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Iodine supply is crucial during pregnancy to ensure that the proper thyroid function of mother and baby support fetal brain development. Little is known about iodine status or its dietary determinants in pregnant women in the Republic of Cyprus. We therefore recruited 128 pregnant women at their first-trimester ultrasound scan to a cross-sectional study. We collected spot-urine samples for the measurement of urinary iodine concentration (UIC, µg/l) and creatinine concentration (Creat, g/l), the latter of which allows us to correct for urine dilution and to compute the iodine-to-creatinine ratio (UI/Creat). Women completed a FFQ and a general questionnaire. We used a General Linear model to explore associations between maternal and dietary characteristics with UI/Creat. The median UIC (105 µg/l) indicated iodine deficiency according to the WHO criterion (threshold for adequacy = 150 µg/l), and the UI/Creat was also low at 107 µg/g. Only 32 % (n 45) of women reported the use of iodine-containing supplements; users had a higher UI/Creat than non-users (131 µg/g v. 118 µg/g), though this difference was NS in the adjusted analysis (P = 0·37). Of the dietary components, only egg intake was significantly associated with a higher UI/Creat in adjusted analyses (P = 0·018); there was no significant association with milk, dairy products or fish intake. Our results suggest that pregnant women in Cyprus have inadequate iodine status and are at risk of mild-to-moderate iodine deficiency. Further research on dietary sources in this population is required. [ABSTRACT FROM AUTHOR]

Background Mild-to-moderate iodine deficiency, particularly in pregnancy, is prevalent; this is of concern because observational studies have shown negative associations with child neurodevelopment. Although neither the benefits nor the safety of iodine supplementation in pregnancy in areas of mild-to-moderate deficiency are well researched, such supplementation is increasingly being recommended by health authorities in a number of countries. Objectives By reviewing the most recent published data on the effects of iodine supplementation in mildly-to-moderately deficient pregnant women on maternal and infant thyroid function and child cognition, we aimed to determine whether the evidence was sufficient to support recommendations in these areas. Methods A systematic review of randomized controlled trials (RCTs), non-RCT interventions, and observational studies was conducted. To identify relevant articles, we searched the PubMed and Embase databases. We defined mild-to-moderate iodine deficiency as a baseline median urinary iodine concentration (UIC) of 50–149 µg/L. Eligible studies were included in meta-analyses. Results In total, 37 publications were included—10 RCTs, 4 non-RCT interventions, and 23 observational studies. Most studies showed no effect of iodine supplementation on maternal or infant thyroid-stimulating hormone and free thyroxine. Most RCTs found that supplementation reduced maternal thyroglobulin and in 3 RCTs, it prevented or diminished the increase in maternal thyroid volume during pregnancy. Three RCTs addressed child neurodevelopment; only 1 was adequately powered. Meta-analyses of 2 RCTs showed no effect on child cognitive [mean difference (MD): −0.18; 95% CI: −1.22, 0.87], language (MD: 1.28; 95% CI: −0.28, 2.83), or motor scores (MD: 0.28; 95% CI: −1.10, 1.66). Conclusions There is insufficient good-quality evidence to support current recommendations for iodine supplementation in pregnancy in areas of mild-to-moderate deficiency. Well-designed RCTs, with child cognitive outcomes, are needed in pregnant women who are moderately deficient (median UIC < 100 µg/L). Maternal intrathyroidal iodine stores should be considered in future trials by including appropriate measures of preconceptional iodine intake. This review was registered at www.crd.york.ac.uk/prospero as CRD42018100277. [ABSTRACT FROM AUTHOR]

