Human requirements of iodine & safe use of iodised salt.
Ranganathan S,1, Reddy V.
National Institute of Nutrition, Hyderabad.
Indian J Med Res. 1995 Nov;102:227-32.
https://www.ncbi.nlm.nih.gov/pubmed/8675243
Household Salt Iodine Content Estimation with the Use of Rapid Test Kits and Iodometric Titration Methods
Ashwini Kumar Nepal,1 Prem Raj Shakya,2 Basanta Gelal,3 Madhab Lamsal,4 David A Brodie,5 and Nirmal Baral6
J Clin Diagn Res. 2013 May; 7(5): 892–895.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3681063/
Year : 2013 | Volume : 2 | Issue : 4 | Page : 239-244
"Iodized salt, a boon or bane?": A retrospective study
Eswar Ganti1, Seshaiah Venkata Kurada1, Srijana Pakalapati1, Srinivasa Rao Dana1, Madhavi Pothukuchi2
1 Department of Medicine, Government Siddhartha Medical College, Vijayawada, Andhra Pradesh, India
2 Department of Community Medicine, Government Siddhartha Medical College, Vijayawada, Andhra Pradesh, India
Results: There was statistically significant association of hypothyroidism with excess usage of iodized salt, with hypertension and diabetes.
Conclusion: Excess iodine, through global iodization of table salt can lead to hypothyroidism, which is more associated with hypertension and diabetes, the two most important diseases commonly encountered in the community. So, iodine supplementation should be restricted to pockets of iodine deficiency only.
http://www.jdrntruhs.org/article.asp?issn=2277-8632;year=2013;volume=2;issue=4;spage=239;epage=244;aulast=Ganti
In countries where iodine has been added to table salt, the rates of autoimmune thyroid disease have risen.
https://chriskresser.com/iodine-for-hypothyroidism-like-gasoline-on-a-fire/
Effects of Increased Iodine Intake on Thyroid Disorders
Xin Sun, Zhongyan Shan, and Weiping Teng
Endocrinol Metab (Seoul). 2014 Sep; 29(3): 240–247.
Iodine is required for the production of thyroid hormones. Although iodine supplementation should be implemented to prevent and treat IDDs, iodine intake must be maintained at a safe level. The majority of excessive iodine exposure cases does not generally result in apparent clinically fatal consequences but could be harmful. More than adequate or excessive iodine levels are unsafe and may lead to hypothyroidism and autoimmune thyroiditis, especially for susceptible populations with recurring thyroid disease, the elderly, fetuses, and neonates. TSH levels are increasing in the Chinese population and the consequences of excessive iodine should be closely investigated.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4192807/
Iodine Excess as an Environmental Risk Factor for Autoimmune Thyroid Disease
Yuqian Luo,1 Akira Kawashima,1 Yuko Ishido,1 Aya Yoshihara,1 Kenzaburo Oda,1 Naoki Hiroi,2 Tetsuhide Ito,3 Norihisa Ishii,4 and Koichi Suzuki1,*
Int J Mol Sci. 2014 Jul; 15(7): 12895–12912.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4139880/
Excess Iodine Intake and Its Thyroid Impact
2019
There are several hypotheses, mechanism through which excess iodine results in thyroid dysfunction, including that excess iodine induces the production of cytokines and chemokines, leading to the recruitment of immunocompetent cells into the thyroid, which, together with the processing of excessive intrathyroid iodine, could induce oxidative stress, thereby increasing lipid oxidation and tissue damage. The inclusion of iodine in thyroglobulin (Tg) has been shown to induce greater Tg antigenicity, thus putting the individual at higher risk of thyroid autoimmunity [9, 10].
The thyroid gland has an intrinsic mechanism of adaptation to excessive iodine. As such, the so-called “acute Wolff–Chaikoff effect” may be explained by the generation of inhibitor substances (namely, iodolactones, iodine aldehydes, and iodine lipids) that impact the thyroid peroxidase (TPO) activity; the subsequent decrease in intrathyroid deiodinases leads to a reduction in the synthesis of thyroid hormones [11, 12]. In most individuals who experience rapid onset of excessive iodine, this effect is transient and recovers upon the occurrence of another phenomenon called “escape” from (or “adaptation” to) the acute Wolff–Chaikoff effect, which is associated with a reduced expression of the sodium-iodide symporter (NIS), a mediator of the active transport system by which iodine is shuttled from the circulation into the thyroid cell.
The decline in the NIS expression presents approximately 24 hours after acute iodine excess; the subsequent reduction in intrathyroid iodine concentration and in the levels of “iodinated” substances inhibits the synthesis of thyroid hormones and—under normal conditions—reinitiates the production of such hormones [13, 14]. In vulnerable individuals, such as those with thyroid antibodies present, individuals with a history of thyroiditis, radioactive iodine users, or individuals on medications such as amiodarone, interferon-α, or lithium, inter alia, the Wolff–Chaikoff escape phenomenon may fail, leading to permanent hypothyroidism. Likewise, in susceptible patients, including those with nontoxic nodular goiter, latent Graves’ disease (also known as Basedow’s), or those residing in areas with extended and severe iodine deficiencies, excess iodine may lead to hyperthyroidism; this condition and its underlying pathology is known as the “Jod-Basedow phenomenon.”
https://www.hindawi.com/journals/jnme/2019/6239243/
Diet and Thyroid Disease
Anitha Vadekeetil*
Department of Microbiology, India
ACTA SCIENTIFIC NUTRITIONAL HEALTH
Volume 3 Issue 4 April 2019
Iodized salt and multivitamin tablets are other sources of iodine. One teaspoon of iodized salt contains 284 ug of iodine and one gram of seaweed contains around 2 mg of iodine. Recommended dietary intake of iodine for adult men and women is 150 ug and for pregnant and lactating women is 220 ug and 290 ug respectively
https://www.actascientific.com/ASNH/pdf/ASNH-03-0221.pdf
