Two thirds of the body’s iodine is in the thyroid gland. It plays a major role in thyroid health, thus controlling metabolism. The thyroid is involved in reproduction, nerve and muscle function, breakdown of proteins and fats, hair and nail growth, and oxygen use by the cells. Iodine deficiency is most common in people living in underdeveloped countries.
Iodine is an essential trace element for thyroid hormones synthesis. An inadequate iodine diet affects thyroid function. It is well known that iodine deficiency (ID) often occurs in remote inland areas, promoting the appearance of impairments that affect all age groups from foetus until adult age. ID is one of the principal causes of impaired cognitive development in children. Cretinism is the most severe form of cognitive impairment, which can be observed due to ID during pregnancy and is irreversible. Some other undesirable facets of ID in pregnancy include prenatal mortality, low birth weight, and low intellectual quotient. Since 1990, the World Health Organization (WHO) has coordinated an international program for the prevention of ID in a special resolution. In 1993, WHO, UNICEF and International Council for the Control of iodine deficiency (ICCIDD) adopted iodized salt as the main strategy for the control of ID. About 1.92 billion people suffer from ID throughout the world.
Iodine metabolism is closely related to thyroid hormone synthesis. A certain amount of inorganic iodide is actively cleared from blood plasma by the thyroid gland and stored in the lumen of follicular cells as iodine compound. An active co-transporter exists into the thyroid gland cells known as NIS (sodium iodide symporter). NIS is expressed in many other tissues, including salivary gland, mammary gland, and gastric mucosa (1). TSH (thyroid stimulating hormone) is the principal regulator of NIS expression (2).
Thyroid hormone synthesis begins with the oxidation of iodide and its incorporation into iodotyrosines such as mono-iodotyrosine and di-iodotyrosine. These precursors of thyroid hormones are incorporated into thyroglobulin considered as a pool of thyroid hormone: thyroxin (T4) and 3,5,3-tri-iodothyronine(T3).
Today, iodine intake is moderately deficient in nine countries, mildly deficient in 21 countries and 112 countries are classified as having adequate iodine intake (3). Excess of iodine intake occurs in ten countries but authors underlined the fact that hyperthyroidism risks are still less important if they are compared to the benefits of ID elimination (4).
Iodine deficiency and the resulting low levels of thyroid hormone can cause women to stop ovulating, leading to infertility. Excessive maternal iodine intake can have adverse consequences for the mother and foetus. Deficiency of iodine happens more often in women than in men, and is more common in pregnant women and older children. Iodine deficiency caused several pathologies, such as endemic goitre, devastating neurocognitive impairments and mental health illnesses (5); foetal and prenatal mortalities also occur.
Human chorionic gonadotrophin (HCG) concentrations increase respectively in foetal and maternal compartments to ensure a reliable free thyroxin (FT4) level. Through the first and second trimesters of pregnancy, there is a much lower concentration of FT4 in the foetal circulation than in the mother’s, making her the principal source of thyroid hormones. During the third semester, thyroid hormone supply to the foetus is mainly from the foetal gland (6). Maternal thyroid hormone synthesis is under the control of HCG stimulation.
Brain cell organization appears from the 6th month of gestation and hence the damage mainly affects the proliferation of neurons.
Sources of Iodine
Compared to terrestrial plants which contain only trace amounts of iodine (0.001 mg g−1), marine plants have high iodine concentrations of 0.5–0.8 mg/ g. There is a wide amount of variation in the iodine content of some common foods, which is not well reflected by package labelling. The manufacture of bread with iodized salt and the supplemental iodine for pregnant women are predicted to be effective interventions to lift iodine intakes in New Zealand.
The oceans are the worldwide repository of iodine; very little of the earth’s iodine is actually found in soil. Iodized table salt with iodine added is the main food source of iodine. Kelp is the most common vegetable seafood that is a rich iodine source. While fish has the highest natural iodine concentration and as such is an excellent source, milk and dairy products are the main determinants of iodine intake in the Norwegian population. Iodization of cow fodder in Norway provides an efficient alternative to universal salt iodization. Some of the better sources of iodine are dried seaweed, cod, iodized salt, baked potato with peel, dairy products, shrimp, navy beans, baked turkey breast and boiled egg. Sea salt is not iodized and is not a good source.
Iodine in health and disease
In endemic zones, subjects suffer from hypothyroidism, which is manifested by a decrease of FT4, a TSH increase and FT3 levels which are still within the normal ranges (7). TSH is both the main growth and differentiation factor for thyrocytes. It stimulates their multiplication and it is the leading cause of goitre formation. TSH act via thyrocytes receptor sites, localized mainly in the basal membranes of follicle cells. Other growth regulators are involved including epidermal growth factor, insulin, and insulin-like growth factor 1 (8). In general, enlargement of the thyroid gland begins as an adaptive process to low iodine intake. Goitre represents both the tip of the iceberg (9) and damage from iodine deficiency.
Many other substances can also affect iodine balance and thyroid metabolism termed as goitrogens (10). These goitrogenic substances interfere with the biosynthesis of thyroid hormones. About 100 natural and synthetic substances have been characterized as thyroidal disruptors (9). Goitrogens substances promote goitre formations, especially when iodine intake is low and if they have been consumed for a long duration. Some anions, such as perchlorate, thiocyanate, bromated nitrates and cholate impair the rate of iodine trapping by NIS. Perchlorate has the greatest potential decrease thyroid gland iodine uptake and has been found in foods, such as cow’s milk or beer (9,11). Thiocyanate also exists in foods, like cassava, broccoli, Brussels sprouts and high plasmatic concentrations have been associated with smoking cigarettes (12). Some pollutants, like dioxins, polychlorinated biphenyls, polybrominated diphenylethers and bisphenol-A may impair thyroid activity. Micronutrient deficiency, such as selenium and vitamin A may result in cases of goitre (13,14). Selenium is a cofactor of deiodinase I, so deficiency of this element may decrease kinetic conversion from T4 to T3. Furthermore, vitamin A supplementation in moderate ID is beneficial to reduce goitre rate by modulating TSH-gene activity (15).
Iodine deficiency has been shown in UK schoolgirls (3) and in pregnant women in the past decade; (6–8) and one recent study showed the extent to which UK iodine deficiency is associated with adverse childhood outcomes (16). Although these results are from a study started 21 years ago, they are applicable to the present UK situation because the level of iodine deficiency recorded is similar to that in a recent study of UK pregnant women. It concludes that maternal iodine deficiency in pregnancy might have been overlooked as a preventable cause of developmental delay in UK children since poorer cognitive development can set children on a trajectory for poorer school attainment, examination grades, and employment opportunities. At the population level, even a slightly lower than average IQ affects economic success and productivity: a one-point increase in a nation’s average IQ has been associated with a persistent annual increase in gross domestic product per person.
In the early 1990s, pregnant women and the health professionals advising them would have been unaware of the need for additional iodine beyond the 140 μg per day recommended for adults, with no separate recommendation for pregnancy. Unsurprisingly therefore, these women, from a region that was part of the old UK goitre belt are deficient by WHO criteria that recommend an iodine intake of 250 μg per day in pregnancy. The scarcity of dietary guidance and the fact that the UK has not adopted a national salt-iodisation programme means that iodine intake is left entirely to chance through individual food choices.
New data indicate iodine increases concentrations of insulin-like growth factor 1 and insulin-like growth factor-binding protein 3, and improves somatic growth (17).
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Keywords:-iodine, thyroid, cognitive health, diabetes