissue. The frequency of moderate to severe lymphoid infiltrate in
females rose from 2 of 12 (16.6%) in the preprophylaxis period to 34 of 114
(28.0%) in the last 25 yr after prophylaxis. After salt prophylaxis, thyroiditis
was more frequent in patients with papillary carcinoma (36.2%) than in those with
nonpapillary tumors (14.7%) (chi(2), p < 0.02). These observations indicate that
a high dietary intake of iodine may be associated with a high frequency of
papillary carcinoma and thyroiditis, and that thyroiditis is more commonly
associated with papillary carcinoma than with other thyroid tumors. The
occurrence of non-Hodgkin's lymphomas only in the postprophylaxis period may be
linked to an increase in thyroiditis.Saudi Med J. 2007 Jul;28(7):1034-8.
The effect of iodine prophylaxis on the frequency of thyroiditis and thyroid
tumors in Southwest, Iran.
Soveid M, Monabbati A, Sooratchi L, Dahti S.
Department of Internal Medicine, Shiraz University of Medical Sciences, Nemazee
Hospital, Shiraz, Iran. msoveid@sums.ac.ir
OBJECTIVE: To investigate the effect of the salt iodization program, which was
initiated in 1989 on frequencies of thyroiditis and papillary carcinoma in Fars
province of Iran, which was previously an iodine deficient area. METHODS: Four
hundred and eighty-two thyroidectomy specimens belonging to the pre-iodization
period from 1983 to 1988, and 466 post iodization specimens from 1998 to 2003
were re-examined for presence of lymphocytic infiltration and types of thyroid
tumors. This study was carried out in Shiraz University of Medical Sciences,
Iran. RESULTS: The frequency of lymphocytic infiltration in non-neoplastic
specimens increased from 30-60.5% after salt iodization (p<0.001). Background of
lymphocytic infiltration in neoplastic specimens also increased from 18.5-61%
after iodine prophylaxis (p<0.001). The frequency of papillary carcinoma in
neoplastic specimens increased from 15-43% (p=0.01) and that of follicular
adenoma decreased from 69-32.5% (p<0.0001). CONCLUSION: Salt iodization is
associated with an increased occurrence of histologic thyroiditis and papillary
carcinoma.Biol Trace Elem Res. 2007 Oct 20 [Epub ahead of print]
Safe Range of Iodine Intake Levels: A Comparative Study of Thyroid Diseases in
Three Women Population Cohorts with Slightly Different Iodine Intake Levels.
Teng X, Shi X, Shan Z, Jin Y, Guan H, Li Y, Yang F, Wang W, Tong Y, Teng W.
Department of Endocrinology and Metabolism, The First Affiliated Hospital, China
Medical University, No. 155 Nanjing Bei Street, Heping District, Shenyang,
Liaoning Province, 110001, People's Republic of China, tengxiaochun@126.com.
Iodine excess may lead to thyroid diseases. Our previous 5-year prospective
survey showed that the prevalence and incidence of hypothyroidism or autoimmune
thyroiditis increased with iodine intake. The aim of the present study was to
investigate the optimal range of iodine intake by comparing the prevalence of
thyroid diseases in three areas with slightly different levels of iodine intake.
In 2005, 778 unselected women subjects from three areas with different iodine
intake levels were enrolled. Levels of serum thyroid hormones, thyroid
autoantibodies, and urinary iodine were measured, and thyroid B ultrasounds were
performed. Among the subjects with mildly deficient iodine intake, those with
adequate intake, and those with more than adequate intake, the prevalence of
clinical and subclinical hypothyroidism was 0, 1.13, and 2.84%, respectively (P =
0.014); that of thyroid goiter was 24.88, 5.65, and 11.37%, respectively (P <
0.001); that of serum thyrotropin values was1.01, 1.25, and 1.39 mIU/l,
respectively; and that of serum thyrotropin/thyroglobulin ratio was 7.98, 6.84,
and 5.11, respectively (P < 0.001). In conclusion, median urinary iodine 100~200
mug/l may reflect the safe range of iodine intake levels. Serum
thyrotropin/thyroglobulin ratio might be a better index of evaluating iodine
status.Endocrinology. 2007 Jun;148(6):2747-52. Epub 2007 Mar 8.
