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Licensed Unlicensed Requires Authentication Published by De Gruyter May 7, 2015

An explanation of the pathophysiology of adverse neurodevelopmental outcomes in iron deficiency

  • Ioannis Bakoyiannis EMAIL logo , Eleana Gkioka , Afrodite Daskalopoulou , Laskarina-Maria Korou , Despina Perrea and Vasilios Pergialiotis

Abstract

Iron deficiency (ID) is a major public health problem worldwide among children aged 0–12 months. Several factors seem to contribute to the iron-deficient state in infancy, including insufficient antenatal and neonatal iron supplementation, exclusive breastfeeding, and early umbilical cord clamping after birth. The most concerning complications of ID, except for anemia, are related to altered long-term neurodevelopment. Clinical studies have shown a negative impact of ID anemia on fetal and neonatal behavior including impairments of motor maturity, autonomic response, memory/learning, and mood. ID-induced defects during infancy seem to persist later in life, even after ID treatment. The underlying mechanisms involve dysfunctional myelination, neurotransmission alterations, and altered synaptogenesis and/or dendritogenesis. The purpose of the present review is to summarize these mechanisms and to provide recommendations for future clinical research in the field.


Corresponding author: Ioannis Bakoyiannis, Laboratory of Experimental Surgery and Surgical Research N.S. Christeas, Athens University Medical School, 15 Kandanou Street, GR-11526 Ampelokipoi, Greece, e-mail:

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Received: 2015-3-10
Accepted: 2015-4-1
Published Online: 2015-5-7
Published in Print: 2015-8-1

©2015 by De Gruyter

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