Iodine deficiency in infancy - a risk for cognitive development.
Summary of "Iodine deficiency in infancy - a risk for cognitive development."
Severe iodine deficiency during pregnancy seriously influences fetal brain development and in the worst case induces cretinism. Recent studies have shown that even a mild iodine deficiency during pregnancy and during the first years of life adversely affects brain development. The World Health Organisation (WHO) considers iodine deficiency as the most common preventable cause of early childhood mental deficiency. In this context, the insufficient production of the four iodine atoms containing thyroxine seems to play a causal role, i. e., due to the iodine substrate deficiency the neuronally particularly relevant free-thyroxine level falls. Due to the very limited iodine storage capacity, the infantile thyroid is eminently dependent on an adequate and steady iodine supply. In the first month of life, when milk is the only energy- and nutrient provider, infants fed a commercial formula regularly have a sufficient iodine supply. However, breastfed infants, who depend on maternal iodine status, frequently show an inadequate iodine intake. Furthermore, iodine intake is critical when complementary food (CF) is introduced. Especially homemade CF is poor in iodine, but also commercial CFs are only partly fortified. A simultaneous inadequate iodine supply of the breastfeeding mother and the preferential use of mostly iodine-poor organic milk cannot ensure an adequate iodine supply of the infant. In terms of an improvement of nutrient supply, especially concerning an unhindered brain development, the corresponding German reference value for iodine intake of infants until age 4 month should be raised from currently 40 microg/d to at least 60 microg/d (WHO-reference: 90 microg/d).
Forschungsinstitut für Kinderernährung, Dortmund.
This article was published in the following journal.
Name: Deutsche medizinische Wochenschrift (1946)
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/20665419
- DOI: http://dx.doi.org/10.1055/s-0030-1262446
Medical and Biotech [MESH] Definitions
A condition in infancy or early childhood due to an in-utero deficiency of THYROID HORMONES that can be caused by genetic or environmental factors, such as thyroid dysgenesis or HYPOTHYROIDISM in infants of mothers treated with THIOURACIL during pregnancy. Endemic cretinism is the result of iodine deficiency. Clinical symptoms include severe MENTAL RETARDATION, impaired skeletal development, short stature, and MYXEDEMA.
A form of IODINE deficiency disorders characterized by an enlargement of the THYROID GLAND in a significantly large fraction of a POPULATION GROUP. Endemic goiter is common in mountainous and iodine-deficient areas of the world where the DIET contains insufficient amount of iodine.
Stable iodine atoms that have the same atomic number as the element iodine, but differ in atomic weight. I-127 is the only naturally occurring stable iodine isotope.
Congenital or postnatal overgrowth syndrome most often in height and occipitofrontal circumference with variable delayed motor and cognitive development. Other associated features include advanced bone age, seizures, NEONATAL JAUNDICE; HYPOTONIA; and SCOLIOSIS. It is also associated with increased risk of developing neoplasms in adulthood. Mutations in the NSD1 protein and its HAPLOINSUFFICIENCY are associated with the syndrome.
Unstable isotopes of iodine that decay or disintegrate emitting radiation. I atoms with atomic weights 117-139, except I 127, are radioactive iodine isotopes.
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