Background: Severe iodine deficiency during pregnancy can cause intellectual disability, presumably through inadequate placental transfer of maternal thyroid hormone to the fetus. The association between mild-to-moderate iodine deficiency and child neurodevelopmental problems is not well understood.Objectives: We investigated the association of maternal iodine status during pregnancy with child attention-deficit hyperactivity disorder (ADHD) and autistic traits.Methods: This was a collaborative study of 3 population-based birth cohorts: Generation R (n = 1634), INfancia y Medio Ambiente (n = 1293), and the Avon Longitudinal Study of Parents and Children (n = 2619). Exclusion criteria were multiple fetuses, fertility treatment, thyroid-interfering medication use, and pre-existing thyroid disease. The mean age of assessment in the cohorts was between 4.4 and 7.7 y for ADHD symptoms and 4.5 and 7.6 y for autistic traits. We studied the association of the urinary iodine-to-creatinine ratio (UI/Creat) <150 μg/g-in all mother-child pairs, and in those with a urinary-iodine measurement at ≤18 weeks and ≤14 weeks of gestation-with the risk of ADHD or a high autistic-trait score (≥93rd percentile cutoff), using logistic regression. The cohort-specific effect estimates were combined by random-effects meta-analyses. We also investigated whether UI/Creat modified the associations of maternal free thyroxine (FT4) or thyroid-stimulating hormone concentrations with ADHD or autistic traits.Results: UI/Creat <150 μg/g was not associated with ADHD (OR: 1.2; 95% CI: 0.7, 2.2; P = 0.56) or with a high autistic-trait score (OR: 0.8; 95% CI: 0.6, 1.1; P = 0.22). UI/Creat <150 μg/g in early pregnancy (i.e., ≤18 weeks or ≤14 weeks of gestation) was not associated with a higher risk of behavioral problems. The association between a higher FT4 and a greater risk of ADHD (OR: 1.3; 95% CI: 1.0, 1.6; P = 0.017) was not modified by iodine status.Conclusions: There is no consistent evidence to support an association of mild-to-moderate iodine deficiency during pregnancy with child ADHD or autistic traits. [ABSTRACT FROM AUTHOR]

Background: Thyroid hormone is essential for optimal fetal brain development. Evidence suggests that both low and high maternal thyroid hormone availability may have adverse effects on child neurodevelopmental outcomes, but the effect on behavioral problems remains unclear. We studied the association of maternal thyrotropin (TSH) and free thyroxine (fT4) concentrations during the first 18 weeks of pregnancy with child attention-deficit hyperactivity disorder (ADHD). Methods: A total of 7669 mother–child pairs with data on maternal thyroid function and child ADHD were selected from three prospective population-based birth cohorts: INfancia y Medio Ambiente (INMA; N = 1073, Spain), Generation R (N = 3812, The Netherlands), and Avon Longitudinal Study of Parents and Children (ALSPAC; N = 2784, United Kingdom). Exclusion criteria were multiple pregnancy, fertility treatment, usage of medication affecting the thyroid, and pre-existing thyroid disease. We used logistic regression models to study the association of maternal thyroid function with the primary outcome, ADHD, assessed via the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV) criteria by parents and/or teachers at a median child age of 4.5 to 7.6 years, and with the secondary outcome, an ADHD symptom score above the 90th percentile. Effect modification by gestational age and sex was tested with interaction terms and stratified analyses. Results: Overall, 233 (3%) children met the criteria for ADHD. When analyzed continuously, neither fT4 nor TSH was associated with a higher risk of ADHD (odds ratio [OR] 1.1, 95% confidence interval [CI 1.0–1.3], p = 0.060 and OR 0.9 [CI 0.9–1.1], p = 0.385, respectively) or with high symptom scores. When investigating effect modification by gestational age, a higher fT4 was associated with symptoms above the 90th percentile but only in the first trimester (for fT4 per 1 SD: OR 1.2 [CI 1.0–1.4], p = 0.027). However, these differential effects by gestational age were not consistent. No significant effect modification by sex was observed. Conclusions: We found no clear evidence of an association between maternal thyroid function and child ADHD. [ABSTRACT FROM AUTHOR]

Iodine deficiency is present in certain groups of the UK population, notably in pregnant women; this is of concern as iodine is required for fetal brain development. UK milk is rich in iodine and is the principal dietary iodine source. UK sales of milk-alternative drinks are increasing but data are lacking on their iodine content. As consumers may replace iodine-rich milk with milk-alternative drinks, we aimed to measure the iodine concentration of those available in the UK. Using inductively coupled plasma-MS, we determined the iodine concentration of seven types of milk-alternative drink (soya, almond, coconut, oat, rice, hazelnut and hemp) by analysing forty-seven products purchased in November/December 2015. For comparison, winter samples of conventional (n 5) and organic (n 5) cows' milk were included. The median iodine concentration of all of the unfortified milk-alternative drinks (n 44) was low, at 7-3 µg/kg, just 1-7% of our value for winter conventional cows' milk (median 438 µg/kg). One brand (not the market leader), fortified its soya, oat and rice drinks with iodine and those drinks had a higher iodine concentration than unfortified drinks, at 280, 287 and 266 µg/kg, respectively. The iodine concentration of organic milk (median 324 µg/kg) was lower than that of conventional milk. Although many milk-alternative drinks are fortified with Ca, at the time of this study, just three of forty-seven drinks were fortified with iodine. Individuals who consume milk-alternative drinks that are not fortified with iodine in place of cows' milk may be at risk of iodine deficiency unless they consume alternative dietary iodine sources. [ABSTRACT FROM AUTHOR]

