Thyroglobulin in smoking mothers and their newborns at delivery suggests autoregulation of placental iodide transport overcoming thiocyanate inhibition.

BACKGROUND: Placental transport of iodide is required for fetal thyroid hormone production. The sodium iodide symporter (NIS) mediates active iodide transport into the thyroid and the lactating mammary gland and is also present in placenta. NIS is competitively inhibited by thiocyanate from maternal smoking, but compensatory autoregulation of iodide transport differs between organs. The extent of autoregulation of placental iodide transport remains to be clarified. OBJECTIVE: To compare the impact of maternal smoking on thyroglobulin (Tg) levels in maternal serum at delivery and in cord serum as markers of maternal and fetal iodine deficiency. METHODS: One hundred and forty healthy, pregnant women admitted for delivery and their newborns were studied before the iodine fortification of salt in Denmark. Cotinine in urine and serum classified mothers as smokers (n=50) or nonsmokers (n=90). The pregnant women reported on intake of iodine-containing supplements during pregnancy and Tg in maternal serum at delivery and in cord serum were analyzed. RESULTS: In a context of mild-to-moderate iodine deficiency, smoking mothers had significantly higher serum Tg than nonsmoking mothers (mean Tg smokers 40.2 vs nonsmokers 24.4 µg/l, P=0.004) and so had their respective newborns (cord Tg 80.2 vs 52.4 µg/l, P=0.006), but the ratio between Tg in cord serum and maternal serum was not significantly different in smokers compared with nonsmokers (smoking 2.06 vs nonsmoking 2.22, P=0.69). CONCLUSION: Maternal smoking increased the degree of iodine deficiency in parallel in the mother and the fetus, as reflected by increased Tg levels. However, placental iodide transport seemed unaffected despite high thiocyanate levels, suggesting that thiocyanate-insensitive iodide transporters alternative to NIS are active or that NIS in the placenta is autoregulated to keep iodide transport unaltered.

Iodine nutrition in breast-fed infants is impaired by maternal smoking.

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.

Thiocyanate in food and iodine in milk: from domestic animal feeding to improved understanding of cretinism.

Transport of iodine in the mammary gland into breast milk plays a central role in various fields of prevention of thyroid diseases. First, a sufficient content of iodine in the mother's milk is necessary for normal brain development in the breastfed child. This is attained by expression during lactation in the mammary gland of the sodium iodide symporter (NIS), also responsible for iodine transport in the thyroid. Milk iodine content varies with the iodine intake of the mother, and urinary iodine excretion in groups of mothers seems to be a valuable indicator of the iodine status of their breastfed children. Second, iodine in dairy products provides a considerable part of iodine intake in many populations. Thiocyanate from rapeseed feeding of cows decreases milk iodine content, probably by competitive inhibition of NIS in the mammary gland. Alterations in feeding of dairy cows may alter the iodine content of consumer milk, and this may influence the risk of thyroid diseases in the population. Thiocyanate inhibition of iodine transport into milk may also be operative in humans with a high thiocyanate intake. This could further impair iodine status in breastfed children in low-iodine intake areas of the world. It can be speculated that a low-iodine content of mother's milk because of inhibition of NIS in the mammary gland may be one factor of importance for development of myxedematous cretinism.