Iodine Deficiency In Pregnancy Research Articles

Iodine deficiency in pregnancy, infancy and childhood and its consequences for brain development

Iodine deficiency during foetal development and early childhood is associated with cognitive impairment. Randomised clinical studies in school-aged children encountered in the literature indicate that cognitive performance can be improved by iodine supplementation, but most studies suffer from methodological constraints. Tests to assess cognitive performance in the domains that are potentially affected by iodine deficiency need to be refined. Maternal iodine supplementation in areas of mild-to-moderate iodine deficiency may improve cognitive performance of the offspring, but randomised controlled studies with long-term outcomes are lacking. Studies in infants or young children have not been conducted. The best indicators for iodine deficiency in children are thyroid-stimulating hormone (TSH) in newborns and thyroglobulin (Tg) in older children. Urinary iodine may also be useful but only at the population level. Adequate salt iodisation will cover the requirements of infants and children as well as pregnant women. However, close monitoring remains essential.

Iodine deficiency in pregnancy and the effects of maternal iodine supplementation on the offspring: a review

The World Health Organization (WHO) recently increased their recommended iodine intake during pregnancy from 200 to 250 μg/d and suggested that a median urinary iodine (UI) concentration of 150–249 μg/L indicates adequate iodine intake in pregnant women. Thyrotropin concentrations in blood collected from newborns 3–4 d after birth may be a sensitive indicator of even mild iodine deficiency during late pregnancy; a < 3% frequency of thyrotropin values > 5 mU/L indicates iodine sufficiency. New reference data and a simple collection system may facilitate use of the median UI concentration as an indicator of iodine status in newborns. In areas of severe iodine deficiency, maternal and fetal hypothyroxinemia can cause cretinism and adversely affect cognitive development in children; to prevent fetal damage, iodine should be given before or early in pregnancy. Whether mild-to-moderate maternal iodine deficiency produces more subtle changes in cognitive function in offspring is unclear; no controlled intervention studies have measured long-term clinical outcomes. Cross-sectional studies have, with few exceptions, reported impaired intellectual function and motor skills in children from iodine-deficient areas, but many of these studies were likely confounded by other factors that affect child development. In countries or regions where < 90% of households are using iodized salt and the median UI concentration in school-age children is < 100 μg/L, the WHO recommends iodine supplementation in pregnancy and infancy.

S29-02 Thyroid hormones and the psychomotor development of the newborn

Iodine is a trace element which is essential for the synthesis of thyroid hormones. If maternal iodine deficiency in pregnancy is severe, fetal brain damage will occur. This damage is irreversible after birth. Mild/moderate iodine deficiency during pregnancy and early postnatal life is associated with neuro/psycho-intellectual deficits in infants and children. The severity is not only related to the degree of iodine deficiency, but also to the developmental phase during which it is suffered, the most severe being the consequence of iodine deficiency during the first two trimesters of pregnancy. The close involvement between human brain development and thyroid hormones is widely accepted. The effects of T3 on the central nervous system are mediated by the regulation of the expression of genes that synthesize proteins implicated in cerebral neurogenesis, neuronal migration and differentiation, axonal outgrowth, dendritic ontogeny, and synaptogenesis. They are also necessary for cerebellar neurogenesis (predominantly during early postnatal life), gliogenesis (predominantly during late fetal life to 6 months postnatally), and myelogenesis (during the second trimester of gestation to 2 years of postnatal life). From clinical studies on the effect of iodine deficiency of both mother and fetus it becomes clear that T4 is required for brain development during gestation.Low T4 levels during neonatal life could be a negative factor contributing to the neurodevelopmental problems of very preterm infants. Indeed, retrospective studies have shown a relationship between hypothyroxinemia and developmental delay and an increased risk of disabling cerebral palsy.

A case for universal salt iodisation to correct iodine deficiency in pregnancy: another salutary lesson from Tasmania

To assess the impact of iodine fortification of bread on the iodine status of pregnant women, and to determine if studies of iodine levels in school-age children were indicative of women's gestational iodine status. Urinary iodine surveys of pregnant Tasmanian women before and after bread was fortified with iodine in October 2001. 285 women attending the Royal Hobart Hospital (RHH) antenatal clinic from 1 October 2000 to 30 September 2001 and 517 women attending the RHH antenatal clinic or primary health care centres in 2003-2006. Median urinary iodine concentration (UIC) for comparison against the World Health Organization recommendation of of 150-249 microg/L for pregnant women. Before supplementation, the median UIC of the 285 women attending the RHH antenatal clinic was 76 microg/L. After supplementation, median UICs were 81 microg/L for 288 women attending primary health care centres and 86 microg/L for 229 women attending the RHH antenatal clinic. Differences in mean UIC were not significant for either the antenatal clinic group (P=0.237) or the primary health care group (P=0.809) compared with the pre-supplementation group. Iodine deficiency in pregnancy persists despite being corrected in Tasmanian children. Successful iodine supplementation must target reproductive-age and pregnant women and be substantiated by ongoing monitoring during pregnancy and lactation. A robust national program for correcting iodine deficiency is urgently needed. Mandatory universal salt iodisation has international endorsement, and should be considered the preferred strategy for eliminating iodine deficiency in Australia.