Seafood intake in pregnancy has been positively associated with childhood cognitive outcomes which could potentially relate to the high vitamin D content of oily fish. However, whether higher maternal vitamin D status (serum 25-hydroxyvitamin D (25(OH)D)) in pregnancy is associated with a reduced risk of offspring suboptimal neurodevelopmental outcomes is unclear. A total of 7065 mother–child pairs were studied from the Avon Longitudinal Study of Parents and Children cohort who had data for both serum total 25(OH)D concentration in pregnancy and at least one measure of offspring neurodevelopment (pre-school development at 6–42 months; ‘Strengths and Difficulties Questionnaire’ scores at 7 years; intelligence quotient (IQ) at 8 years; reading ability at 9 years). After adjustment for confounders, children of vitamin D-deficient mothers (<50·0 nmol/l) were more likely to have scores in the lowest quartile for gross-motor development at 30 months (OR 1·20; 95 % CI 1·03, 1·40), fine-motor development at 30 months (OR 1·23; 95 % CI 1·05, 1·44) and social development at 42 months (OR 1·20; 95 % CI 1·01, 1·41) than vitamin D-sufficient mothers (≥50·0 nmol/l). No associations were found with neurodevelopmental outcomes, including IQ, measured at older ages. However, our results suggest that deficient maternal vitamin D status in pregnancy may have adverse effects on some measures of motor and social development in children under 4 years. Prevention of vitamin D deficiency may be important for preventing suboptimal development in the first 4 years of life. [ABSTRACT FROM AUTHOR]

Background: Though iodine deficiency in pregnancy is a matter of public-health concern, a functional measure of iodine status is lacking. The thyroid-specific protein thyroglobulin (Tg), which reflects thyroid size, has shown promise as a functional measure in studies of children and adults, but data in pregnancy are sparse. In a cohort of mildly to moderately iodine-deficient pregnant women, this study aimed to explore whether serum Tg is a sensitive functional biomarker of iodine status and to examine longitudinal change in Tg with gestational age. Method: A total of 230 pregnant women were recruited at an antenatal clinic at 12 weeks of gestation to the Selenium in PRegnancy INTervention study, in Oxford, United Kingdom. Repeated measures of urinary iodine-to-creatinine ratio, serum thyrotropin (TSH), and Tg at 12, 20, and 35 weeks of gestation were made. Women were dichotomized by their iodine-to-creatinine ratio (<150 or ≥150 μg/g) to group them broadly as iodine deficient or iodine sufficient. Women with thyroid antibodies were excluded; data and samples were available for 191 women. Results: Median Tg concentrations were 21, 19, and 23 μg/L in the first, second, and third trimesters, respectively. In a linear mixed model, controlling for confounders, Tg was higher in the <150 μg/g group than it was in the ≥150 μg/g group ( p < 0.001) but there was no difference in TSH ( p = 0.27). Gestational week modified the effect of iodine status on TSH ( p = 0.01) and Tg ( p = 0.012); Tg did not increase with gestational week in the ≥150 μg/g group, but it did in the <150 μg/g group, and TSH increased more steeply in the <150 μg/g group. Conclusions: Low iodine status (<150 μg/g) in pregnancy is associated with higher serum Tg, suggesting that the thyroid is hyperstimulated by iodine deficiency, which causes it to enlarge. Tg is a more sensitive biomarker of iodine status in pregnancy than is TSH. [ABSTRACT FROM AUTHOR]

Concern has been expressed recently that Se may increase the risk of type 2 diabetes, but this has not been tested in a randomised-controlled trial (RCT) in pregnant women. We took advantage of having stored plasma samples from the Se in Pregnancy Intervention (SPRINT) RCT of Se supplementation in pregnancy to test the effect of Se supplementation on a marker of insulin resistance in UK pregnant women. Because our blood samples were not fasted, we measured plasma adiponectin concentration, a recognised marker of insulin resistance that gives valid measurements in non-fasted samples, as diurnal variability is minor and there is no noticeable effect of food intake. In SPRINT, 230 primiparous UK women were randomised to treatment with Se (60 μg/d) or placebo from 12 weeks of gestation until delivery. We hypothesised that supplementation with Se at a nutritional level would not exacerbate the fall in adiponectin concentration that occurs in normal pregnancy, indicating the lack of an adverse effect on insulin resistance. Indeed, there was no significant difference between the two groups in the change in adiponectin from 12 to 35 weeks (P=0·938), nor when the analysis was restricted to the bottom or top quartiles of baseline whole-blood Se (P=0·515 and 0·858, respectively). Cross-sectionally, adiponectin concentration was not associated with any parameter of Se status, either at 12 or 35 weeks. It is reassuring that a nutritional dose of Se had no adverse effect on the concentration of adiponectin, a biomarker of insulin resistance, in pregnant women of modest Se status. [ABSTRACT FROM AUTHOR]

