Abstract

Iodine is a trace element essential for the synthesis of triodothyronine (T3) and thyroxine (T4). Inadequate intake of iodine leads to insufficient production of these hormones, which play a vital role in the process of early growth and development of most organs, especially the brain. The neurological sequele of iodine deficiency are mediated by thyroid hormone deficiency, varying from minimal brain function to a syndrome of severe intellectual disability. All the basic processes of neurogenesis: cellular proliferation, differentiation, migration, and selective cell death are impaired during period of brain growth spurt. Evidence suggests alterations in synaptology, neurons, myelin sheaths, glial cells, and morphology of cerebrum and cerebellum in severe iodine deficiency. Foetal thyroid ontogenesis occurs after the first trimester. Until then foetus is dependent on maternal T4. A thyroid dependent event important for subsequent brain development occurs in the beginning of the third trimester of pregnancy.

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