Induction of goitrous hypothyroidism by dietary iodide in SJL mice.
Li HS, Carayanniotis G.
Faculty of Medicine, Memorial University of Newfoundland, St. John's,
Newfoundland, Canada.
Prolonged intake of large amounts of iodide has been reported to increase the
incidence of goiter and/or hypothyroidism in humans as well as animals prone to
spontaneous autoimmune thyroiditis. In the current study, we investigated the
role of dietary iodide on the development of hypothyroidism, as well as
thyroiditis, in strains of mice that do not develop spontaneous autoimmune
thyroiditis. Intake of 0.05% NaI via drinking water for 10 wk induced
hypothyroidism in SJL/J mice as indicated by elevated TSH and depressed total
T(4) values in serum and formation of colloidal goiter with an inactive flattened
thyroid epithelium. Hypothyroidism did not appear to have an autoimmune basis
because only focal mononuclear cell infiltrates were found intrathyroidally, and
antithyroglobulin antibodies or increased organification of iodide were not
detected. These phenomena were not observed in similarly treated CBA/J mice,
suggesting polymorphisms in genes controlling events downstream of iodide uptake
by thyrocytes. Interestingly, RT-PCR analysis indicated that unlike CBA/J, SJL/J
mice could not down-regulate Na/I symporter gene expression during the NaI
treatment. No significant temporal or strain differences were observed regarding
the expression of thyroglobulin, pendrin, thyroid peroxidase, and DUOX1 and DUOX2
genes after NaI intake. Our results point to the generation of a mouse model for
the study of iodine-induced hypothyroidism, which does not seem to have an
autoimmune basis.J Endocrinol Invest. 2003;26(2 Suppl):49-56.
Iodine excess and thyroid autoimmunity.
Bournaud C, Orgiazzi JJ.
Service d'Endocrinologie, Diabétologie et Maladies Métaboliques, Centre
Hospitalier Lyon-Sud, 69495 Pierre-Bénite Cedex, France.
Epidemiological studies, as well as animal models, indicate that iodine might be
an immunogenic agent for the thyroid gland, at least in subjects predisposed to
thyroid autoimmunity. This review presents data, either epidemiological or
experimental, obtained in different conditions: constant and stable iodine
status, either deficient, sufficient or excessive; long-term iodine prophylaxis;
temporary supplementation with iodide (6-12 months) or iodised oil. Moreover, we
also discuss data obtained in the general population, among subjects with
euthyroid goiter, or autoimmune goiter, or even in women prone to post-partum
thyroid diseases. It is concluded that the significant increase in the prevalence
of autoimmune thyroid diseases in populations living in iodine sufficient areas
should not prevent the implementation of the iodine prophylaxis.J Immunol. 2002 Jun 1;168(11):5907-11.
Enhanced iodination of thyroglobulin facilitates processing and presentation of a
cryptic pathogenic peptide.
Dai YD, Rao VP, Carayanniotis G.
Division of Endocrinology, Faculty of Medicine, Memorial University of
Newfoundland, St. John's, Newfoundland, Canada.
Increased iodine intake has been associated with the development of experimental
autoimmune thyroiditis (EAT), but the biological basis for this association
remains poorly understood. One hypothesis has been that enhanced incorporation of
iodine in thyroglobulin (Tg) promotes the generation of pathogenic T cell
determinants. In this study we sought to test this by using the pathogenic
nondominant A(s)-binding Tg peptides p2495 and p2694 as model Ags. SJL mice
challenged with highly iodinated Tg (I-Tg) developed EAT of higher severity than
Tg-primed controls, and lymph node cells (LNC) from I-Tg-primed hosts showed a
higher proliferation in response to I-Tg in vitro than Tg-primed LNC reacting to
Tg. Interestingly, I-Tg-primed LNC proliferated strongly in vitro against p2495,
but not p2694, indicating efficient and selective priming with p2495 following
processing of I-Tg in vivo. Tg-primed LNC did not respond to either peptide.