Assessment of iodine intake in mildly iodine-deficient pregnant women by a new automated kinetic urinary iodine determination method

Maternal iodine deficiency can compromise the thyroid status of the mother, fetus and newborn child. Therefore, it is important to assess the iodine excretion level of groups of pregnant women. In this study we aimed to determine iodine intake in pregnancy using a recently reported automated kinetic method for urinary iodine determination. Urinary iodine measurements of 123 pregnant women (18 first, 28 second and 77 third trimester) were carried out using a new automated kinetic assay based on the Sandell-Kolthoff reaction at 37 degrees C and its kinetic measurement at 340 nm in a random-access automated analyzer after ammonium persulfate digestion at 95 degrees C in a water bath with +/-0.1 degree C precision. Statistical analyses were carried out using SPSS software. Whole group, first trimester, second trimester and third trimester urinary iodine concentrations (mean+/-SD) in pregnant women were 1.13+/-0.81, 1.08+/-0.71, 0.86+/-0.58 and 1.27+/-0.87 micromol/L, respectively. The urinary iodine concentration significantly increased with gestational age (p<0.05). We found that our study group was mildly iodine-deficient according to WHO criteria. Furthermore, the pregnant women were found to be mildly iodine-deficient in the first and third trimesters and moderately so in the second trimester. The only statistical difference was between second and third trimester values (p<0.05). Even though the increased iodine deficiency in the second trimester is not useful for early detection of iodine deficiency in pregnancy, the severity of this deficiency in the second trimester may lead to important effects on thyroid metabolism for both mother and fetus. Our study suggests that the iodine excretion of pregnant women living in iodine-deficient areas could be assessed using this fast and automated method.

Biochemical Hypothyroidism Secondary to Iodine Deficiency Is Associated with Poor School Achievement and Cognition in Bangladeshi Children

Iodine deficiency in pregnancy leads to poor cognitive function in the offspring; however, the effect of concurrent iodine deficiency on school-aged children is not clear. Several studies have shown that school children in iodine-deficient villages have poorer cognitive function than children in iodine-sufficient villages. However, villages differ in many factors that may also detrimentally affect children's development. In addition, the children's nutritional and health status has not usually been taken into account. In this study, we compared the cognitive function and school achievement levels of 170 children who had recently had low thyroxine (T4) levels [T4 ≤ 45 nmol/L (hypothyroid)] with children who had not had low T4 levels [T4 ≥70 nmol/L (euthyroid)]. The children were matched for school and grade level and came from the same iodine-deficient regions in rural Bangladesh. They were given a battery of cognitive, motor and school achievement tests. We also measured their nutritional status, examined their stools for geohelminths and assessed their home environments. A factor analysis of cognitive and motor function tests yielded two factors, a general cognitive factor and a fine motor factor. The children's height and arm circumference, experience of hunger, parental characteristics and stimulation in the home made independent contributions to their test scores. Controlling for these variables, the hypothyroid children performed worse than the euthyroid children on reading and spelling and the general cognitive factor. These findings indicate that a large number of disadvantages including hypothyroidism are related to the poor development of these children.

Iodine deficiency in pregnancy in Denmark. Regional variations and frequency of individual iodine supplementation.

Iodine requirements are increased during pregnancy and lactation and adequate iodine intake is important for normal brain development of the fetus/newborn child. The aim of the present study was to evaluate the extent to which this increase in iodine requirement is met in pregnant women living in various regions of Denmark. One hundred and fifty-two healthy pregnant women admitted to five different Danish departments of obstetrics participated in the study. Iodine status was evaluated by measurement of iodine in spot urine at day five after delivery and by careful history of the intake of iodine containing vitamin/mineral tablets. Approximately one third of the women had received tablets containing iodine. In women who had not received iodine supplementation urinary iodine was low with a median value of 39.7 micrograms/g creatinine (Aalborg 28, Randers 33, Ringkøbing 34, Arhus 43 and Copenhagen 62 micrograms/g creatinine). These values are far below internationally recommended levels. The consequences remain to be evaluated and no firm recommendations can be given. It seems reasonable, however, to recommend a high intake of food containing iodine (e.g. milk products) during pregnancy and lactation. Since nearly all the women took some kind of vitamin/mineral supplementation it could be considered to advocate intake of vitamin/mineral tablets containing iodine.

Elimination of Mental Defect due to Iodine Deficiency by the Year 2000

The WHO estimates one billion people to be at risk of iodine deficiency disorders of which mental defect is the most significant feature. Of these, 20 million are estimated to be suffering from some degree of preventable mental defect due mainly to the effects of iodine deficiency in pregnancy. The elimination of iodine deficiency disorders as a public health problem by the year 2000 has been accepted by the UN system at the World Summit for Children (1990) and the World Health Assembly (1990). In the light of the remarkable progress of national IDD control programs since 1985 there is justifiable confidence that this objective can be realised.