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Iodine Deficiency and the Developing Brain

It is estimated that around 2 billion people worldwide may have an insufficient intake of iodine. Iodine is essential for the synthesis of the thyroid hormones thyroxine (T4) and tri-iodothyronine (T3), and there is increasing evidence for its importance in the early growth and development of many organs, including the brain and central nervous system.

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A deficiency of iodine during pregnancy can lead to conditions such as maternal and foetal goitre, hypothyroidism, intellectual impairment, psychomotor defects and cretinism, a severe and irreversible form of mental retardation characterised by multiple neurological defects such as deaf-mutism, diplegia and squint, as well as dwarfism. On top of this, the risk of miscarriage, still birth and infant mortality is increased. Goitre, hypothyroidism and impaired cognitive function do not just affect infants either – they have also been noted to occur in childhood, adolescence and adulthood when iodine intake is insufficient. 

According to the World Health Organization (WHO), iodine deficiency is the world’s most prevalent, yet easily preventable, cause of brain damage. Although the number of countries in which iodine deficiency is considered a public health problem has halved over the past 10 years, 54 countries are still reported to be iodine deficient, and the reappearance of mild-to-moderate iodine deficiency in some developed countries that were previously considered to have sufficient iodine intake is of increasing concern. 

Different recommendations for iodine intake have been proposed by several different organisations, making it tricky to know precisely how much is the right amount. The WHO and UNICEF, for example, have recommended a daily dose of 150 µg iodine for women of reproductive age, 250 µg for pregnant and lactating women, and 90 µg for children under 2 years. Nordic Nutritional Recommendations published in 2012 suggested 150 µg/day for men and women over 10 years of age, 175 µg/day for pregnant women, 200 µg/day for lactating women, and amounts increasing from 50 to 120 µg/day for infants and children aged 6 months to 9 years. Meanwhile, adequate intake values for iodine recently proposed in EFSA journal were 150 µg/day for adults, 70-130 µg/day for infants aged 7-11 months and children, 200 µg/day for pregnant women and 200 µg/day for lactating women. 

Iodine, thyroid hormones, and the foetus 

During pregnancy, there is an increased need for maternal thyroid hormone production. Before 12-14 weeks of gestation, the foetus is not able to produce its own T3 and T4, and is completely reliant on maternal thyroid hormones that cross the placenta. Several changes to thyroid physiology occur to accommodate this increased demand and, as iodine is vital to the production of thyroid hormones, they rely on a sufficient intake of iodine. Because of this increased need for iodine during pregnancy, women may be at risk of developing mild iodine deficiency if their intake is not increased, even if it was sufficient before the pregnancy began. 

Although the foetus still relies on maternal thyroid hormones after the onset of its own thyroid hormone production, the first few weeks of pregnancy may be the most sensitive to a deficiency. Thyroid hormones play a crucial role in several neurodevelopmental processes, including neurogenesis, cell migration, synaptogenesis and the differentiation of neuronal and glial cells. A deficiency in early pregnancy can disrupt neural proliferation, alter cell migration, and lead to changes in the structure of the brain. 

Evidence suggests that different brain regions are affected according to the stage of pregnancy that the thyroid hormone deficiency occurs. Basal ganglia, for example, are affected by early thyroid deficiency, while late thyroid dysfunction can influence cerebellar and hippocampal development. The consequences of hypothyroxinaemia depend on its timing and severity, and it is thought that neurological cretinism may be a result of severe hypothyroxinaemia in early pregnancy. 

Iodine in the environment 

For people reliant on locally produced foods for their sustenance, where they live can have a major impact on their iodine status as iodine is not distributed evenly over the Earth’s surface. Seawater is a major source of iodine in the geochemical cycle. Seaweeds and phytoplankton release iodine-containing organic gases into the atmosphere, and these migrate inland where they are deposited in precipitation. This deposited iodine may subsequently be re-volatilised and deposited even further inland. 

Thus, coastal regions tend to be more iodine-rich, while levels tend to decrease the further inland you go. But just living by the coast does not guarantee a sufficient iodine status - the availability of iodine from the soil also affects how much can be taken up by plants, the animals that feed on these plants, and the humans using these plants and animals as sources of food. 

Because of this uneven distribution, communities living in inland areas such as central Africa and Asia, and depending on locally produced food, may be more at risk of developing iodine deficiency disorders. Others at risk include those living in areas subject to frequent flooding and in mountainous regions such as the Himalayas, European Alps and Andes, where iodine may be washed away by rainwater and glaciation. 

For others still, the iodine status of their surrounding environment holds less importance. Many people eat foods every day that originate from numerous different places all over the globe. Nonetheless, it is important for these people to consume the right types of food if they are to have an adequate iodine status. Seafood, milk and dairy products, and eggs are all important sources of iodine in many populations, and iodized salt programmes have gone a long way to reduce the prevalence of iodine deficiency in many places. 