Similarly, the p2495-specific, IL-2-secreting T cell hybridoma clone 5E8 was
activated when I-Tg-pulsed, but not Tg-pulsed, splenocytes were used as APC,
whereas the p2694-specific T cell hybridoma clone 6E10 remained unresponsive to
splenic APC pulsed with Tg or I-Tg. The selective in vitro generation of p2495
was observed in macrophages or dendritic cells, but not in B cells, suggesting
differential processing of I-Tg among various APC. These data demonstrate that
enhanced iodination of Tg facilitates the selective processing and presentation
of a cryptic pathogenic peptide in vivo or in vitro and suggest a mechanism that
can at least in part account for the association of high iodine intake and the
development of EAT.Autoimmunity 1995;20(3):201-6
Excess iodine induces the expression of thyroid solid cell nests in lymphocytic thyroiditis-prone BB/W rats. Zhu YP, Bilous M, Boyages SC. Department of Clinical Endocrinology, Westmead Hospital, Sydney, Australia. Previous epidemiological studies have suggested that lymphocytic thyroiditis and/or an increased iodine intake may be risk factors for the development of thyroid cancer. We previously reported that excess iodine accelerated the development of thyroid lymphocytic infiltration (LI) in the autoimmune BB/W rat model. We also found that excess iodine increased thyroid cell proliferation in a disordered manner. The present study was designed to further explore these observations and to address the question as to whether excess iodine under certain conditions predisposes the thyroid gland to neoplasia. To test this hypothesis, the lymphocytic thyroiditis-prone BB/W rat was exposed to excess iodine in drinking water. Ten BB/W rats at 4 weeks of age were given iodine water (NaI 0.05%) for 10 weeks, whilst another 10 BB/W rats were given tap water and served as controls. Eighteen normal Wistar rats were also divided into excess iodine and control groups, served as a comparison to the BB/W rats. We found that an excess iodine intake accelerated the development of LI in the BB/W rat. Severe LI was usually accompanied by prominent thyroid cell proliferation, evident as numerous microfollicles and cell masses, not forming normal thyroid follicles. Numerous lymphocytes and plasma cells often encroached on these areas of increased cellular proliferation. The surprising feature, and a possible indicator of activated thyroid cell proliferation, was the high incidence of thyroid solid cell nest-like lesions (SCN) in the iodine treated BB/W rats.(ABSTRACT TRUNCATED AT 250 WORDS)Clin Endocrinol (Oxf) 1989 Oct;31(4):453-65
Thyroid autoimmunity in endemic goitre caused by excessive iodine intake.
Boyages SC, Bloot AM, Maberly GF, Eastman CJ, Li M, Qian QD, Liu DR, van der
Gaag RD, Drexhage HA.
Department of Medicine, Westmead Hospital, Sydney, Australia.
The pathophysiology of endemic goitre caused by excessive iodine intake is not
well defined. By interacting with the immune system, iodine excess may trigger
the development of autoimmune thyroid disease such as lymphocytic Hashimoto's
thyroiditis (LT). In an attempt to examine this further, we compared the
presence of thyroid autoantibodies in 29 goitrous children, from an iodine
excess area, and in 26 healthy children, from an iodine sufficient area, of
north central China. Serum was tested for antimicrosomal (MAb),
anti-thyroglobulin (TgAb), second colloid antigen antibodies (CA2-Ab) and TSH
binding inhibitory immunoglobulins (TBII). Affinity chromatographically purified
IgG was tested for thyroid growth-stimulating activity (TGI) by two different
methods: a sensitive cytochemical bioassay (CBA) using guinea-pig thyroid
explants and a mitotic arrest assay (MAA) employing a continuous rat thyroid
cell line (FRTL-5). We found no increased prevalence of LT in patients with
endemic iodine goitre. The levels of MAb, TgAb and CA2-Ab did not differ
significantly between the two groups of children. Further, TBII were not present
in either group. Thyroid growth-stimulating immunoglobulins (TGI) were the major
autoantibodies found in children with goitres caused by iodine excess. In the
CBA, 12 of 20 (60%) goitrous children and 0 of 12 (0% P less than 0.05) healthy
children were positive for TGI. Similar results were found in the MAA, and a
good correlation between results of the CBA and MAA was found (P = 0.003).
