Iodine deficient gestation and

Iodine-Deficient Gestation and Neurodevelopment of 3-Year-Old Children... 

Our aim was to examine the neurodevelopment of a group of 3-year-old children of mothers living in an iodine-deficient area, and to establish the possible existence of a relationship between their performance and maternal iodine nutrition and thyroid function through gestation. 

Goiter was evident from 70 days in the iodine-deficient fetuses and thyroid histology revealed evidence of hyperplasia from 56 days gestation. The increase in thyroid weight was associated with a reduction in fetal thyroid iodine content and greatly reduced plasma T values associated with greatly reduced plasma T levels in the mother (Table 3). 

Universal thyroxine supplementation in extreme preterm infants does not improve neurodevelopmental outcome (van Wassenaer et al., 1997a). However, subgroup analysis of the developmental scores of infants <27 weeks gestation in the thyroxine group, compared to placebo, were increased by 18 points, but decreased by 10 points in infants of 27—29 weeks. Thyroxine supplementation may be detrimental in some infants and there are no indications, apart from gestation, why this should be so. With this uncertainty, we believe that the correction of iodine deficiency is the first and safest approach to the correction of hypothyroxinemia. 

Recently, a WHO technical consultation group met to review the maternal iodine requirements during gestation (Benoist et al, 2007). Consideration was given to the fact that the amount recommended should be sufficient to prevent brain damage or thyroid function disorders due to iodine deficiency during pregnancy. There is a lack of data to indicate an optimal intake. Therefore, conclusions were reached after evaluation of the efficiency of gut absorption of iodine, the estimated metabolic needs, and the typical daily losses in the feces and urine. 

Iodine Deficiency in Preterm Babies Born at iess than 30 Weeks of Gestation and Aiterations in their Neurodeveiopment... 

The risk of abnormal development is further aggravated because mother and offspring are exposed to iodine deficiency during gestation and the postnatal period. 

Further studies in sheep of the effect of correction of iodine deficiency by iodized oil injection at 100 days gestation (end of second trimester) revealed only partial correction of the effect on brain strucmre by the end of gestation (Potter et al.y 1984). This requires follow-up with observations of behavior and neurological stams into the postnatal period. Such studies could also be carried out in marmosets (primate model) with greater relevance to humans. However, the finding in sheep is consistent with observations in humans that the injection of iodized oil in the latter half of pregnancy may not prevent cretinism in the infant (Pharoah et al., 1971). Similar observations have been made by Cao et al. (1994) in China. 

Cretinism is a condition of severe physical and mental retardation due to iodine deficiency, and specifically due to deficiency of thyroid hormones during early pregnancy. This condition is irreversible, even after treatment with thyroid hormones or iodine soon after birth, but can be corrected if treatment with iodine starts prior to or early in gestation. 

Iodine deficiency has been recognized as the most frequent cause, after starvation, of preventable mental defects, affecting hundreds of million people to different degrees. The eradication of iodine deficiency has been approved in resolutions or declarations from most of the international conferences and organisms (United Nations, UNICEF, WHO, FAO, ICCIDD). Adequate iodine nutrition is important for the prevention of brain damage that could be irreversible by birth, and is only preventable when administered very early in gestation. 

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