Salivary iodine concentrations (SIC) and urinary iodine concentrations are correlated. This study aimed to verify the use of SIC as a biomarker for estimating iodine intake in pregnant and lactating women and to diagnose abnormal thyroid function. A cross-sectional study was conducted in northern Xinjiang, China. Participants provided venous blood, random urine, saliva and milk samples. A total of 607 pregnant and 171 lactating women volunteered to participate in the study. The average daily iodine intake was calculated for each participant. Pregnant women were divided according to trimester. The median daily iodine intake was 436·41 μg/d in the first trimester, 425·83 μg/d in the second trimester and 430·56 μg/d in the third trimester. The average daily iodine intake in lactating women was 416·16 μg/d. Different indicators were used to diagnose excessive iodine intake (> 500 μg/d). Among pregnant women, SIC had an AUC of 0·62 (P < 0·01), sensitivity of 51·75 % and specificity of 65 %. Among lactating women, SIC had an AUC of 0·63 (P = 0·03), sensitivity of 43·52 % and specificity of 85 %. SIC was an effective biomarker for diagnosing abnormal thyroid function (P = 0·03). In conclusion, this study demonstrated that SIC is a reliable biomarker for evaluating both iodine nutrition status and abnormal thyroid function in pregnant and lactating women.

The aim of this study was to explore the status of thyroid peroxidase antibody (TPOAb) and thyroglobulin antibody (TGAb) in three areas with differing water iodine concentrations; and to discuss the relationships between these two thyroid antibodies and thyroid diseases in the three areas. We investigated 2503 adults from three areas. Urinary iodine concentrations, thyroid stimulating hormone (TSH), free thyroxine (FT4), free triiodothyronine (FT3), TPOAb, TGAb and thyroid volume (TV) were measured, and thyroid ultrasonography was performed. The positivity rates of TGAb(+), TPOAb(+) and TGAb(+) and TPOAb(+) or TGAb(+) were significantly higher in iodine fortification (IF) areas than iodine adequate (IA) areas (all P < 0·05). In IF and iodine excess areas, the positivity rates of TPOAb(+), TGAb(+) and TPOAb(+) or TGAb(+) significantly increased with age (all P for trend < 0·05). The levels of TSH, TV and the prevalence of overt hypothyroidism, subclinical hypothyroidism and goitre were significantly elevated in the thyroid antibody-positive groups in the three areas, but the FT3 was diminished (all P < 0·010). Positivity for TPOAb and TGAb was associated with an increased risk of subclinical hypothyroidism in the three areas. In areas with different median water iodine, positivity for both TPOAb and TGAb was associated with elevated TSH values. Notably, with the increased levels of TPOAb, the frequency of abnormally elevated TSH increased dramatically in the three areas.

Adequate iodine nutrition during infancy is required for normal thyroid function and, subsequently, brain development. However, data on infant iodine status in the first year of life are scarce. This study aimed to describe infant iodine status and further explore its associations with maternal iodine nutrition, breast-feeding status and thyroid function. In this cohort study, 113 infants were followed up at ages 3, 6 and 11 months in Norway. Infant and maternal urinary iodine concentration (UIC), maternal iodine intake, breast milk iodine concentration (BMIC), breast-feeding status and infant thyroid function tests were measured. The median infant UIC was 82 µg/l at the age of 3 months and below the WHO cut-off of 100 µg/l. Infant UIC was adequate later in infancy (median 110 µg/l at ages 6 and 11 months). Infant UIC was associated positively with maternal UIC (β = 0·33, 95 % CI (0·12, 0·54)), maternal iodine intake (β = 0·30, 95 % CI (0·18, 0·42)) and BMIC (β = 0·46, 95 % CI (0·13, 0·79)). Breastfed infants had lower median UIC compared with formula-fed infants at ages 3 months (76 v. 190 µg/l) and 6 months (105 v. 315 µg/l). Neither infant UIC nor BMIC were associated with infant thyroid function tests. In conclusion, breastfed infants in Norway are at risk of insufficient iodine intake during the first months of life. Maternal iodine nutrition is important for providing sufficient iodine intake in infants, and awareness of promoting adequate iodine nutrition for lactating women should be prioritised.

