Iodine status of postpartum women and their infants aged 3, 6 and 12 months: Mother and Infant Nutrition Investigation (MINI).

To alleviate the re-emergence of iodine deficiency in New Zealand, two strategies, the mandatory fortification of bread with iodised salt (2009) and a government-subsidised iodine supplement for breast-feeding women (2010), were introduced. Few studies have investigated mother and infant iodine status during the first postpartum year; this study aimed to describe iodine status of mothers and infants at 3, 6 and 12 months postpartum (3MPP, 6MPP and 12MPP, respectively). Partitioning of iodine excretion between urine and breast milk of exclusive breast-feeding (EBF) women at 3MPP was determined. In total, eighty-seven mother-infant pairs participated in the study. Maternal and infant spot urinary iodine concentration (UIC) and breast milk iodine concentration (BMIC) were determined. The percentage of women who took iodine-containing supplements decreased from 46 % at 3MPP to 6 % at 12MPP. Maternal median UIC (MUIC) at 3MPP (82 (46, 157) µg/l), 6MPP (85 (43, 134) µg/l) and 12MPP (95 (51, 169) µg/l) were <100 µg/l. The use of iodine-containing supplements increased MUIC and BMIC only at 3MPP. Median BMIC at all time points were below 75 µg/l. Infant MUIC at 3MPP (115 (69, 182) µg/l) and 6MPP (120 (60, 196) µg/l) were below 125 µg/l. Among EBF women at 3MPP, an increased partitioning of iodine into breast milk (highest proportion 60 %) was shown at lower iodine intakes, along with a reduced fractional iodine excretion in urine (lowest proportion 40 %), indicating a protective mechanism for breastfed infants' iodine status. In conclusion, this cohort of postpartum women was iodine-deficient. Iodine status of their breastfed infants was suboptimal. Lactating women who do not consume iodine-rich foods and those who become pregnant again should take iodine-containing supplements.

Iodine-fortified toddler milk improves dietary iodine intakes and iodine status in toddlers: a randomised controlled trial.

PURPOSE: We aimed to evaluate the effectiveness of consuming iodine-fortified toddler milk for improving dietary iodine intakes and biochemical iodine status in toddlers. METHODS: In a 20-week parallel randomised controlled trial, healthy 12-20-month-old children were assigned to: Fortified Milk [n = 45; iodine-fortified (21.1 µg iodine/100 g prepared drink) cow's milk], or Non-Fortified Milk (n = 90; non-fortified cow's milk). Food and nutrient intakes were assessed with 3-day weighed food records at baseline, and weeks 4 and 20. Urinary iodine concentration (UIC) was measured at baseline and 20 weeks. RESULTS: At baseline, toddlers' median milk intake was 429 g/day. There was no evidence that milk intakes changed within or between the groups during the intervention. Toddlers' baseline geometric mean iodine intake was 46.9 µg/day, and the median UIC of 43 µg/L in the Fortified Milk group and 55 µg/L in the Non-Fortified Milk group indicated moderate and mild iodine deficiency, respectively, with this difference due to chance. During the intervention, iodine intakes increased by 136% (p < 0.001) and UIC increased by 85 µg/L (p < 0.001) in the Fortified Milk group compared to the Non-Fortified Milk group. The 20-week median UIC was 91 µg/L in the Fortified Milk group and 49 µg/L in the Non-Fortified Milk group. CONCLUSIONS: Consumption of ≈ 1.7 cups of iodine-fortified toddler milk per day for 20 weeks can increase dietary iodine intakes and UIC in healthy iodine-deficient toddlers. This strategy alone is unlikely to provide sufficient intake to ensure adequate iodine status in toddlers at risk of mild-to-moderate iodine deficiency.

Association Between Maternal Iodine Intake in Pregnancy and Childhood Neurodevelopment at Age 18 Months.

