Iodine is an essential halogen that is the only known component of the thyroid hormones — the thyroxine (T4) and the triiodothyronine (T3) — and it is therefore essential for the regulation of the basal metabolic rate, for the development of the central nervous system, for the growth and the maturation of all tissues, and for the maintenance of the normal physiological function in all organs. The thyroid gland actively concentrates the iodine from the blood (by the sodium-iodide symporter, NIS, on the basolateral membrane of the thyroid follicular cells) and incorporates it into the tyrosine residues of the thyroglobulin protein (by the thyroid peroxidase enzyme) to form the monoiodotyrosine (MIT), the diiodotyrosine (DIT), the T4, and the T3. Without adequate iodine, the thyroid hormone synthesis is impaired, the T4 and T3 levels in the blood fall, the TSH (thyroid-stimulating hormone) rises in an attempt to stimulate the thyroid hormone synthesis, the thyroid gland hypertrophies (enlarges) to trap more iodine, and the goitre develops — the hallmark of the iodine deficiency. In severe iodine deficiency, the T4 and T3 levels are so low that the cretinism develops in the developing foetus and infant — a condition of the irreversible mental retardation, the growth retardation, the deaf-mutism, and the motor spasticity that is one of the most devastating consequences of any nutritional deficiency. The typical dietary iodine intake is 100-300mcg daily (from the iodised salt, the seafood, and the dairy products), and the RDA is 150mcg daily for adults — but the iodine deficiency is the most common cause of the preventable intellectual disability worldwide, affecting approximately 2 billion people, and it is particularly common in the inland mountainous areas where the iodine has been washed out of the soil by the glacial action and by the rainfall.
Iodine and the Thyroid Hormone Synthesis
The thyroid hormone synthesis is a complex, multi-step process that begins with the active transport of the iodide from the blood into the thyroid follicular cell by the sodium-iodide symporter (NIS) — this is the rate-limiting step in the thyroid hormone synthesis, and it is regulated by the TSH (which increases the NIS expression and activity) and by the iodine availability (which down-regulates the NIS expression through the Wolff-Chaikoff effect). Once inside the thyroid follicular cell, the iodide is oxidised by the thyroid peroxidase (TPO) enzyme (in the presence of hydrogen peroxide) to the reactive iodine species that can then iodinate the tyrosine residues of the thyroglobulin (TG) protein — this iodination of the tyrosine residues produces the MIT (one iodine atom per tyrosine) and the DIT (two iodine atoms per tyrosine), which are then coupled by the TPO enzyme to form the T4 (two DIT molecules coupled) and the T3 (one MIT and one DIT molecule coupled). The T4 and the T3 are then stored in the colloid of the thyroid follicle as part of the thyroglobulin protein, and they are released into the blood by the proteolysis of the thyroglobulin (in response to the TSH stimulation) — the T4 is the predominant hormone that is secreted by the thyroid (approximately 80mcg/day), and it is converted to the more metabolically active T3 (by the type 1 and type 2 deiodinase enzymes) in the peripheral tissues, particularly in the liver, the kidneys, and the brain.
The clinical importance of the iodine for the thyroid hormone synthesis is underscored by the observation that the iodine deficiency is the most common cause of the preventable intellectual disability worldwide. The iodisation of the salt (which was introduced in the 1920s and which has been implemented in most countries) has dramatically reduced the prevalence of the iodine deficiency and of the cretinism — making the iodised salt one of the most successful public health interventions in history. The universal salt iodisation (USI) programme, which is endorsed by the WHO and UNICEF, aims to ensure that all edible salt is iodised, and it has been implemented in over 120 countries — but it is estimated that approximately 2 billion people worldwide still have inadequate iodine intake, and the iodine deficiency remains one of the most important public health problems in the developing world.
Practical Application
For general iodine supplementation for the thyroid health, the evidence-based approach is to supplement with 150-300mcg of iodine daily (as potassium iodide or as kelp extract — the forms that are well absorbed and well utilised by the thyroid). The RDA of iodine is 150mcg daily for adults, 220mcg daily for pregnant women, and 290mcg daily for lactating women — and the tolerable upper intake level is 1100mcg daily for adults (above which the iodine can cause the iodine-induced hyperthyroidism and the autoimmune thyroiditis in susceptible individuals). The iodine is found in high concentrations in the seaweed (kelp, wakame, nori), in the iodised salt, in the seafood (particularly the shellfish and the saltwater fish), and in the dairy products. For comprehensive thyroid support, iodine pairs well with the selenium (which is required for the deiodinase enzymes that convert the T4 to the T3 and which also protects the thyroid from the oxidative damage — approximately 50% of the people with the thyroid disease are selenium deficient), with the zinc (which is required for the TSH receptor function and for the thyroid hormone action in the peripheral tissues), with the iron (which is required for the thyroid peroxidase activity and for the production of the hydrogen peroxide in the thyroid), and with the vitamin D (which has immunomodulatory effects and which is increasingly recognised as an important determinant of the autoimmune thyroid disease risk).
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