Maximal TGI activity in dose-response CBA showed a good relation with clinical
goitre size (r = 0.63; P less than 0.05) indicating a possible
pathophysiological role for these antibodies. We conclude that endemic iodine
goitre is not associated with Hashimoto's lymphocytic thyroiditis. Nevertheless,
autoimmune growth factors such as TGI may play a primary role in the
pathogenesis of thyroid growth in this condition.Science 1985 Oct 18;230(4723):325-7
Induction of autoimmune thyroiditis in chickens by dietary iodine.
Bagchi N, Brown TR, Urdanivia E, Sundick RS. Clinical studies have suggested that excess dietary iodine promotes autoimmune
thyroiditis; however, the lack of a suitable animal model has hampered
investigation of the phenomenon. In this study, different amounts of potassium
iodide were added to the diets of chicken strains known to be genetically
susceptible to autoimmune thyroiditis. Administration of iodine during the first
10 weeks of life increased the incidence of the disease, as determined by
histology and the measurement of autoantibodies to triiodothyronine, thyroxine,
and thyroglobulin. Further support for the relation between iodine and
autoimmune thyroiditis was provided by an experiment in which iodine-deficient
regimens decreased the incidence of thyroid autoantibodies in a highly
susceptible strain. These results suggest that excessive consumption of iodine
in the United States may be responsible for the increased incidence of
autoimmune thyroiditis.Am J Clin Nutr. 2005 Apr;81(4):840-4.
High thyroid volume in children with excess dietary iodine intakes.
Zimmermann MB, Ito Y, Hess SY, Fujieda K, Molinari L.
Human Nutrition Laboratory, Swiss Federal Institute of Technology, Zurich,
Switzerland. michael.zimmermann@ilw.agrl.ethz.ch
BACKGROUND: There are few data on the adverse effects of chronic exposure to high iodine intakes, particularly in children. OBJECTIVE: The objective of the study was to ascertain whether high dietary intakes of iodine in children result in high thyroid volume (Tvol), a high risk of goiter, or both. DESIGN: In an international sample of 6-12-y-old children (n = 3319) from 5 continents with iodine intakes ranging from adequate to excessive, Tvol was measured by ultrasound, and the urinary iodine (UI) concentration was measured. Regressions were done on Tvol and goiter including age, body surface area, sex, and UI concentration as covariates. RESULTS: The median UI concentration ranged from 115 microg/L in central Switzerland to 728 microg/L in coastal Hokkaido, Japan. In the entire sample, 31% of children had UI concentrations >300 microg/L, and 11% had UI concentrations >500 microg/L; in coastal Hokkaido, 59% had UI concentrations >500 microg/L, and 39% had UI concentrations >1000 microg/L. In coastal Hokkaido, the mean age- and body surface area-adjusted Tvol was approximately 2-fold the mean Tvol from the other sites combined (P < 0.0001), and there was a positive correlation between log(UI concentration) and log(Tvol) (r = 0.24, P < 0.0001). In the combined sample, after adjustment for age, sex, and body surface area, log(Tvol) began to rise at a log(UI concentration) >2.7, which, when transformed back to the linear scale, corresponded to a UI concentration of approximately 500 microg/L. CONCLUSIONS: Chronic iodine intakes approximately twice those recommended-indicated by UI concentrations in the range of 300-500 microg/L-do not increase Tvol in children. However, UI concentrations >/=500 microg/L are associated with increasing Tvol, which reflects the adverse effects of chronic iodine excess.