There are limited and inconsistent data suggesting that mild iodine deficiency in pregnancy might be associated with poorer developmental outcomes in children. Between 2011 and 2015, we conducted a prospective cohort study in Australia examining the relationship between maternal iodine intake in pregnancy and childhood neurodevelopment, assessed using Bayley Scales of Infant and Toddler Development, Third Edition (Bayley-III), in 699 children at 18 months. Maternal iodine intake and urinary iodine concentration (UIC) were assessed at study entry (<20 weeks' gestation) and at 28 weeks' gestation. Maternal iodine intake in the lowest (<220 µg/day) or highest (≥391 µg/day) quartile was associated with lower cognitive, language, and motor scores (mean differences ranged from 2.4 (95% confidence interval (CI): 0.01, 4.8) to 7.0 (95% CI: 2.8, 11.1) points lower) and higher odds (odds ratios ranged from 2.7 (95% CI: 1.3, 5.6) to 2.8 (95% CI: 1.3, 5.7)) of cognitive developmental delay (Bayley-III score <1 SD) compared with mothers with an iodine intake in the middle quartiles. There was no association between UIC in pregnancy and Bayley-III outcomes regardless of whether UIC and the outcomes were analyzed as continuous or categorical variables. Both low and high iodine intakes in pregnancy were associated with poorer childhood neurodevelopment in this iodine-sufficient population.

Development of Databases on Iodine in Foods and Dietary Supplements.

Iodine is an essential micronutrient required for normal growth and neurodevelopment; thus, an adequate intake of iodine is particularly important for pregnant and lactating women, and throughout childhood. Low levels of iodine in the soil and groundwater are common in many parts of the world, often leading to diets that are low in iodine. Widespread salt iodization has eradicated severe iodine deficiency, but mild-to-moderate deficiency is still prevalent even in many developed countries. To understand patterns of iodine intake and to develop strategies for improving intake, it is important to characterize all sources of dietary iodine, and national databases on the iodine content of major dietary contributors (including foods, beverages, water, salts, and supplements) provide a key information resource. This paper discusses the importance of well-constructed databases on the iodine content of foods, beverages, and dietary supplements; the availability of iodine databases worldwide; and factors related to variability in iodine content that should be considered when developing such databases. We also describe current efforts in iodine database development in the United States, the use of iodine composition data to develop food fortification policies in New Zealand, and how iodine content databases might be used when considering the iodine intake and status of individuals and populations.

Maternal adherence with recommendations for folic acid and iodine supplements: A cross-sectional survey.

We conducted a survey of 535 New Zealand women to determine supplement use pre-pregnancy, during pregnancy and while breastfeeding to evaluate adherence with national recommendations for folic acid and iodine supplementation. Our findings suggest that despite these women being well-educated and motivated to complete an online survey, there was low adherence to recommendations for folic acid and iodine supplements. Only 38% of women reported supplement intake that met both folic acid and iodine recommendations. This cross-sectional survey provides information useful to policy makers, clinicians and researchers seeking to protect and promote maternal and infant health.

Iodine Supplementation of Mildly Iodine-Deficient Adults Lowers Thyroglobulin: A Randomized Controlled Trial.

CONTEXT: An inverse relationship between thyroglobulin (Tg) and urinary iodine concentration (UIC) has been found in children, potentially making Tg a viable blood marker of iodine status. The application of Tg in adults is unknown. OBJECTIVE: The objective of the study was to determine the efficacy of Tg to assess iodine status in adults. DESIGN: This was a randomized, double-blind, placebo-controlled, clinical trial. SETTING: The study was conducted in Dunedin, New Zealand. PARTICIPANTS: Mildly iodine deficient adults (n = 112) aged 18­40 years participated in the study. INTERVENTION: Participants were supplemented with 150 µg of iodine as potassium iodate or placebo daily for 24 weeks. At baseline and 24 weeks, participants provided five casual urine samples for UIC determination; serum TSH and free T4 (FT4) was also measured. Tg was determined at baseline and 8, 16, and 24 weeks. MAIN OUTCOME MEASURES: A change in Tg concentration between the iodine-supplemented and placebo groups at 24 weeks. RESULTS: At baseline, the overall median UIC was 65 µg/L, confirming that participants were mildly iodine deficient (ie, median UIC between 50 and 99 µg/L). The overall median Tg was 16.6 µg/L; TSH and FT4 were within normal reference ranges. At 24 weeks, the median UIC of the placebo and supplemented groups was significantly different, 79 and 168 µg/L, respectively (P < .001). Tg in the iodine-supplemented group decreased by 12%, 20%, and 27% compared with the placebo group at 8 (P = .045), 16 (P < .001), and 24 weeks (P < .001); there were no significant changes in TSH and FT4. CONCLUSION: Improved iodine status as assessed by UIC was associated with a concomitant decrease in Tg concentration, demonstrating that Tg is a useful biomarker of iodine status in a group of adults.