Background: Low selenium status in pregnancy has been associated with a number of adverse conditions. In nonpregnant populations, the selenium status or response to supplementation has been associated with polymorphisms in dimethylglycine dehydrogenase (DMGDH), selenoprotein P (SEPP1) and the glutathione peroxidases [cytosolic glutathione peroxidase (GPx1) and phospholipid glutathione peroxidase (GPx4)]. Objective: We hypothesized that, in pregnant women, these candidate polymorphisms would be associated with selenium status in early pregnancy, its longitudinal change, and the interindividual response to selenium supplementation at 60 μg/d. Design: With the use of stored samples and data from the United Kingdom Selenium in Pregnancy Intervention (SPRINT) study in 227 pregnant women, we carried out genetic-association studies, testing for associations between selenium status, its longitudinal change, and response to supplementation and common genetic variation in DMGDH (rs921943), SEPP1 (rs3877899 and rs7579), GPx1 (rs1050450) and GPx4 (rs713041). Selenium status was represented by the concentration of whole-blood selenium at 12 and 35 wk of gestation, the concentration of toenail selenium at 16 wk of gestation, and plasma glutathione peroxidase (GPx3) activity at 12 and 35 wk of gestation. Results: Our results showed that DMGDH rs921943 was significantly associated with the whole-blood selenium concentration at 12 wk of gestation (P = 0.032), which explained ≤2.0% of the variance. This association was replicated with the use of toenail selenium (P = 0.043). In unsupplemented women, SEPP1 rs3877899 was significantly associated with the percentage change in whole-blood selenium from 12 to 35 wk of gestation (P = 0.005), which explained 8% of the variance. In supplemented women, SEPP1 rs3877899 was significantly associated with the percentage change in GPx3 activity from 12 to 35 wk of gestation (P = 0.01), which explained 5.3% of the variance. Selenium status was not associated with GPx1, GPx4, or SEPP1 rs7579. Conclusions: In agreement with previous studies, we show that the genetic variant rs921943 in DMGDH is significantly associated with selenium status in United Kingdom pregnant women. Notably, our study shows that women who carry the SEPP1 rs3877899 A allele are better able to maintain selenium status during pregnancy, and their GPx3 activity increases more with supplementation, which suggests better protection from low selenium status. The SPRINT study was registered at www.isrctn.com as ISRCTN37927591. [ABSTRACT FROM AUTHOR]

Adequate iodine intake is important during pregnancy as it is a component of the thyroid hormones that are crucial for fetal brain and neurological development. While randomized controlled trials in severe iodine deficiency have shown that iodine deficiency in pregnancy causes impaired offspring cognition, less is known of the effects in regions of mild/mild-to-moderate deficiency. The United Kingdom is now classified as mildly iodine deficient by the World Health Organization, based on a 2011 national study of 14-15-year-old schoolgirls. As pregnancy is the most critical time for brain development, we evaluated iodine status in pregnant women in Surrey (n = 100) and Oxford (n = 230). The median urinary iodine concentration was 85.3 μg/L in Surrey women, considerably lower than the WHO/United Nations Children's Fund/International Council for the Control of Iodine Deficiency Disorders cut-off of 150 μg/L. Oxford women had similarly low status. We investigated whether that level of iodine deficiency was associated with adverse child cognitive effects using stored samples and data from the Avon Longitudinal Study of Parents and Children cohort. In adjusted analyses, we found a significant association between low maternal iodine status in early pregnancy (urinary iodine-to-creatinine ratio <150 μg/g) such that children had an approximately 60% greater risk of being in the bottom quartile of scores for verbal intelligence quotient, reading accuracy and comprehension. UK women who might become pregnant should ensure they have adequate iodine status to avoid compromising their children's brain development. [ABSTRACT FROM AUTHOR]