Maternal thyroid hormones facilitate optimal foetal neurodevelopment; however, the exact role of the thyroid hormones on specific cognitive outcomes is unknown. The present study aimed to investigate associations between maternal thyroid function and neurodevelopmental outcomes in the Seychelles Child Development Study (SCDS) Nutrition 2 cohort (n 1328). Maternal free thyroid hormones (fT3, fT4 and fTSH) were assessed at 28 weeks’ gestation with a range of child cognitive outcomes analysed at 20 months. Dietary iodine intake was analysed for a subset of women through a Food Frequency Questionnaire. Linear regression analysis was used to test associations between serum concentrations of maternal thyroid hormones and child neurodevelopment outcomes. Thyroid hormones were analysed as continuous data and categorised as quintiles. 95% of mothers had optimal thyroid function based on fTSH concentrations. Overall, the present study shows that maternal thyroid function is not associated with neurodevelopmental outcomes in this high fish-eating population. However, a positive association, using quintiles for fT3, was reported for the Mental Developmental Index, between Q3 v. Q4 (β 0⋅073; P 0⋅043) and for Q3 v. Q5 (β value 0⋅086; P 0⋅018). To conclude, mothers in our cohort, who largely have optimal thyroid function and iodine intakes, appear able to regulate thyroid function throughout pregnancy to meet neurodevelopmental needs. However, it is possible that minor imbalances of fT3, as indicated from our secondary analysis, may impact offspring neurodevelopment. Further investigation of the relationship between maternal thyroid function and infant neurodevelopment is warranted, particularly in populations with different dietary patterns and thereby iodine intakes.

The present study reports on first-trimester reference ranges of plasma mineral Se/Zn/Cu concentration in relation to free thyroxine (FT4), thyrotropin (TSH) and thyroid peroxidase antibodies (TPO-Ab), assessed at 12 weeks’ gestation in 2041 pregnant women, including 544 women not taking supplements containing Se/Zn/Cu. The reference range (2·5th–97·5th percentiles) in these 544 women was 0·72–1·25 µmol/l for Se, 17·15–35·98 µmol/l for Cu and 9·57–16·41 µmol/l for Zn. These women had significantly lower mean plasma Se concentration (0·94 (sd 0·12) µmol/l) than those (n 1479) taking Se/Zn/Cu supplements (1·03 (sd 0·14) µmol/l; P < 0·001), while the mean Cu (26·25 µmol/l) and Zn (12·55 µmol/l) concentrations were almost identical in these sub-groups. Women with hypothyroxinaemia (FT4 below reference range with normal TSH) had significantly lower plasma Zn concentrations than euthyroid women. After adjusting for covariates including supplement intake, plasma Se (negatively), Zn and Cu (positively) concentrations were significantly related to logFT4; Se and Cu (but not Zn) were positively and significantly related to logTSH. Women taking additional Se/Zn/Cu supplements were 1·46 (95 % CI 1·09, 2·04) times less likely to have elevated titres of TPO-Ab at 12 weeks of gestation. We conclude that first-trimester Se reference ranges are influenced by Se-supplement intake, while Cu and Zn ranges are not. Plasma mineral Se/Zn/Cu concentrations are associated with thyroid FT4 and TSH concentrations. Se/Zn/Cu supplement intake affects TPO-Ab status. Future research should focus on the impact of trace mineral status during gestation on thyroid function.

Iodine intake affects the occurrence of thyroid disorders. However, the association of iodine intake with longevity remains to be described. This led us to perform a 20 years’ follow-up on participants from the Randers–Skagen (RaSk) study. Residents in Randers born in 1920 (n 210) and Skagen born in 1918–1923 (n 218) were included in a clinical study in 1997–1998. Mean iodine content in drinking water was 2 µg/l in Randers and 139 µg/l in Skagen. We collected baseline data through questionnaires, performed physical examinations and measured iodine concentrations in spot urine samples. Income data were retrieved from Danish registries. We performed follow-up on mortality until 31 December 2017 using Danish registries. Complete follow-up data were available on 428 out of 430 of participants (99·5 %). At baseline, the median urinary iodine concentration was 55 µg/l in Randers and 160 µg/l in Skagen residents. Participants were long-term residents with 72·8 and 92·7 % residing for more than 25 years in Randers and Skagen, respectively. Cox regression showed that living in Skagen compared with Randers was associated with a lower hazard ratio (HR) of death in both age- and sex-adjusted analyses (HR 0·60, 95 % CI 0·41, 0·87, P = 0·006), but also after adjustment for age, sex, number of drugs, Charlson co-morbidity index, smoking, alcohol and income (HR 0·60, 95 % CI 0·41, 0·87, P = 0·008). Residing in iodine-replete Skagen was associated with increased longevity. This indicates that long-term residency in an iodine-replete environment may be associated with increased longevity compared with residency in an iodine-deficient environment.

