Iodine is a halogen element that is an essential component of the thyroid hormones — thyroxine (T4, which contains four iodine atoms) and triiodothyronine (T3, which contains three iodine atoms). The thyroid hormones are the primary regulators of the basal metabolic rate in the human body — they increase the oxygen consumption of all metabolically active tissues, they stimulate the protein synthesis, they regulate the lipid metabolism, they promote the carbohydrate absorption, and they are essential for the normal development of the brain and of the nervous system in the foetus and in the young child. The iodine deficiency is one of the most common nutritional deficiencies in the world — it affects approximately 2 billion people globally, and it is the leading cause of the preventable mental retardation and of the goitre (the enlargement of the thyroid gland that is the visible hallmark of the iodine deficiency). The primary dietary sources of iodine are the iodised salt, the seafood (particularly the fish and the shellfish), the seaweed (particularly the kelp, the nori, and the kombu), and the dairy products (particularly the milk and the yoghurt, which are sources of iodine in countries where the iodine-containing fertilisers are used on the pastures). The global public health intervention of the iodised salt programme (which was launched in the 1990s and which has been implemented in most countries of the world) has dramatically reduced the incidence of the iodine deficiency disorders (IDD), and it is considered one of the most cost-effective public health interventions in the world.
Thyroid Hormone Synthesis and the Iodine Metabolism
The thyroid gland synthesises the thyroid hormones from the iodine and from the tyrosine residues of the thyroglobulin protein — the T4 is synthesised first (with the incorporation of the two iodine atoms onto each tyrosine ring) and is then partially deiodinated to T3 (by the type 1 and type 2 deiodinase enzymes) in the thyroid gland and in the peripheral tissues. The process of the thyroid hormone synthesis is called the organification of the iodine — the iodide ions (I-) are taken up from the blood by the sodium-iodide symporter (NIS) on the basolateral membrane of the thyroid follicular cell, they are transported to the apical membrane, they are oxidised to iodine (I2) by the thyroid peroxidase enzyme (TPO) in the presence of the hydrogen peroxide, and the iodine is then covalently attached to the tyrosine residues of the thyroglobulin protein at the colloid interface. This organification of the iodine is the essential step in the thyroid hormone synthesis, and it is the step that is blocked by the thionamide drugs (propylthiouracil, methimazole, carbimazole) that are used in the treatment of the hyperthyroidism — by inhibiting the TPO enzyme, these drugs prevent the organification of the iodine and thereby reduce the synthesis of the thyroid hormones.
The clinical importance of the iodine for the thyroid hormone synthesis is underscored by the observation that the iodine deficiency produces the goitre (the enlargement of the thyroid gland that is the compensatory response to the reduced iodine availability) and the hypothyroidism (the reduced synthesis and secretion of the thyroid hormones, with the low T4 and the high TSH that is the hallmark of the underactive thyroid). The goitre is the visible manifestation of the iodine deficiency — the thyroid gland enlarges in an attempt to capture more iodine from the blood, and this enlargement produces the characteristic swelling in the neck that is the hallmark of the iodine deficiency. The hypothyroidism that accompanies the iodine deficiency produces the classic symptoms of the underactive thyroid — the fatigue, the weight gain, the cold intolerance, the constipation, the dry skin, the hair loss, the bradycardia, and the depression — and in the severe cases, it produces the myxoedema coma (the life-threatening exacerbation of the hypothyroidism that is characterised by the extreme hypothermia, the bradycardia, the hypotension, and the coma).
Iodine Deficiency Disorders and the Prevention of the Cretinism
The most devastating consequence of the iodine deficiency is the cretinism — the severe developmental disorder that affects the children who are born to iodine-deficient mothers and that is characterised by the irreversible mental retardation, the deaf mutism, the spasticity, the growth failure, and the sexual infantilism. The cretinism is the extreme end of the spectrum of the iodine deficiency disorders (IDD), which also include the milder forms of the neurodevelopmental impairment (including the reduced IQ, the impaired cognitive function, and the decreased school performance) that affect the children who are mildly to moderately iodine deficient during the foetal development and the early childhood. The prevention of the cretinism and of the other IDD is one of the most important public health priorities in the iodine-deficient regions of the world, and it is achieved primarily through the iodised salt programme — the addition of the potassium iodate to the table salt, which ensures that the entire population of a country has access to the iodine that is required for the normal thyroid hormone synthesis and for the normal brain development.
Practical Application
For general iodine supplementation, the evidence-based approach is to ensure an intake of 150mcg of iodine daily for adults (as the RDA of 150mcg daily for both men and women), primarily through the use of the iodised salt in cooking and at the table. The iodised salt contains approximately 45mcg of iodine per gram of salt, and the typical intake of salt of 5-10g daily provides approximately 225-450mcg of iodine — which is slightly above the RDA but well within the safe range (the tolerable upper intake level is 1,100mcg daily for adults). For people who do not use the iodised salt (because they have high blood pressure and are limiting their salt intake, or because they live in a region where the iodised salt is not available), the iodine supplementation at 150mcg daily (as the potassium iodide or as the kelp extract) is recommended, particularly for the women of childbearing age, for the pregnant women, and for the breastfeeding women, who have the highest iodine requirements. For comprehensive thyroid and metabolic support, iodine pairs well with the selenium (which is required for the deiodinase enzymes that convert T4 to T3), with the zinc (which is required for the thyroid hormone receptor function), with the iron (whose deficiency impairs the thyroid hormone synthesis), and with the tyrosine (which is the amino acid precursor of the thyroid hormones).
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