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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.

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., (© 2017 The Royal Australian and New Zealand College of Obstetricians and Gynaecologists.)

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., Competing Interests: The authors declare no conflicts of interest.

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.

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., (Copyright © 2014 Elsevier Inc. All rights reserved.)

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.

Background: The New Zealand population has both marginal selenium status and mild iodine deficiency. Adequate intakes of iodine and selenium are required for optimal thyroid function., Objective: The aim of the study was to determine whether low selenium and iodine status compromises thyroid function in an older New Zealand population., Design: We investigated the effects of selenium and iodine supplementation in a double-blind, randomized, placebo-controlled trial in 100 Dunedin volunteers aged 60-80 y. Participants received 100 microg Se/d as l-selenomethionine, 80 microg I, 100 microg Se + 80 microg I, or placebo for 3 mo. Thyroid-stimulating hormone (TSH), free triiodothyronine (T(3)), free thyroxine (T(4)), thyroglobulin, plasma selenium, whole-blood glutathione peroxidase (GPx) activity, and urinary iodine concentrations (UICs) were measured., Results: Plasma selenium (P < 0.0001) and whole-blood GPx activity (P<0.0001) increased from baseline to week 12 in the selenium and selenium plus iodine groups in comparison with the placebo group. Median UIC at baseline was 48 microg/L (interquartile range: 31-79 microg/L), which is indicative of moderate iodine deficiency. UIC increased in the iodine and selenium plus iodine groups and was significant only for the iodine group (P = 0.0014). Thyroglobulin concentration decreased by 24% and 13% of baseline in the iodine and selenium plus iodine groups in comparison with the placebo group (P = 0.009 and P = 0.108, respectively). No significant treatment effects were found for TSH, free T(3), free T(4), or ratio of T(3) to T(4)., Conclusions: Additional selenium improved GPx activity but not the thyroid hormone status of older New Zealanders. Iodine supplementation alleviated the moderate iodine deficiency and reduced elevated thyroglobulin concentrations. No synergistic action of selenium and iodine was observed. The trial was registered at www.anzctr.org.au/registry/ as ACTRN012605000368639.