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.
Biofeedback is a method of pelvic floor rehabilitation using a surface electrode inserted into the vagina and a catheter in the rectum. Forty women with genuine urinary stress incontinence were randomized to compare the efficacy of physiotherapy and physiotherapy in combination with biofeedback. The effect of the treatment was determined by a standardized pad-weighing test. Long-term status was determined using a questionnaire after 2-3 years. Thirty-four women completed the treatment. The study showed a statistically significant better improvement in the biofeedback group. The long-term effect in the biofeedback group seemed better and the patients were more motivated for training afterwards.
In moderately iodine-deficient, pregnant, thyroid peroxidase antibody (TPO-Ab)-positive women the role of iodine supplementation in the development of postpartum thyroid dysfunction (PPTD) was studied in a placebo-controlled, randomized, double blind trial. Screening for TPO-Ab was performed in early pregnancy in a population of healthy pregnant Danish women with no previous diagnosed thyroid disease (prevalence, 117 of 1,284; 9.1%). The participants were randomized, stratified according to TPO-Ab level, to three groups. All participants received a daily vitamin and mineral tablet with 150 microg iodine or no iodine. The +/+ group received iodine during pregnancy and the postpartum period, the +/- group received iodine during pregnancy only, and the -/- group received no iodine supplementation. A total of 66 TPO-Ab positive women were followed, and in the postpartum period sera were collected at 8-week interval for biochemical evaluation of thyroid function and antibody level. Compliance was evaluated by 24-h urinary iodine measurements. PPTD developed in 55% of the participants. In 67% of the cases abnormal TSH was accompanied by abnormalities in thyroid hormones, whereas 33% had abnormal serum TSH only. There was no statistically significant difference in the frequency of PPTD in the three groups: +/+ group, 59% (95% confidence interval, 36-79%); +/- group, 60% (36-81%); and -/- group, 46% (26-67%). There were also no differences in the severity of the PPTD, as evaluated by duration and grade of deviation of TSH and thyroid hormones from normality. The occurrence, severity, and type of PPTD predominantly depended on the TPO-Ab level: TPO-Ab below 200 U/L at screening, 35% developed PPTD; TPO-Ab of 200-900 U/L, 54%; and TPO-Ab above 900 U/L, 75% developed PPTD. Women with low levels of antibodies predominantly remained euthyroid or had hyperthyroidism only, whereas women with high antibody levels had hyperthyroidism followed by hypothyroidism or hypothyroidism only. We conclude that iodine supplementation (150 microg) during pregnancy and the postpartum period to TPO-Ab-positive women living in an area with mild to moderate iodine deficiency did not induce or worsen PPTD. The study confirmed that screening for TPO-Ab in early pregnancy can predict women at high risk for development of PPTD.
In a prospective investigation, 99 very preterm infants (gestational age (GA) 24 32 weeks, birthweight 560-2,255 g) were studied during the first 4 weeks of life. The infants were divided into two groups: infants born extremely early (GA <28 weeks, n = 20) and infants of GA 28 - 32 weeks; the groups were then subdivided into critically ill or not. Diagnostic blood sampling and blood transfusion events were recorded. In total, 1905 blood samples (5,253 analysis) were performed, corresponding to 0.7 samples (1.9 analysis) per day per infant. The highest frequencies were found during the first week, in infants with extremely low GA and in critically ill infants. The mean blood loss and transfusion volume values were 13.6 ml/kg and 6.3 ml/kg, respectively. In total, 19 infants (19%) received 34 transfusions corresponding to 0.3 transfusions per infant. Thirteen out of 20 infants of extremely low GA received 28 blood transfusions, corresponding to 27.0 ml/kg of blood on average during the study period. Four developed late anaemia; thus, in total, 14 (70%) of the infants born extremely early received 35 transfusions during the first 3 months of life, corresponding to a total mean of 34.8 ml/kg. For the extremely preterm infants a significant correlation between sampled and transfused blood volume was found (mean 37.1 and 33.3 ml/kg, respectively, r = + 0.71, p = 0.0003). The most frequently requested analyses were glucose, sodium and potassium. Few blood gas analyses were requested (1.9/ infant). No blood losses attributable to excessive generous sampling were detected. The results show an acceptable low frequency of sampling and transfusion events for infants of GA 28-32 weeks. The study emphasizes the necessity of thorough reflection and monitoring of blood losses when ordering blood sampling in extremely preterm, critically ill infants.
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.
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