Iodine deficiency fetal

Potter BJ, Mano MT, Balling GB, Rogers PS, Martin DM and Hetzel BS (1981) Reversal of brain retardation in iodine-deficient fetal sheep. In Howell I, McC, Gawthome JM, White CL, eds. Trace Element Metabolism in Man and Animals, pp. 313-315. Springer Verlag Berlin, Heidelberg, New York. 

Hetzel, B. S., and Mano, M, T. 1989). A review of experimental studies of iodine deficiency during fetal development. J. Nutr. 119,145-151. 

United Nations to alleviate iodine deficiency. Iodine is required for the thyroid hormones, thyroxine and triiodothyronine, that regulate the metabohc rate and O2 consumption of cells. Iodine is also intimately involved in the control of growth and development, particularly during fetal and infant life. 

A second example of an application of the controlled-release technology developed by Rhone-Poulenc is the Rhodifuse lode system (ref. 6). This system is commercialized by Rhone-Poulenc RORER for the treatment of iodine deficiency. Lack of iodine in the diet can cause serious disorders such as goiter and cretinism in adults, growth disorders in children, and fetal death in pregnant women. This... 

Various maternal metabolic dysfunctions can cause fetal cerebral palsy. An example is maternal iodine deficiency and resulting hypothyroxinemia (abnormally low concentration of blood thyroxine). 

The pituitary and brain, as well as brown adipose tissue, contain DI2 and DI3, which catalyze 5 - and 5-deiodination, respectively. Selenium deficiency alone has no effect on thyroid weight in rats, whereas iodine deficiency results in a 60% increase, and concurrent iodine and selenium deficiency results in a thyroid weight 148% above that of control animals. The principal physiological role of DI2 is the local intracellular production of T3. The role of DI3 has been proposed to protect fetal tissue from high levels of T3 and T4 during development by converting them to r T3 and r T4, respectively (Sunde 1997) (r = reverse). 

When iodine requirements are not met, TH synthesis is reduced, resulting in enlargement of the thyroid gland to compensate for this reduction. In adults, mild iodine deficiency (ID) is associated with nontoxic nodular goiter and, less often, with toxic nodular goiter, due to increases in the constitutive (thyrotropin-independent) growth and functional potential of some clones of thyroid cells. In pregnancy, this can result in fetal neurodevelopmental deficits and mental retardation. 

A. Brain damage caused by maternal/fetal/neonatal iodine deficiency A. Brain damage caused by maternal hypothyroidism ... 

The realization that iodine deficiency in pregnancy has a pronounced effect on fetal, neonatal and childhood brain function has resulted in a large body of knowledge on the effects of thyroid hormone on brain and nervous-system development (see Grave, 1977 DeLong et ai, 1989 Stanbury, 1994 Bemal, 2002). 

Pregnant and lactating women and neonates are the main targets of the effects of iodine deficiency, because of the impact of maternal, fetal and neonatal hypothyroxinemia on... 

Table 52.3 Special features of iodine deficiency related to fetal and immediate postnatal growth...

The demonstration of the prevention of cretinism with iodized oil in a double-blind controlled trial in Papua New Guinea established the causal role of iodine deficiency in cretinism by an effect on the developing fetal brain (Pharoah et al, 1971). Cretinism could not be prevented unless the iodized oil was given before pregnancy, as injection during pregnancy was ineffective (Table 62.2). 

Early correction of hypothyroidism due to congenital defects in neonates has now become a standard practice in most developed countries in order to prevent longterm brain damage (Dussault and Glorieux, 1989). The more severe the fetal hypothyroidism, as indicated by bone retardation, the more Hkely are residual effects (Dussault and Glorieux, 1989). Such considerations indicate the urgent need for a preventive approach to the correction of iodine deficiency for developing countries, because treatment of individual cases is not usually possible. 

Three mechanisms have been suggested for the effect of iodine deficiency on fetal brain development. 

It was concluded that both maternal and fetal thyroid hormones were involved in the effect of iodine deficiency... 

Other studies in the iodine-deficient rat confirm low fetal brain T3 levels despite a five-fold to ten-fold increase... 

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