Maternal Iodine Deficiency and Brain Disorders

Ahmed RG
  • Endocrinology & Metabolic Syndrome, January 2016, OMICS Publishing Group
  • DOI: 10.4172/2161-1017.1000223

Iodine and Brain Disorders

What is it about?

Thyroid Hormones (THs) play an essential role in development and hormone deficiency during critical phases in fetal life may lead to severe and permanent brain damage. Maternal iodine deficiency is considered the most common cause of fetal TH deficiency, but the problem may also arise in the fetus/neonates. Due to defects in fetal thyroid gland development or hormone synthesis, clinical symptoms at birth are often mild as a result of compensatory maternal TH supply. A shortage of THs starting at the early stages of pregnancy results in neurological deficits that cannot be rescued by exogenous TH addition at later stages. Neonates are more sensitive than adults to the effects of iodine deficiency. Thus, these disturbances may lead to abnormalities in the neuronal network and may result in mental retardation and other neurological defects, including impaired motor skills and visual processing. Thus, iodine defenses programmes can avoid adverse neurodevelopmental consequences in mothers and their offspring.

Why is it important?

Defects in synaptic architecture induced by TH insufficiencies, as well as deficiencies in protein substrates involved in complex signaling pathways serious for synaptic plasticity, culminate to disturb hippocampal neurophysiological function. An irregular laminar distribution has been described in the auditory cortex of hypothyroid rats, including an increased number of neurons in layers V/VI, a concomitant diminution in layers II to IV, and the abnormal presence of neurons in the subcortical white matter. Finally, a reduction, or absence, of TH during brain maturation yields molecular, morphological and functional alterations in hippocampus. Interestingly, the neurodevelopmental impairments induced by hypothyroxinemia suggest an independent role of T4.


Ahmed R. G. (Author)
Division of Anatomy and Embryology, Zoology department, Faculty of Science, Beni-Suef University, Egypt.

Whatever the mechanisms, the reported data require a reevaluation of which disturbance could result in irreversible and permanent damage to the developing thyroid-brain axis. The resolution of this review will require additional evidence at a molecular level either demonstrating a direct action of the THs on the fetal brain or additional evidence supporting the suggestion that the observed effects of maternal iodine deficiency on fetal development are explained by impaired gestation. Thus, the adverse effects of maternal hypothyroidism on fetal development are mediated directly by loss of the maternal hormones contribution to the fetus, indirectly by metabolic impairment of gestation, or both. In addition, future attention should be focused on identifying a non-genomic approach because of there is scant evidence and these actions of TH differ across the developmental time and brain region.

The following have contributed to this page: Ahmed R. G.