Multicenter StudyHokkaido Igaku Zasshi 1994 May;69(3):614-26. [Screening for thyroid dysfunction in adults residing in Hokkaido Japan: in relation to urinary iodide concentration and thyroid autoantibodies]
[Article in Japanese] Konno N, Iizuka N, Kawasaki K, Taguchi H, Miura K, Taguchi S, Murakami S, Hagiwara K, Noda Y, Ukawa S. Department of Internal Medicine, Hokkaido Central Hospital for Social Health Insurance, Sapporo, Japan. The prevalence of thyroid dysfunction and its relation to thyroid autoantibodies (TAA) and urinary iodide concentration (UI) was studied in apparently healthy adults in Sapporo (n = 4110) (Sapporo group), and in five coastal areas of Hokkaido (n = 1061) (coastal group) which produce iodine-rich seaweed (kelp). The frequency of above normal UI (high UI) in the morning urinary samples of coastal group was 10.8%, significantly higher than that of Sapporo group (6.4%) (p < 0.001). Frequency of positive TAA in both groups were similar. In Sapporo group TAA was positive in 6.4% of males and 13.8% of females with an age-related increase. The overall prevalence of hyperthyroidism (TSH < 0.15 mU/L) in coastal group (0.6%) was similar to that in Sapporo group (1.1%), while that of hypothyroidism (TSH > 5.0 mU/L) in coastal group (3.8%) was significantly higher than that in Sapporo group (1.3%) (P < 0.001). The frequency of high UI correlated significantly with that of hypothyroidism with negative TAA (r = 0.829, P < 0.05), but not with positive TAA, or with that of hyperthyroidism. Hypothyroidism was more prevalent in TAA negative subjects with high UI than with normal UI. Moreover, serum TSH and thyroglobulin levels were higher and free T4 level was lower in former than in latter group. These results indicate that 1) the prevalence of TAA negative hypothyroidism in iodine sufficient areas may be associated with the amount of iodine ingested, 2) this hypothyroidism is more prevalent and marked in subjects consuming further excess amounts of iodine, and 3) excessive intake of iodine should be considered an etiology of hypothyroidism in addition to chronic thyroiditis in these areas.Endocrinol Metab Clin North Am 1987 Jun;16(2):327-42
Environmental factors affecting autoimmune thyroid disease.
Safran M, Paul TL, Roti E, Braverman LE.
Department of Medicine, University of Massachusetts Medical Center, Worcester.
A number of environmental factors affect the incidence and progression of
autoimmune thyroid disease. Exposure to excess iodine, certain drugs, infectious
agents and pollutants, and stress have all been implicated.Acta Endocrinol (Copenh) 1978 Aug;88(4):703-12
A case of Hashimoto's thyroiditis with thyroid immunological abnormality
manifested after habitual ingestion of seaweed.
Okamura K, Inoue K, Omae T.
An interesting case of iodide induced goitre with immunological abnormalities is
described. The patient who was sensitive to synthetic penicillin had previously
been treated for exudative pleuritis, congestive heart failure and acute renal
failure. Following recovery, he began to ingest large amounts of seaweed after
which he developed goitrous hypothyroidism. It was of interest that the serum
level of gamma-globulin increased, and subsequently the antithyroid microsomal
antibody became strongly positive, suggesting that thyroidal autoimmune
processes had been precipitated. Biopsy of the thyroid gland revealed chronic
thyroiditis, with evidence suggesting extreme stimulation by TSH. Hight
thyroidal uptake of 131I, positive perchlorate discharge test and biochemical
analysis of the thyroidal soluble protein showed severe impairment of hormone
synthesis following continuous accumulation of excess iodide. While there is
evidence suggesting that increased iodide may be an important factor in the
initiation of Hashimoto's thyroiditis, this may result from the marked increased
sensitivity of Hashimoto's gland to the effects of iodine. Thus an occult lesion
could be unmasked in this manner. The mechanism by which iodide mediates this
effect is not clear.…
[more studies at link]