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Salt, iodine, and thyroid and all we need to know: Part 1

Updated: Apr 15

To understand all this there are three things to understand.

1.      Need of iodine in body, how much and what happens if excess iodine is undertaken.

2.      How nature makes iodine and how salt is fortified with iodine, and

3.      And is excess of causing health issues.

And the conclusions are almost every one is taking excess salt hence as consequence excess iodine and sodium but since sodium is not talked here, we escape.

Excess iodine is harmful and hence possibly we cannot cut salt quickly consumption using other natural salts in some ratio in diet is healthier.


Iodine, a trace element, is an essential component of thyroid hormones thyroxine (T4) and triiodothyronine (T3), which are critical for liver, kidney, muscle, brain and central nervous system function. Iodine regulates overall metabolism and plays a critical role in fetal and child neurodevelopment, organ, and tissue function. A healthy adult body contains 15–20 mg of iodine, of which 70–80% is in the thyroid gland. For the developing fetus, deficiency is one of the greatest causes of preventable intellectual disability, thus iodine status of pregnant and women of reproductive age is a recognized international concern.


In the human gut iodine is metabolized to iodide and in healthy adults > 90% is absorbed. Once in circulation, it mainly accumulates in the thyroid gland or is excreted by the kidney, with small amounts accumulating in the salivary glands, mammary gland or choroid plexus. Clearance by the kidney is constant, while uptake by the thyroid is dependent upon iodine status and intake. When iodine supply is sufficient, uptake by the thyroid may be ≤10%, whereas it can exceed 80% due to chronic deficiency. After active transport into the thyroid, iodide is stored in the thyroglobulin (Tg) protein before undergoing conversion into T3 and T4. The hormones T3 and T4 enter circulation bound to carrier proteins and then target tissues; however, T3 is the primary physiologically active form and preferentially binds to its receptors. Both free T3 and T4 are assessed in serum by immunoassay. However, serum thyroid stimulating hormone (TSH) is the best marker of individual thyroid status and is used clinically for this purpose. The hormones T3 and T4 do not change sufficiently as a result of iodine deficiency to be clinically useful.

Over 90% of ingested iodine is excreted in the urine by the kidneys, which is why measurement of UIC is considered one of the best biomarkers of recent dietary iodine intake. The hormone TSH, secreted by the pituitary gland, is the main regulator of T3 and T4 metabolism through a negative feedback loop regulated by thyroid hormones and modulated by TSH-releasing hormone. In addition to signaling degradation of Tg and release of T3 and T4 into the circulation, TSH also increases iodine uptake; therefore, an elevated TSH concentration is generally a symptom of hypothyroidism, while low TSH levels indicate hyperthyroidism.


Adverse Consequences of Excess Iodine Intake

A median UIC of > 299 µg/L indicates possible excess. In the U.S. the IOM has set the UL for iodine intake at 1100 µg/day for adult men and women, which includes pregnant and lactating women 19 years and older, although the consequences of excess intake are far less detrimental than too little. Excessive iodine intake may lead to hyperthyroidism, autoimmune thyroid disease, and papillary cancer–a type of thyroid cancer (Dunn et.el 2001) In healthy adults, high levels can reduce thyroid hormone production, leading to higher TSH stimulation, causing hypothyroidism and eventually thyroid growth and development of diffuse goiters (Dunn 2006,Zimmerman et. El .2020, Carle 2014). In populations that are chronically iodine deficient, sudden increase and excess iodine intake leads to iodine-induced hyperthyroidism, which primarily occurs in older individuals with nodular goiter (Zimmerman).


The iodine in nature and its contribution to problem:


Iodine is the heaviest stable halogen element and primarily exists in nature as iodide (I-), the form typically used to produce supplements and iodized table salt in the form of potassium iodide (KI). It can also be found naturally as iodate (IO3-), another form used to fortify table salt as potassium iodate (KIO3). Iodide is naturally in soil and seawater, which affects the iodine content of produce. However, in many regions surface soils are depleted of iodide. Since iodide is found in seawater, it volatizes into the atmosphere and can return to the soil, in non-coastal regions this cycle is incomplete and as a consequence plant foods and drinking water are depleted. Therefore, historically iodine deficiency was seen in populations from inland regions (central Asia and Africa, central and eastern Europe, the central U.S.), mountainous areas (Alps, Andes, Atlas, Himalayas) and those with frequent flooding (Southeast Asia).


Now it raises a special problem for country like India with huge coastal belt and two strong monsoons that will be carrying iodine for soil right to end to end ----that’s why before we started iodized salt mountain region had high goiter issues and possibly had people had lesser % of hyperthyroidism.

But since no data exists about it, a lot of it's logical conclusions.


But bottom line is excess iodized salt means even excessive iodine and add to that natural iodine especially around coastal belt our consumption of salt must be relooked. Excess iodized salt is simple if there are 5 members in home your monthly salt intake must be 750 gms. And add iodine coming from food, even lesser.


In part 2 we will talk of options of different non iodized salts like Himalayan pink rock salt, lake salt of sambhar and other salts from sea.


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