Abstract
Iodine is a necessary micronutrient for the production of thyroid hormones and normal human development. Despite the significant worldwide strategies for the prevention and control of iodine deficiency, it is still a prevalent public health issue, especially in pregnant women. Severe iodine deficiency during pregnancy and neonatal period is associated with many major and irreversible adverse effects, including an increased risk of pregnancy loss and infant mortality, neonatal hypothyroidism, cretinism, and neuropsychomotor retardation. We will review the impact of severe iodine deficiency on maternofetal, neonatal, and offspring outcomes. We will also discuss its epidemiology, classification of iodine deficiency severity, and current recommendations to prevent iodine deficiency in childbearing age and pregnant women.
Highlights
Dietary iodine is an essential micronutrient for thyroid hormone synthesis, and adequate thyroid hormone production is required for normal human development [1]
Iodine deficiency can affect fetal programming through imprinting of central nervous system cells and exert postnatal effects [4]. These adverse effects are driven through the role of thyroid hormones [thyroxine (T4) and tri-iodothyronine (T3)] in neurological development, as they are required for normal neuronal migration, myelination, and synaptic transmission and plasticity during fetal and early post-natal life [5, 6]
We provide an overview of the epidemiology of Severe iodine deficiency (SID) during pregnancy and its consequences on maternofetal, neonatal, and offspring outcomes
Summary
Dietary iodine is an essential micronutrient for thyroid hormone synthesis, and adequate thyroid hormone production is required for normal human development [1]. Sustained deficiency in iodine intake results in a reduction of thyroid hormone production and action, and significant adverse health effects, especially in pregnant women and their offspring [2]. Iodine deficiency can affect fetal programming through imprinting of central nervous system cells and exert postnatal effects [4]. These adverse effects are driven through the role of thyroid hormones [thyroxine (T4) and tri-iodothyronine (T3)] in neurological development, as they are required for normal neuronal migration, myelination, and synaptic transmission and plasticity during fetal and early post-natal life [5, 6]. We provide an overview of the epidemiology of SID during pregnancy and its consequences on maternofetal, neonatal, and offspring outcomes
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