Background: Iodine is required throughout pregnancy for thyroid hormone production, which is essential for fetal brain development. Studies of iodine status in pregnant women from the United Kingdom (UK) have focused on early gestation (<16 wk). Data on the effect of advancing gestation on urinary iodine excretion are conflicting, with suggestions of both an increase and a decrease. Objectives: The aims were to evaluate iodine status in a cohort of UK pregnant women and to explore how it changes throughout gestation. Design: We used samples and data from 230 UK pregnant women who were recruited to the Selenium in PRegnancy INTervention study. Iodine concentration was measured in spot-urine samples that were collected at ~12, 20, and 35 wk of gestation; creatinine concentration was also measured to correct for urine dilution. A linear mixed model was used to explore the effect of gestational week on iodine-to-creatinine ratio, with change in season, body mass index, daily milk intake, and maternal age controlled for. Results: The median urinary iodine concentration from urine samples collected at all time points (n = 662) was 56.8 mg/L, and the iodine-to-creatinine ratio was 116 mg/g, thus classifying this cohort as mildly-to-moderately iodine deficient. The median iodine-to-creatinine ratios at 12, 20, and 35 wk were 102.5, 120.0, and 126.0 mg/g, respectively. Only 3% of women were taking iodine-containing prenatal supplements. The iodine-to-creatinine ratio increased with advancing gestation, and there was a significant interaction between gestational week and season (P = 0.026). For a 1-wk increase in gestation, the iodine-to-creatinine ratio increased by a factor of 1.05 (95% CI: 1.02, 1.08) in winter and by a factor of 1.04 (95% CI: 1.00, 1.08) in summer. Conclusions: This group of UK pregnant women was mildly-to-moderately iodine deficient at all trimesters, which is of public health concern. The finding that the iodine-to-creatinine ratio increased over the course of gestation may not be generalizable to populations with different iodine status from ours and merits further investigation. This trial was registered at www.isrctn.com as ISRCTN37927591. [ABSTRACT FROM AUTHOR]

Dietary intake/status of the trace mineral Se may affect the risk of developing hypertensive conditions of pregnancy, i.e. pre-eclampsia and pregnancy-induced hypertension (PE/PIH). In the present study, we evaluated Se status in UK pregnant women to establish whether pre-pregnant Se status or Se supplementation affected the risk of developing PE/PIH. The samples originated from the SPRINT (Selenium in PRegnancy INTervention) study that randomised 230 UK primiparous women to treatment with Se (60 μg/d) or placebo from 12 weeks of gestation. Whole-blood Se concentration was measured at 12 and 35 weeks, toenail Se concentration at 16 weeks, plasma selenoprotein P (SEPP1) concentration at 35 weeks and plasma glutathione peroxidase (GPx3) activity at 12, 20 and 35 weeks. Demographic data were collected at baseline. Participants completed a FFQ. UK pregnant women had whole-blood Se concentration lower than the mid-range of other populations, toenail Se concentration considerably lower than US women, GPx3 activity considerably lower than US and Australian pregnant women, and low baseline SEPP1 concentration (median 3·00, range 0·90–5·80 mg/l). Maternal age, education and social class were positively associated with Se status. After adjustment, whole-blood Se concentration was higher in women consuming Brazil nuts (P= 0·040) and in those consuming more than two seafood portions per week (P= 0·054). A stepwise logistic regression model revealed that among the Se-related risk factors, only toenail Se (OR 0·38, 95 % CI 0·17, 0·87, P= 0·021) significantly affected the OR for PE/PIH. On excluding non-compliers with Se treatment, Se supplementation also significantly reduced the OR for PE/PIH (OR 0·30, 95 % CI 0·09, 1·00, P= 0·049). In conclusion, UK women have low Se status that increases their risk of developing PE/PIH. Therefore, UK women of childbearing age need to improve their Se status. [ABSTRACT FROM PUBLISHER]

As intra-thyroidal iodine stores should be maximised before conception to facilitate the increased thyroid hormone production during pregnancy, women who are planning to become pregnant should ideally consume 150 μg iodine/d (US RDA). As few UK data exist for this population group, a cross-sectional study was carried out at the University of Surrey to assess the iodine intake and status of women of childbearing age. Total iodine excretion was measured from 24 h urine samples in fifty-seven women; iodine intake was estimated by assuming that 90 % of ingested iodine was excreted. The average iodine intake was also estimated from 48 h food diaries that the participants completed. The median urinary iodine concentration value (63·1 μg/l) indicated the group to be mildly iodine deficient by WHO criteria. By contrast, the median 24 h urinary iodine excretion value (149·8 μg/24 h) indicated a relatively low risk of iodine deficiency. The median estimated iodine intake, extrapolated from urinary excretion, was 167 μg/d, whereas it was lower, at 123 μg/d, when estimated from the 48 h food diaries. Iodine intake estimated from the food diaries and 24 h urinary iodine excretion were strongly correlated (r 0·75, P< 0·001). The intake of milk, eggs and dairy products was positively associated with iodine status. The iodine status of this UK cohort is probably a best-case scenario as the women were mostly nutrition students and were recruited in the winter when milk-iodine content is at its highest; further study in more representative cohorts of UK women is required. The present study highlights the need for revised cut-off values for iodine deficiency that are method- and age group-specific. [ABSTRACT FROM PUBLISHER]