Effects of anemia at different stages of gestation on infant outcomes.

OBJECTIVES: Maternal anemia is a public health challenge worldwide. The present study aims to explore the effects of maternal anemia at different stages of gestation on postnatal growth and neurobehavioral development in infants. METHODS: A cohort of pregnant Indian women were followed from 13 to 22 wk gestation (i.e., second trimester; n = 211), 29 to 42 wk gestation (i.e., third trimester; n = 178); their infants were followed to ∼3 wk (n = 147) postpartum. Data collected included information on sociodemographic and health-related factors, including anemia (i.e., low hemoglobin status), maternal and infant anthropometric data, and infant neurobehavioral data. A mixed logistic regression model was used to examine the impact of anemia during pregnancy on maternal and infant outcomes (i.e., anthropometric growth parameters and infant neurobehavioral development). RESULTS: The prevalence of maternal anemia was 41% and 55% (P < 0.001), and iron deficiency anemia was 3.6% and 5.6%, respectively, in the second trimester and third trimester. Infants of pregnant women who were not anemic in the second trimester were 0.26 standard deviations (SD) heavier (P = 0.029), 0.50 SD taller (P = 0.001), and had 0.26 SD larger head circumference (P = 0.029) compared with infants of anemic pregnant women. Infants of pregnant women who were not anemic in the third trimester had orientation scores 3.88 higher (P = 0.004) than infants of women who were anemic. CONCLUSIONS: Our findings indicate that maternal anemia in the second trimester of gestation influences postnatal infant growth and underscores the necessity of alleviating anemia in young women in the early stages of gestation.

Urinary iodine concentration of New Zealand adults improves with mandatory fortification of bread with iodised salt but not to predicted levels.

PURPOSE: To measure the iodine status and iodine intake of New Zealand adults 18-64 years of age following mandatory fortification of bread with iodine. METHODS: A cross-sectional survey of NZ adults living in Dunedin and Wellington during February-November 2012. Three hundred and one men and women aged 18-64 years randomly selected from the New Zealand Electoral Roll completed a 24-h urine collection, a demographic and iodine-specific food frequency questionnaire (FFQ), and had height and weight measured. Urine collections were analysed for iodine and reported as median urinary iodine concentration (UIC) µg/L and median urinary iodine excretion (UIE) µg/day. The FFQ was used to estimate iodine intake with and without discretionary iodised salt use. RESULTS: The median UIC for all adults was 73 µg/L, indicative of mild iodine deficiency. The mean urinary volume was 2.0 L. As an estimate of iodine intake, the median UIE was 127 µg/day. Estimated iodine intake, using the FFQ which included discretionary iodised salt use, was 132 µg/day. Iodine intakes were associated with UIC (P = 0.040) and UIE (P = 0.003), but not with bread iodine intake and iodised salt use. CONCLUSION: Using the WHO/UNICEF/ICCIDD target for iodine sufficiency (a UIC of >100 µg/L) based on school-aged children with a mean urinary volume of 1.0 L, the iodine status of NZ adults does not reach adequate levels (73 µg/L). A more realistic parameter in a population with a higher urinary volume excretion (2.0 L) is the UIE. A median UIE of 127 µg/day suggests that the iodine status of NZ adults is now likely to be adequate.

The effect of iodine supplementation in pregnancy on early childhood neurodevelopment and clinical outcomes: results of an aborted randomised placebo-controlled trial.

