Department of Zoology, Faculty of Science, Beni-Suef University, Beni-Suef, Egypt
Received date: November 19, 2015; Accepted date: January 04, 2016; Published date: January 18, 2016
Citation: Ahmed RG (2016) Maternal Iodine Deficiency and Brain Disorders. Endocrinol Metab Syndr 5:223. doi:10.4172/2161-1017.1000223
Copyright: © 2016 Ahmed RG. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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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.