Pre-eclampsia is a serious hypertensive condition of pregnancy associated with high maternal and fetal morbidity and mortality. Se intake or status has been linked to the occurrence of pre-eclampsia by our own work and that of others. We hypothesised that a small increase in the Se intake of UK pregnant women of inadequate Se status would protect against the risk of pre-eclampsia, as assessed by biomarkers of pre-eclampsia. In a double-blind, placebo-controlled, pilot trial, we randomised 230 primiparous pregnant women to Se (60 μg/d, as Se-enriched yeast) or placebo treatment from 12 to 14 weeks of gestation until delivery. Whole-blood Se concentration was measured at baseline and 35 weeks, and plasma selenoprotein P (SEPP1) concentration at 35 weeks. The primary outcome measure of the present study was serum soluble vascular endothelial growth factor receptor-1 (sFlt-1), an anti-angiogenic factor linked with the risk of pre-eclampsia. Other serum/plasma components related to the risk of pre-eclampsia were also measured. Between 12 and 35 weeks, whole-blood Se concentration increased significantly in the Se-treated group but decreased significantly in the placebo group. At 35 weeks, significantly higher concentrations of whole-blood Se and plasma SEPP1 were observed in the Se-treated group than in the placebo group. In line with our hypothesis, the concentration of sFlt-1 was significantly lower at 35 weeks in the Se-treated group than in the placebo group in participants in the lowest quartile of Se status at baseline (P= 0·039). None of the secondary outcome measures was significantly affected by treatment. The present finding that Se supplementation has the potential to reduce the risk of pre-eclampsia in pregnant women of low Se status needs to be validated in an adequately powered trial. [ABSTRACT FROM PUBLISHER]

Iodine is a key component of the thyroid hormones which are crucial for brain development. Adequate intake of iodine in pregnancy is important as in utero deficiency may have lifelong consequences for the offspring. Data on the iodine status of UK pregnant women are sparse, and there are no such data for pregnant women in the South East of the UK. A total of 100 pregnant women were recruited to a cross-sectional study carried out at the Royal Surrey County Hospital, Guildford, at their first-trimester visit for an ultrasound scan. The participants provided a spot-urine sample (for the measurement of urinary iodine concentration (UIC) and creatinine concentration) and 24 h iodine excretion was estimated from the urinary iodine:creatinine ratio. Women completed a general questionnaire and a FFQ. The median UIC (85·3 μg/l) indicated that the group was iodine deficient by World Health Organisation criteria. The median values of the iodine:creatinine ratio (122·9 μg/g) and of the estimated 24 h iodine excretion (151·2 μg/d) were also suggestive of iodine deficiency. UIC was significantly higher in women taking an iodine-containing prenatal supplement (n 42) than in those not taking such a supplement (P< 0·001). In the adjusted analyses, milk intake, maternal age and iodine-containing prenatal supplement use were positively associated with the estimated 24 h urinary iodine excretion. Our finding of iodine deficiency in these women gives cause for concern. We suggest that women of childbearing age and pregnant women should be given advice on how to improve their iodine status through dietary means. A national survey of iodine status in UK pregnant women is required. [ABSTRACT FROM PUBLISHER]