BACKGROUND: Concern that mild iodine deficiency in pregnancy may adversely affect neurodevelopment of offspring has led to recommendations for iodine supplementation in the absence of evidence from randomised controlled trials. The primary objective of the study was to investigate the effect of iodine supplementation during pregnancy on childhood neurodevelopment. Secondary outcomes included pregnancy outcomes, maternal thyroid function and general health. METHODS: Women with a singleton pregnancy of fewer than 20 weeks were randomly assigned to iodine (150 µg/d) or placebo from trial entry to birth. Childhood neurodevelopment was assessed at 18 months by using Bayley Scales of Infant and Toddler Development (Bayley-III). Iodine status and thyroid function were assessed at baseline and at 36 weeks' gestation. Pregnancy outcomes were collected from medical records. RESULTS: The trial was stopped after 59 women were randomly assigned following withdrawal of support by the funding body. There were no differences in childhood neurodevelopmental scores between the iodine treated and placebo groups. The mean cognitive, language and motor scores on the Bayley-III (iodine versus placebo, respectively) were 99.4 ± 12.2 versus 101.7 ± 8.2 (mean difference (MD) -2.3, 95 % confidence interval (CI) -7.8, 3.2; P = 0.42), 97.2 ± 12.2 versus 97.9 ± 11.5 (MD -0.7, 95 % CI -7.0, 5.6; P = 0.83) and 93.9 ± 10.8 versus 92.4 ± 9.7 (MD 1.4, 95 % CI -4.0, 6.9; P = 0.61), respectively. No differences were identified between groups in any secondary outcomes. CONCLUSIONS: Iodine supplementation in pregnancy did not result in better childhood neurodevelopment in this small trial. Adequately powered randomised controlled trials are needed to provide conclusive evidence regarding the effect of iodine supplementation in pregnancy. TRIALS REGISTRATION: The trial was registered with the Australian New Zealand Clinical Trials Registry at http://www.anzctr.org.au . The registration number of this trial is ACTRN12610000411044 . The trial was registered on 21 May 2010.

Iron status of pregnant Indian women from an area of active iron supplementation.

OBJECTIVE: The aim of this study was to investigate the iron status of pregnant tribal women from Ramtek, Nagpur, Maharashtra, India using a combination of indices. METHODS: A community-based observational study was conducted to assess iron status using a convenience sample of pregnant Indian tribal women from Ramtek. Pregnant women were recruited at 13 to 22 wk gestation (first visit; n = 211) and followed to 29 to 42 wk gestation (second visit; n = 177) of pregnancy. Sociodemographic and anthropometric data; iron supplement intake; and blood samples for estimating hemoglobin (Hb), serum ferritin (SF), soluble transferrin receptor (sTfR), and C-reactive protein (CRP) were obtained. RESULTS: The mean (SD) Hb concentration at recruitment was 106 (15) g/L and 106 (14) g/L at the second visit; 41% of the women at recruitment and 55% at second visit were anemic (14% higher, P < 0.001). No women at recruitment and 3.7% at second visit had SF concentration < 15 ng/mL; and 3.3% at recruitment and 3.9% at the second visit had sTfR > 4.4 ng/mL (0.6% higher, P = 0.179). Almost 62% and 71% of pregnant women used iron supplements at both visits, respectively. Iron supplement intake > 7 d in the preceding month improved the Hb concentration by 3.23 g/L and reduced sTfR concentration by 13%; women who were breastfeeding at the time of recruitment had 11% higher SF concentration. CONCLUSIONS: The iron indices suggest that pregnant tribal women of central India, although anemic, had good iron status. Use of iron supplements > 7 d in the preceding month improved iron status; however, non-iron-deficiency anemia persisted in this group.

Mandatory fortification of bread with iodised salt modestly improves iodine status in schoolchildren.

Iodine deficiency has re-emerged in many parts of the world including the UK, Australia and New Zealand (NZ). In 2009, the NZ government introduced the mandatory fortification of bread with iodised salt as a strategy to improve iodine intakes. The aim of the present study was to assess the impact of fortification on the iodine status of NZ schoolchildren. A school-based cluster survey was used to randomly select schools from two NZ cities. Children aged 8-10 years were administered a general questionnaire, and asked to provide a casual urine and finger-prick blood sample. The median urinary iodine concentration (UIC) of the children (n 147) was 113 µg/l, which falls between 100 and 199 µg/l indicating adequate iodine status; 12 % of children had a UIC < 50 µg/l and 39 % had a UIC < 100 µg/l. The median serum thyroxine concentration was 115 nmol/l. The median serum thyroglobulin (Tg) concentration was 10.8 µg/l and falls in the 10.0-19.9 µg/l range indicative of mild iodine deficiency, suggesting that these children still had enlarged thyroid glands. When compared with the median UIC of 68 µg/l reported in the 2002 NZ Children's Nutrition Survey, the UIC of children in the present study had increased, which is probably caused by the addition of iodised salt to bread. However, the elevated concentration of Tg in these children suggests that the increase in UIC is not sufficient to ensure that thyroid volume has normalised. The fortification of other staple foods, in addition to bread, should be considered to ensure good iodine status in NZ children.