Despite this, mild-to-moderate iodine deficiency has been reported in several countries where iodine intake was thought to be sufficient. As even a mild thyroid hormone deficiency during early pregnancy can negatively affect the cognitive development of the offspring, this is a matter of great concern.  

Iodine deficiency in unexpected places 

The UK is one such country that it is not as iodine sufficient as was once thought. Results of a cross-sectional study carried out in Guildford, UK, for example, suggested that the women who took part in the study were iodine deficient by WHO criteria.

Unlike in other countries where iodized salt has had a great impact on the prevalence of iodine deficiency, it may not have had such a great effect on iodine intake in the UK. A study looking at the availability of iodized table salt in the UK showed that its availability was low and that it only contributes a small percentage to the total UK salt intake. In addition, public health campaigns have encouraged reduced salt consumption. 

The consumption of organic milk instead of regular milk could also be decreasing the intake of iodine for some. One study showed that organic milk purchased in the UK was 42.1% lower in iodine than conventional milk. Given that milk is a major source of iodine in UK diets, and that some women actively choose to consume organic foods during pregnancy, this too could have important implications. In trying to make healthy food choices, women may inadvertently be lowering their intake of iodine at a time they need it the most. 

Dairy products are also an important contributor to the iodine status of the population in the USA. Another study found that the iodine status of pregnant women in the USA was borderline sufficient. Similarly to the UK, the population in the USA has traditionally been considered iodine sufficient, but median urinary iodine concentrations have decreased by 50% since the 1970s. The results of this study raised concerns about the iodine status of women who do not consume dairy products, and it was suggested that they might be at risk of iodine deficiency. 

A lack of knowledge about dietary sources of iodine may be contributing to the problem. Another study conducted in New South Wales, Australia, which looked at the knowledge, attitudes and practices of pregnant women regarding the intake of iodine and folic acid, found them to have a limited knowledge of dietary sources of these nutrients. 

Effects on cognitive performance 

While not extreme, the level of iodine deficiency in the UK has nonetheless been associated with adverse effects on the neurological development of the offspring. A further study which examined the maternal iodine status of UK mothers in the first trimester of pregnancy and compared it with the IQ of their offspring at 8 years of age and reading ability at 9 years of age, showed that children of women with an iodine-to-creatinine ratio of less than 150 µg/g, an amount corresponding to iodine deficiency in pregnancy, were more likely to have scores in the lowest quartile for verbal IQ, reading accuracy and reading comprehension than were those of mothers with ratios of 150 µg/g or more. Furthermore, scores were shown to worsen from 150 µg/g or more, to 50-150 µg/g to less than 50 µg/g.

Further evidence also corroborates the link between iodine deficiency and poor cognitive outcome. A review looking at the connection between nutrition and brain development in early life reported that there was a 13.5 IQ point difference between individuals living in iodine-sufficient and iodine-deficient areas, and that 4-7 year old children in an iodine-deficient region of China whose mothers were given iodine during pregnancy performed better on a psychomotor test than those who were supplemented beginning at 2 years of age. 

Another review reported that Chinese infants with a higher level of cord blood TSH had a lower mental developmental index, and that there was an increased risk of neurocognitive developmental delay in the offspring when maternal iodine supplementation was delayed. It was further reported that the children of mothers receiving 300 µg of iodine during pregnancy had a significantly higher psychomotor development index than those not receiving any supplementation. 

One further review on the cognitive and psychomotor development of children in Europe whose mothers suffered from mild iodine deficiency during pregnancy concluded that iodine supplementation from the first trimester until the end of pregnancy may decrease the risk of cognitive and psychomotor development delay in the offspring. 

In contrast, a study looking at the safety and effectiveness of maternal iodine supplementation with regard to child neuropsychological development in Spain found that maternal consumption of 150 µg/g iodine or more from supplements was related to a 1.5-fold increase in the odds of a psychomotor score less than 85 and a 1.7-fold increase in the odds of a mental score less than 85. 

These results did not support a beneficial impact of maternal iodine supplementation on neuropsychological development of infants from iodine-sufficient or mildly iodine-deficient areas, but rather showed an association between iodine supplements with a poorer mental and psychomotor achievement in the study areas. The association was found to be more pronounced in children whose mothers consumed iodized salt, suggesting an excess of iodine intake. 

Despite these results, there is an increasing body of evidence demonstrating the adverse effects of iodine deficiency on the developing infant, even in countries that are only classified as mildly iodine deficient, and it has been suggested that women of childbearing age and pregnant women should be given advice on how to improve their iodine status through dietary means.

(Image Credit: DanEvans at www.pixabay.com)

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