This review describes historical iodine deficiency in the UK, gives current information on dietary sources of iodine and summarises recent evidence of iodine deficiency and its association with child neurodevelopment. Iodine is required for the production of thyroid hormones that are needed for brain development, particularly during pregnancy. Iodine deficiency is a leading cause of preventable brain damage worldwide and is associated with impaired cognitive function. Despite a global focus on the elimination of iodine deficiency, iodine is a largely overlooked nutrient in the UK, a situation we have endeavoured to address through a series of studies. Although the UK has been considered iodine-sufficient for many years, there is now concern that iodine deficiency may be prevalent, particularly in pregnant women and women of childbearing age; indeed we found mild-to-moderate iodine deficiency in pregnant women in Surrey. As the major dietary source of iodine in the UK is milk and dairy produce, it is relevant to note that we have found the iodine concentration of organic milk to be over 40% lower than that of conventional milk. In contrast to many countries, iodised table salt is unlikely to contribute to UK iodine intake as we have shown that its availability is low in grocery stores. This situation is of concern as the level of UK iodine deficiency is such that it is associated with adverse effects on offspring neurological development; we demonstrated a higher risk of low IQ and poorer reading-accuracy scores in UK children born to mothers who were iodine-deficient during pregnancy. Given our findings and those of others, iodine status in the UK population should be monitored, particularly in vulnerable subgroups such as pregnant women and children. [ABSTRACT FROM PUBLISHER]

Background: Preterm birth occurs in 5%-13% of pregnancies. It is a leading cause of perinatal mortality and morbidity and has adverse long-term consequences for the health of the child. Because of the role selenium plays in attenuating inflammation, and because low concentrations of selenium have been found in women with preeclampsia, we hypothesized that low maternal selenium status during early gestation would increase the risk of preterm birth. Methods: White Dutch women with a singleton pregnancy (n = 1197) were followed prospectively from 12 weeks' gestation. Women with thyroid disease or type 1 diabetes were excluded. At delivery, 1129 women had complete birth-outcome data. Serum concentrations of selenium were measured during the 12th week of pregnancy. Deliveries were classified as preterm or term, and preterm births were subcategorized as iatrogenic, spontaneous or the result of premature rupture of the membranes. Results: Of the 60 women (5.3%) who had a preterm birth, 21 had premature rupture of the membranes and 13 had preeclampsia. The serum selenium concentration at 12 weeks' gestation was significantly lower among women who had a preterm birth than among those who delivered at term (mean 0.96 [standard deviation (SD) 0.14] µmol/L v. 1.02 [SD 0.13] µmol/L; t = 2.9, p = 0.001). Women were grouped by quartile of serum selenium concentration at 12 weeks' gestation. The number of women who had a preterm birth significantly differed by quartile (X2 = 8.01, 3 degrees of freedom], p < 0.05). Women in the lowest quartile of serum selenium had twice the risk of preterm birth as women in the upper three quartiles, even after adjustment for the occurrence of preeclampsia (adjusted odds ratio 2.18, 95% confidence interval 1.25-3.77). Interpretation: Having low serum selenium at the end of the first trimester was related to preterm birth and was independent of the mother having preeclampsia. Low maternal selenium status during early gestation may increase the risk of preterm premature rupture of the membranes, which is a major cause of preterm birth. [ABSTRACT FROM AUTHOR]

Objective. Postpartum depression is a common complication of childbirth, and its prevention is an important public-health issue because of its negative effects on mother, infant, and family. The present randomized, double-blind, placebo-controlled trial was conducted to examine the effect of prenatal selenium supplementation on the postpartum depression level in Iranian women. Design. A total of 166 primigravid pregnant women in the first trimester of pregnancy, were randomized to receive 100 μg of selenium ( n = 83) or a placebo ( n = 83) per day until delivery. The symptoms of postpartum depression were evaluated during the eight weeks following delivery by means of the Edinburgh Postnatal Depression Scale (EPDS). Serum selenium concentrations were measured at baseline and at the end of study. Results. There was no significant difference in demographic characteristics and perceived social support between the selenium and control groups at baseline ( p > 0.05). There were 22 drop-outs in the selenium-supplemented group and 19 in the placebo group. Forty-four women in the selenium group and 41 women in the placebo group completed the trial and the EPDS questionnaire. Selenium supplementation was associated with a significant increase in mean serum selenium concentration at term ( p < 0.001) but remained unchanged in the control group. The mean EPDS score in the selenium group was significantly lower than that of the control group ( p < 0.05). Conclusion. These findings suggest that supplementation with selenium during pregnancy might be an effective approach for the prevention of postpartum depression. [ABSTRACT FROM AUTHOR]