Assessing iodine intakes in pregnancy and strategies for improvement.

An adequate intake of iodine in the diet of pregnant women is important to ensure normal growth and development of the fetus. It is difficult, however, to accurately determine iodine intakes using traditional methods of dietary assessment, primarily because the contribution of iodised salt use, at the table and in cooking, to total iodine intake is difficult to quantify. Given the limitations of dietary assessment, biochemical indices in blood and urine are typically used to assess iodine status in children and adults. Although reference ranges exist for thyroid hormones, there has been no consensus on the cut-offs needed in pregnancy to diagnose iodine deficiency. In contrast, a median urinary iodine concentration (UIC) of 150-249 µg/L has been established to determine the adequate iodine status of a group of pregnant women. However, the large intra-individual variation in UIC from either spot or 24h urine samples means that UIC cannot be used to assess iodine status in an individual pregnant woman. The difficulty in determining if an individual pregnant woman is iodine deficient is problematic for cross-sectional studies examining associations between iodine status in pregnancy and developmental outcomes in the child.

The effect of maternal iodine status on infant outcomes in an iodine-deficient Indian population.

BACKGROUND: An adequate intake of iodine during pregnancy is essential for the synthesis of maternal thyroid hormones needed to support normal fetal development. This study aimed to assess the iodine status of pregnant tribal Indian women and their infants and to determine the impact of maternal iodine status on infant growth and behavior. METHODS: A prospective, observational study was undertaken to assess the iodine status of tribal pregnant Indian women living in Ramtek, northeast of Nagpur, India. Pregnant women were recruited at 13-22 weeks gestation (n=220), visited a second time at 33-37 weeks gestation (n=183), and again visited at 2-4 weeks postpartum with their infants. Sociodemographic, anthropometric, and biochemical data, including household salt, blood, and urine samples were obtained from pregnant women. Urine samples, anthropometric, and neonatal behavioral data were collected from infants. RESULTS: The median urinary iodine concentration (MUIC) at recruitment (mean gestation=17.5 weeks) of mothers was 106 µg/L, which declined to 71 µg/L at the second visit (mean gestation=34.5 weeks) similar to the postpartum MUIC of 69 µg/L, indicating that these women were iodine deficient. Infant (mean age=2.5 weeks) MUIC was 168 µg/L. Median maternal thyroid stimulating hormone (TSH) and free thyroxine (FT(4)) concentrations at first and second visits were 1.71 and 1.79 mIU/L and 14.4 and 15.4 pmol/L, respectively; 20.0% of women at first visit had TSH >97.5th percentile and 1.4% had FT(4) <2.5th percentile. Salt iodine concentration was a significant predictor of maternal UIC (p<0.001), and postpartum maternal UIC was a significant predictor of infant UIC (p<0.001). For every pmol/L increase in maternal FT(4) concentration at first visit, both infant weight-for-age Z-score and length-for-age Z-score increased by 0.05 units. There was no relationship between maternal UIC, FT(4), or TSH at first visit and neonatal behavior. CONCLUSIONS: Despite three quarters of the women in this study having access to adequately iodized salt (i.e., >15 ppm), these pregnant tribal Indian women were iodine deficient. Increasing the iodine content of salt deemed adequately iodized and iodine supplementation are two strategies that might improve the iodine status of these pregnant women and, consequently, the growth of their infants.

Minimal impact of excess iodate intake on thyroid hormones and selenium status in older New Zealanders.

