Sheila Skeaff

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.

Iodine Deficiency in Pregnancy: The Effect on Neurodevelopment in the Child

Iodine is an integral part of the thyroid hormones, thyroxine (T4) and tri-iodothyronine (T3), necessary for normal growth and development. An adequate supply of cerebral T3, generated in the fetal brain from maternal free T4 (fT4), 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 fT4) 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.

Thyroglobulin as a Biomarker of Iodine Deficiency: A Review

BACKGROUND Thyroglobulin, produced exclusively by the thyroid gland, has been proposed to be a more sensitive biomarker of iodine status than thyrotropin or the thyroid hormones triiodothyronine and thyroxine. However, evidence on the usefulness of thyroglobulin (Tg) to assess iodine status has not been extensively reviewed, particularly in pregnant women and adults. SUMMARY An electronic literature search was conducted using the Cochrane CENTRAL, Web of Science, PubMed, and Medline to locate relevant studies on Tg as a biomarker of iodine status. Since urinary iodine concentration (UIC) is the recommended method to assess iodine status in populations, only studies that clearly reported both Tg and UIC were included. For the purpose of this review, a median Tg <13 μg/L and a median UIC ≥100 μg/L (UIC ≥150 μg/L for pregnant women) were used to indicate adequate iodine status. We excluded studies conducted in subjects with either known thyroid disease or those with thyroglobulin antibodies. The search strategy and selection criteria yielded 34 articles of which nine were intervention studies. The majority of studies (six of eight) reported that iodine-deficient pregnant women had a median Tg ≥13 μg/L. However, large observational studies of pregnant women, including women with adequate and inadequate iodine status, as well as well-designed intervention trials that include both Tg and UIC, are needed. In adults, the results were equivocal because iodine-deficient adults were reported to have median Tg values of either <13 or ≥13 μg/L. Only studies in school-aged children showed that iodine-sufficient children typically had a median Tg <13 μg/L. Some of the inconsistent results may be partially explained by the use of different methodological assays and failure to assess assay accuracy using a certified reference material. CONCLUSIONS These data suggest that Tg does hold promise as a biomarker of iodine deficiency. However, it is associated with limitations. A median Tg cutoff of 13 μg/L warrants further investigation, particularly in adults or pregnant women, as there is a lack of both observational and intervention studies in these groups.

Dietary intakes of 6-24-month-old urban South Island New Zealand children in relation to biochemical iron status.

OBJECTIVE To investigate food sources and intakes of iron, and dietary factors associated with serum ferritin levels in 6-24-month-old children. DESIGN A cross-sectional survey employing proportionate cluster sampling was conducted in 1998/1999. Dietary intakes were assessed using a non-consecutive 3-day weighed food record. Serum ferritin and C-reactive protein were analysed from non-fasting venepuncture blood samples and general sociodemographic data were collected. SETTING Cities of Christchurch, Dunedin and Invercargill, New Zealand. SUBJECTS Randomly selected healthy 6-24-month-old non-breast-feeding children (n = 226). RESULTS Total iron intakes (+/- standard deviation (SD)) among non-breast-feeding infants (< 12 months old; n = 42) and toddlers (> or = 12 months old; n = 184) were 8.4 +/- 2.9 mg day(-1) and 5.0 +/- 2.5 mg day(-1), respectively. Fifteen per cent of infants and 66% of toddlers were at risk of inadequate iron intakes. Main sources of dietary iron were infant formula (60%) for infants and cereals (31%) for toddlers. Meat contributed on average 2% and 10% of dietary iron in the infant and toddler diets, respectively. Dietary factors positively associated with serum ferritin were intakes of iron and vitamin C, whereas intakes of calcium and dietary fibre were negatively associated. For each 1% increase in percentage of energy from iron-fortified formula concomitant with a 1% decrease from dairy products, there was a 4.2% increased odds of replete iron stores (ferritin > or = 20 microg l(-1)). CONCLUSIONS Toddlers were at higher risk of sub-optimal iron intakes than infants. Results suggest that a diet high in bioavailable iron is important for optimising the iron stores of young children in New Zealand.

