Lack of iodine for thyroid hormone formation during the fetal stage and/or the first years of life may lead to developmental brain damage. During the period of breastfeeding, thyroid function of the infant depends on iodine in maternal milk. We studied healthy, pregnant women admitted for delivery and their newborn infants. Cotinine in urine and serum was used to classify mothers as smokers (n = 50) or nonsmokers (n = 90). Smoking and nonsmoking mothers had identical urinary iodine on d 5 after delivery, but smoking was associated with reduced iodine content in breast milk (smokers 26.0 micro g/liter vs. nonsmokers 53.8 micro g/liter; geometric mean, P < 0.001) and in the infants' urine (smokers 33.3 micro g/liter, vs. nonsmokers 50.4 micro g/liter, P = 0.005). Results were consistent in multivariate linear models and by logistic regression analysis. The odds ratio for smoking vs. nonsmoking mothers to have lower breast milk than urinary iodine content was 8.4 (95% confidence interval, 3.5-20.1). In smokers, iodine transfer into breast milk correlated negatively to urinary cotinine concentration. Smoking mothers had significantly higher serum levels of thiocyanate, which may competitively inhibit the sodium-iodide symporter responsible for iodide transport in the lactating mammary gland. Smoking during the period of breastfeeding increases the risk of iodine deficiency-induced brain damage in the child. Women who breastfeed should not smoke, but if they do, an extra iodine supplement should be considered.
The iodine intake level of the population is of major importance for the occurrence of thyroid disorders in an area. The aim of the present study was to evaluate the importance of drinking water iodine content for the known regional differences in iodine intake in Denmark and for the iodine content of infant formulas.Iodine in tap water obtained from 55 different locations in Denmark varied from <1.0 to 139 mg/l. In general the iodine content was low in Jutland (median 4.1 mg/l) with higher values on Sealand (23 mg/l) and other islands. Preparation of coffee or tea did not reduce the iodine content of tap water with a high initial iodine concentration. A statistically significant correlation was found between tap water iodine content today and the urinary iodine excretion measured in 41 towns in 1967 (r = 0.68, P < 0.001). The correlation corresponded to a basic urinary iodine excretion in Denmark of 43 mg/24 h excluding iodine in water and a daily water intake of 1.7 l. The iodine content of infant formulas prepared by addition of demineralized water varied from 37 to 138 mg/l (median 57 mg/l, n = 18). Hence the final iodine content would depend heavily on the source of water used for preparation.We found that iodine in tap water was a major determinant of regional differences in iodine intake in Denmark. Changes in water supply and possibly water purification methods may influence the population iodine intake level and the occurrence of thyroid disorders.
Comparative epidemiologic studies in areas with low and high iodine intake and controlled studies of iodine supplementation have demonstrated that the major consequence of mild-to-moderate iodine deficiency for the health of the population is an extraordinarily high occurrence of hyperthyroidism in elderly subjects, especially women, with risk of cardiac arrhythmias, osteoporosis, and muscle wasting. The hyperthyroidism is caused by autonomous nodular growth and function of the thyroid gland and it is accompanied by a high frequency of goiter. Pregnant women and small children are not immediately endangered but the consequences of severe iodine deficiency for brain development are grave and a considerable safety margin is advisable. Moreover, a shift toward less malignant types of thyroid cancer and a lower radiation dose to the thyroid in case of nuclear fallout support that mild-to-moderate iodine deficiency should be corrected. However, there is evidence that a high iodine intake may be associated with more autoimmune hypothyroidism, and that Graves' disease may manifest at a younger age and be more difficult to treat. Hence, the iodine intake should be brought to a level at which iodine deficiency disorders are avoided but not higher. Iodine supplementation programs should aim at relatively uniform iodine intake, avoiding deficient or excessive iodine intake in subpopulations. To adopt such a strategy, surveillance programs are needed.
Whereas the consequences of extremes in iodine intake are well described, much less is known about the effect of more moderate variations in maternal iodine intake on fetal thyroid function. The present study performed in Denmark with mild to moderate iodine deficiency dealt with the effect of maternal iodine supplementation on thyroid function in the mother at term and in the fetus/neonate. Serum was collected consecutively from pregnant women at term (n = 144) and from cord blood (n = 139). Forty-nine women had a regular intake of vitamin and mineral tablets with iodine (150 microg/day) during pregnancy, and 95 took no artificial iodine supplementation. Iodine supplementation (+I) induced opposite variations in thyroid function in the mother and the fetus. In +I mothers, TSH was 7.6% lower than in mothers with no supplementation (P < 0.05). In cord blood, on the contrary, TSH was 27.3% higher in the +I group (P < 0.05). The variations were caused by opposite shifts in TSH frequency distribution in mothers and neonates. The association between iodine supplementation and high serum TSH in the neonates was further substantiated by an inverse correlation between thyroglobulin and TSH in cord blood (P < 0.001), whereas no specific pattern was observed in the mothers. High serum thyroglobulin was a marker of low iodine intake in both mothers and neonates. The results suggest that the fetal thyroid, at least in areas of mild iodine deficiency, is more sensitive to the inhibitory effect of iodine than hitherto anticipated.
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