OBJECTIVE: Iodine deficiency has re-emerged in New Zealand, while selenium status has improved. The aim of this study was to investigate the effects of excess iodine intake as iodate on thyroid and selenium status. METHODS: In a randomized controlled trial on older people (mean±s.d. 73±4.8 years; n=143), two groups received >50  mg iodine as iodate/day for 8 weeks because of supplement formulation error, either with 100  µg selenium (Se+highI) or without selenium (highI). Four other groups received 80  µg iodine as iodate/day with selenium (Se+lowI) or without selenium (lowI), selenium alone (Se+), or placebo. Thyroid hormones, selenium status, and median urinary iodine concentration (MUIC) were compared at weeks 0, 8, and 4 weeks post-supplementation. RESULTS: MUIC increased nine- and six-fold in Se+highI and highI groups, decreasing to baseline by week 12. Plasma selenium increased in selenium-supplemented groups (P<0.001). The level of increase in whole blood glutathione peroxidase (WBGPx) in the Se+highI group was smaller than Se+ (P=0.020) and Se+lowI (P=0.007) groups. The decrease in WBGPX in the highI group was greater than other non-selenium-supplemented groups, but differences were not significant. Ten of 43 participants exposed to excess iodate showed elevated TSH (hypothyroidism) at week 8. In all but two, TSH had returned to normal by week 12. In three participants, TSH decreased to <0.10  mIU/l (hyperthyroidism) at week 8, remaining low at week 12. CONCLUSIONS: Excess iodate induced hypothyroidism in some participants and hyperthyroidism in others. Most abnormalities disappeared after 4 weeks. Excess iodate reduced WBGPx activity and resulted in smaller increases in WBGPx after selenium supplementation.

Concurrent micronutrient deficiencies are prevalent in nonpregnant rural and tribal women from central India.

OBJECTIVE: The existence of concurrent micronutrient deficiencies in Indian women of reproductive age has received little attention. This study aimed to comprehensively assess the micronutrient status of nonpregnant rural and tribal women 18-30 y from central India. METHODS: Participants (n = 109) were randomly selected using a stratified (rural-tribal) proportionate-to-population size cluster sampling method from 12 subcenters in Ramtek block, Nagpur. Sociodemographic, anthropometric, dietary, and biochemical data, including blood and urine samples, were obtained. RESULTS: Tribal and rural women had similar sociodemographic characteristics and anthropometric status; 63% of women had a body mass index <18.5 kg/m(2). The median urinary iodine concentration was 215 µg/L (IQR: 127, 319). The mean (SD) concentration of hemoglobin, serum zinc, retinol, and folate was 112 (13) g/L, 10.8 (1.6) µmol/L, 1.2 (0.3) µmol/L, 18.4 (8.4) nmol/L, respectively, with a geometric mean serum vitamin B(12) concentration of 186 pmol/L. The percentage of women with low values for hemoglobin (<120 g/L), serum zinc (<10.7 µmol/L), vitamin B(12) (<148 pmol/L), retinol (<0.7 µmol/L), and folate (<6.8 nmol/L) was 66%, 52%, 34%, 4%, and 2%, respectively. Tribal women had a higher prevalence of zinc deficiency (58% versus 39%, P = 0.054) and concurrent deficiency of any two micronutrients (46% versus 26%; P = 0.034), including zinc and anemia (38% versus 21%, P = 0.024). CONCLUSION: Zinc, vitamin B(12), and iron constitute the principal micronutrient deficiencies in these women. Existing supplementation programs should be extended to include 18- to 30-y-old nonpregnant women as the majority of childbearing occurs within this timeframe.

Iodine deficiency in pregnancy: the effect on neurodevelopment in the child.

Iodine is an integral part of the thyroid hormones, thyroxine (T(4)) and tri-iodothyronine (T(3)), necessary for normal growth and development. An adequate supply of cerebral T(3), generated in the fetal brain from maternal free T(4) (fT(4)), is needed by the fetus for thyroid hormone dependent neurodevelopment, which begins in the second half of the first trimester of pregnancy. Around the beginning of the second trimester the fetal thyroid also begins to produce hormones but the reserves of the fetal gland are low, thus maternal thyroid hormones contribute to total fetal thyroid hormone concentrations until birth. In order for pregnant women to produce enough thyroid hormones to meet both her own and her baby's requirements, a 50% increase in iodine intake is recommended. A lack of iodine in the diet may result in the mother becoming iodine deficient, and subsequently the fetus. In iodine deficiency, hypothyroxinemia (i.e., low maternal fT(4)) results in damage to the developing brain, which is further aggravated by hypothyroidism in the fetus. The most serious consequence of iodine deficiency is cretinism, characterised by profound mental retardation. There is unequivocal evidence that severe iodine deficiency in pregnancy impairs brain development in the child. However, only two intervention trials have assessed neurodevelopment in children of moderately iodine deficient mothers finding improved neurodevelopment in children of mothers supplemented earlier rather than later in pregnancy; both studies were not randomised and were uncontrolled. Thus, there is a need for well-designed trials to determine the effect of iodine supplementation in moderate to mildly iodine deficient pregnant women on neurodevelopment in the child.

