Iodine as Essential Nutrient during the First 1000 Days of Life

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).

Keywords: behavioural disorders; deficiency; foetal programming; iodine; neurodevelopment.

Figure 1

Foetal and neonatal effects of iodine deficiency during pregnancy. The main advance has been that maternal hormone transfer to the foetus during pregnancy is definitely accepted, as well as the existence of damage in the progeny even in the absence of maternal hypothyroidism.

Figure 2

The neuronal migration process is affected by moderately low thyroid hormone levels in early foetal life. The figure shows a disorganized cortical plate where both the radial (blue arrow) and tangential (red arrow) migratory pathways are distorted by maternal hypothyroxinemia (courtesy of Berbel P).