Mild iodine deficiency in a sample of New Zealand schoolchildren.

Objective: To assess the iodine status of New Zealand schoolchildren.Design: A proportionate to population size school-based cluster survey was used to randomly select children from two cities. The indicators used to assess iodine status were urinary iodine, as determined in a casual urine sample, and thyroid volume, as measured by ultrasonography. A qualitative food frequency questionnaire designed to ascertain frequency of consumption over the previous 3 months of foods or food groups that are good sources of dietary iodine, including iodized salt, was administered to each child.Setting: Dunedin and Wellington, New Zealand.Participants: Three-hundred children aged 8–10 y from 30 schools.Results: The median urinary iodine concentration of the children was 6.6 µg/dl (interquartile range, 4.5–9.1). The percentage of children who had urinary iodine levels less than 5 µg/dl was 31.4 (95% confidence interval (CI), 24.2–38.6). Comparison of thyroid volume with 2001 World Health Organization age/sex-specific and age/BSA-specific cut-off values resulted in a goitre prevalence of 11.3% (95% CI, 7.6–15.1) and 12.0% (95% CI, 7.9–16.1), respectively. Almost 30% of the childrens caregivers did not use iodized salt in cooking and 51% of the children did not use iodized salt at the table.Conclusions: Mild iodine deficiency was found in this sample of children. Iodized table salt may no longer be making a significant contribution to the iodine intakes of New Zealand children.Sponsorship: This research was funded by the Health Research Council of New Zealand and the Ministry of Health in New Zealand.

Summary of an NIH Workshop to Identify Research Needs to Improve the Monitoring of Iodine Status in the United States and to Inform the DRI

The Office of Dietary Supplements (ODS) at the NIH sponsored a workshop on May 12-13, 2011, to bring together representatives from various NIH institutes and centers as a first step in developing an NIH iodine research initiative. The workshop also provided an opportunity to identify research needs that would inform the dietary reference intakes for iodine, which were last revised in 2001. Iodine is required throughout the life cycle, but pregnant women and infants are the populations most at risk of deficiency, because iodine is required for normal brain development and growth. The CDC monitors iodine status of the population on a regular basis, but the status of the most vulnerable populations remains uncertain. The NIH funds very little investigator-initiated research relevant to iodine and human nutrition, but the ODS has worked for several years with a number of other U.S. government agencies to develop many of the resources needed to conduct iodine research of high quality (e.g., validated analytical methods and reference materials for multiple types of samples). Iodine experts, scientists from several U.S. government agencies, and NIH representatives met for 2 d to identify iodine research needs appropriate to the NIH mission.

Selenium and iodine supplementation: effect on thyroid function of older New Zealanders.

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.

Iodine fortification: why, when, what, how, and who?

Purpose of reviewTo highlight current issues regarding the role of iodine fortification in correcting and preventing iodine deficiency. Universal salt iodization (USI) is recommended, wherein all salt is iodized; however, a more graduated approach may be warranted. Recent findingsIodine deficiency is widespread and has re-emerged in countries such as Australia, New Zealand and the UK. As well as supplementation in groups such as pregnant and lactating women who have increased iodine requirements, public health strategies to improve iodine intakes include voluntary or mandatory fortification of the food supply. A key player in the process of fortification is the food industry, wherein misperceptions that the addition of iodized salt to foods alters taste and colour still persist and legislation in some countries that prohibits its addition to manufactured foods, can result in a reluctance to support USI. SummaryAmeliorating iodine deficiency on a population level in countries with mild-to-moderate deficiency is warranted. Risk of both inadequate and excess iodine intakes requires regular monitoring to accompany fortification programmes as well as strategies to address subpopulations at risk. More sensitive indicators of recent iodine status are needed to rapidly assess the impact of fortification on improving the status.

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 Childrens 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.

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.