Breast-milk iodine concentration declines over the first 6 mo postpartum in iodine-deficient women.

BACKGROUND: Little is known about the iodine status of lactating mothers and their infants during the first 6 mo postpartum or, if deficient, the amount of supplemental iodine required to improve status. OBJECTIVE: The objective was to determine maternal and infant iodine status and the breast-milk iodine concentration (BMIC) over the first 6 mo of breastfeeding. DESIGN: A randomized, double-blind, placebo-controlled supplementation trial was conducted in lactating women who received placebo (n = 56), 75 µg I/d (n = 27), or 150 µg I/d (n = 26) after their infants' birth until 24 wk postpartum. Maternal and infant urine samples and breast-milk samples were collected at 1, 2, 4, 8, 12, 16, 20, and 24 wk. Maternal serum thyrotropin and free thyroxine concentrations were measured at 24 wk. RESULTS: Over 24 wk, the median urinary iodine concentration (UIC) of unsupplemented women and their infants ranged from 20 to 41 µg/L and 34 to 49 µg/L, respectively, which indicated iodine deficiency (ie, UIC < 100 µg/L). Mean maternal UIC was 2.1-2.4 times higher in supplemented than in unsupplemented women (P < 0.001) but did not differ significantly between the 2 supplemented groups. BMIC in the placebo group decreased by 40% over 24 wk (P < 0.001) and was 1.3 times and 1.7 times higher in women supplemented with 75 µg I/d (P = 0.030) and 150 µg I/d (P < 0.001), respectively, than in unsupplemented women. Thyrotropin and free thyroxine did not differ significantly between groups. CONCLUSION: BMIC decreased in the first 6 mo in these iodine-deficient lactating women; supplementation with 75 or 150 µg I/d increased the BMIC but was insufficient to ensure adequate iodine status in women or their infants. The study was registered with the Australian New Zealand Clinical Trials Registry as ACTRN12605000345684.

Iodine supplementation improves cognition in mildly iodine-deficient children.

BACKGROUND: The effects of severe iodine deficiency during critical periods of brain development are well documented. There is little known about the consequences of milder forms of iodine deficiency on neurodevelopment. OBJECTIVE: The objective was to determine whether supplementing mildly iodine-deficient children with iodine improves cognition. DESIGN: A randomized, placebo-controlled, double-blind trial was conducted in 184 children aged 10-13 y in Dunedin, New Zealand. Children were randomly assigned to receive a daily tablet containing either 150 microg I or placebo for 28 wk. Biochemical, anthropometric, and dietary data were collected from each child at baseline and after 28 wk. Cognitive performance was assessed through 4 subtests from the Wechsler Intelligence Scale for Children. RESULTS: At baseline, children were mildly iodine deficient [median urinary iodine concentration (UIC): 63 microg/L; thyroglobulin concentration: 16.4 microg/L]. After 28 wk, iodine status improved in the supplemented group (UIC: 145 microg/L; thyroglobulin: 8.5 microg/L), whereas the placebo group remained iodine deficient (UIC: 81 microg/L; thyroglobulin: 11.6 microg/L). Iodine supplementation significantly improved scores for 2 of the 4 cognitive subtests [picture concepts (P = 0.023) and matrix reasoning (P = 0.040)] but not for letter-number sequencing (P = 0.480) or symbol search (P = 0.608). The overall cognitive score of the iodine-supplemented group was 0.19 SDs higher than that of the placebo group (P = 0.011). CONCLUSIONS: Iodine supplementation improved perceptual reasoning in mildly iodine-deficient children and suggests that mild iodine deficiency could prevent children from attaining their full intellectual potential. The trial was registered with the Australia New Zealand Clinical Trials Register as ACTRN12608000222347.