Objective: We assessed the impact of selenium, a trace element with antioxidant properties on a simple measure of oxidative stress in pregnant women. Study design: A novel assay of prooxidant-antioxidant balance (PAB) was applied in a double-blind, placebo-controlled study of selenium supplementation in pregnancy. We measured the prooxidant burden and the antioxidant capacity simultaneously in one assay, thereby calculating a redox index. A total of 166 primigravid pregnant women in the first trimester of pregnancy, were randomized to receive 100 μg of selenium (n=83) or placebo (n=83) per day until delivery. PAB values and serum selenium concentrations were measured at baseline and at the end of study. Results: Pretreatment demographic data and biochemical indices including serum selenium concentrations did not differ significantly between the groups. The drop-out rates for the groups were 22/83 and 19/83 for the selenium and placebo groups, respectively. Supplementation with selenium was associated with a significant increase in mean serum selenium concentration (P<0.001) but without significant change in mean PAB value. In contrast, mean serum selenium concentration remained unchanged and mean PAB values increased significantly (P<0.05 in the control group). Conclusion: Our findings suggest that selenium supplementation may reduce oxidative stress associated with pregnancy. [ABSTRACT FROM AUTHOR]

Purpose. To compare the nutritional status of infertile women with non-pregnant fertile age-matched controls and to assess the periconceptional intake of nutritional supplements in pregnancy with an estimation of total micronutrient (diet and supplementary) intake. Design. An assessment of the nutritional status of infertile women and fertile, age-matched non-pregnant controls and a survey of the periconceptional intake of folic acid and other nutritional supplements. Materials and methods. Group 1: a 7-day weighed diet diary and blood tests for magnesium, mineral and pyridoxine status were used to assess the nutritional status of six infertile women and 12 non-pregnant, healthy, age-matched controls. Group 2: the periconceptional dietary intake of folic acid and other nutritional supplements was estimated in 87 pregnant women attending midwife clinics, 36 women attending an assisted conception clinic and 7 women attending a self help group for lesbian pregnancy. Results. In the group of six infertile subjects and 12 fertile controls, there was a non-significant trend for micronutrient intake in the controls to be higher than for the infertile subjects. Comparisons with the UK reference nutrient intake confirmed suboptimal nutrition in all subjects and some controls. Twenty-five per cent of controls and 33% of infertile subjects had subnormal serum selenium consistent with reduced antioxidant defence. There was also a non-significant trend for non-caeruloplasmin copper and cadmium to be higher in the infertile subjects. The combined mean dietary intake for all subjects and controls was similar to the values from the National Diet and Nutrition Survey. Therefore, an approximate value for the total intake of nutrients (diet and supplementation) of the 130 women in the larger survey was calculated using the mean dietary intake of the smaller group as an estimate of the dietary component. This analysis suggested suboptimal total intake for >50% of the subjects for selenium, zinc, magnesium and iodine and borderline total intake for >50% of subjects for vitamins B12, C and E, betacarotene, iron, folate + folic acid and essential fatty acids. Conclusions. Current levels of supplementation with folic acid and other nutrients are failing to compensate for poor mean dietary intake of these nutrients at the time of conception. These nutritional deficiencies are probably important contributory factors in infertility, spontaneous abortion, pregnancy complications and post-partum health problems in the mother and infant (including congenital malformations and postnatal depression). [ABSTRACT FROM AUTHOR]

Background. In view of plans for dietary fortification with folic acid, there is a need to reassess the advice being given in primary care. Patients and professionals may assume that fortification will make preconceptional folic acid supplementation unnecessary, but this is unlikely to be correct. Aim. To calculate the intake of total folic acid and folate at conception and to estimate the impact of fortification on the incidence of neural tube defect (NTD) conceptions. Design. An in-depth investigation of dietary folate intake of 18 women and a survey of preconception supplementation in a group of 130 women, including an assessment of the probable impact of mandatory fortification. Method. Dietary folate intake of six infertile women and 12 age-matched fertile controls was assessed using a 7-day weighed diet diary. Mean values for this group were used as an estimate of local dietary folate intake. Questionnaires about periconceptional intake of supplements that included folic acid in their formulation were given to newly pregnant women attending district midwife clinics, a series of women attending an assisted conception unit and a self-help group of lesbians who were either pregnant or planning a pregnancy. Results. Of the 18 women in the dietary study there was suboptimal dietary folate intake in all infertile subjects and in eight of 12 controls. An approximate value for the combined intake of dietary folate and folic acid in the larger survey (n = 130) was calculated. We estimated that UK dietary fortification will double the number of pregnancies with adequate total folate intake. From previous data on folic acid intake and NTD births we estimate that this will prevent 226-343 conceptions per year in the UK from developing NTD malformations. Conclusions. Fortification should prevent approximately 226-343 conceptions a year from developing NTDs, but 45% of women will still have an inadequate total folate intake, unless supplementation levels improve. [ABSTRACT FROM AUTHOR]