Abstract
Iodine is an essential micronutrient incorporated into thyroid hormones. Although iodine deficiency can lead to a broad spectrum of disorders throughout life, it is most critical in the early stages of development, as the foetal brain is extremely dependent on iodine supply. During the last two decades, our understanding of thyroid physiology during gestation has substantially improved. Furthermore, thyroid hormone receptors have been identified and characterised in placental and embryonic tissues, allowing us to elucidate the maternal-foetal transfer of thyroid hormones. Experimental studies have demonstrated that the cyto-architecture of the cerebral cortex can be irreversibly disturbed in iodine deficiency causing abnormal neuron migratory patterns which are associated with cognitive impairment in children. In this context, the role of iodine as key factor in the programming of foetal and infant neurodevelopment, needs to be revisited with a special focus on areas of mild to moderate iodine deficiency. The objective of this review is to summarize the available evidence from both animals and human studies, for the effect of iodine deficiency (particularly, of maternal hypothyroxinemia) on brain development and neurological or behavioural disorders, such as lower intelligence quotient (IQ) or attention deficit hyperactivity disorder (ADHD).
Highlights
Thyroid hormones intervene directly or indirectly in many metabolic and developmental processes such as thermal and metabolic regulation, somatic growth and development and function of the central nervous system (CNS) [1,2]
It was believed that iodine deficiency (ID) was a problem restricted to certain geographic areas and specific individuals and that it resulted in a well-defined clinical spectrum [7]
The aim of this review is to summarize the current knowledge from both animals and human studies on iodine deficiency as a key factor in foetal programming, on brain development and neurological or behavioural disorders, such as lower intelligence quotient (IQ) or attention deficit hyperactivity disorder (ADHD)
Summary
Thyroid hormones intervene directly or indirectly in many metabolic and developmental processes such as thermal and metabolic regulation, somatic growth and development and function of the central nervous system (CNS) [1,2]. Iodine requirements during gestation increase to fulfil both foetal needs and altered maternal thyroid physiology [3]. Iodine is considered to be an essential micronutrient as it is obtained exclusively through diet or iodine supplements, and it cannot be replaced by any other nutrient in human development [4]. This essentiality becomes even more obvious in the early stages of intrauterine life since adequate iodine intake in pregnancy is needed to achieve optimal foetal neurodevelopment [2,5]. The re-emergence of iodine deficiency in some industrialized countries has reawakened concern about the cognitive consequences of this deficiency [8,9]
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