A high prevalence of thyroid hypofunction has been found in bipolar patients. However, the samples used in previous studies included a high percentage of patients in treatment with lithium and carbamazepine. Since the use of these drugs may explain the high prevalence of thyroid disturbances found in bipolar patients, we designed the present study to assess thyroid function in a sample of bipolar patients who had not been treated previously with lithium or carbamazepine. Patients included in the sample met Research Diagnostic Criteria for bipolar affective disorder. Assessment included determination of serum levels for total tyroxine (T4), total triiodothyronine (T3), and thyrotropin both basally and in response to infusion of 500 mg of Protilerin. The rate of thyroid hypofunction in the total sample (9.2%) was considerably lower than that reported in other studies with bipolar patients undergoing lithium therapy. Five patients (9.2%) showed some thyroid hyperfuncion parameter. Our results do not show significant differences in thyroid function indices between long-term and short-term duration of illness, between outpatients and inpatients, between high and low number of episodes, and between rapid- and non-rapid-cycling cases. Comparison between bipolar I and bipolar II patients shows a statistically significant difference in the values of TSH levels, with the bipolar II group having a higher mean value. Our data suggest that thyroid dysfunction is not related to gender, duration of illness, number of episodes, or rapid-cycling course of illness. The higher TRH-stimulated TSH levels in the bipolar II group could be considered a differential biological feature.

Maternal thyroid dysfunction during pregnancy may contribute to offspring neurobehavioral disorders. In this paper, we investigate the relationship between maternal thyroid function during pregnancy and offspring depression and anxiety. Data were taken from the Avon Longitudinal Study of Parents and Children. A total of 2,920 mother-child pairs were included. Thyroid-stimulating hormone levels, free thyroxine (FT4), and thyroid peroxidase antibodies were assessed during the first trimester of pregnancy because maternal supply is the only source of thyroid hormone for the fetus during the first 12 weeks of gestation. Child symptoms of depression and anxiety were assessed using the Development and Well-Being Assessment at ages 7.5 and 15 years. The odds of presenting with depression and anxiety were estimated using the generalized estimating equation. The level of FT4 during the first trimester of pregnancy was associated with child depression combined at ages 7.5 and 15 (odds ratio = 1.21, 95% confidence interval [1.00, 1.14]. An increase of 1 standard deviation of FT4 during pregnancy increased the odds of child depression by 28% after adjustment made for potential confounders. No association was found among maternal levels of thyroid-stimulating hormone, FT4, and thyroid peroxidase antibodies and childhood anxiety. In conclusion, increased levels of FT4 during the first trimester of pregnancy appear be linked to greater risk of offspring depression.

I deficiency is still a worldwide public health problem, with children being especially vulnerable. No nationwide study had been conducted to assess the I status of Spanish children, and thus an observational, multicentre and cross-sectional study was conducted in Spain to assess the I status and thyroid function in schoolchildren aged 6–7 years. The median urinary I (UI) and thyroid-stimulating hormone (TSH) levels in whole blood were used to assess the I status and thyroid function, respectively. A FFQ was used to determine the consumption of I-rich foods. A total of 1981 schoolchildren (52 % male) were included. The median UI was 173 μg/l, and 17·9 % of children showed UI<100 μg/l. The median UI was higher in males (180·8 v. 153·6 μg/l; P<0·001). Iodised salt (IS) intake at home was 69·8 %. IS consumption and intakes of ≥2 glasses of milk or 1 cup of yogurt/d were associated with significantly higher median UI. Median TSH was 0·90 mU/l and was higher in females (0·98 v. 0·83; P<0·001). In total, 0·5 % of children had known hypothyroidism (derived from the questionnaire) and 7·6 % had TSH levels above reference values. Median TSH was higher in schoolchildren with family history of hypothyroidism. I intake was adequate in Spanish schoolchildren. However, no correlation was found between TSH and median UI in any geographical area. The prevalence of TSH above reference values was high and its association with thyroid autoimmunity should be determined. Further assessment of thyroid autoimmunity in Spanish schoolchildren is desirable.

To answer the question if it is possible for specific psychiatric illnesses to influence the thyroxine-concentration, a group of 376 patients admitted to a psychiatric hospital was studied retrospectively.

13.5% had an elevated thyroxine-concentration and only 0.6% had a low concentration.

Of the group of 145 men, 22.8% was found to have an elevated thyroxine-concentration. In the group of 196 women we found 6.6% to be elevated. A low thyroxine was found in only 0.5% of the women and 0.7% of the men.

In the group with an elevated thyroxine the psychiatric diagnoses of schizophrenia and psychotic disorders NOS are more common (19.6% and 17.4% respectively) than in the group with a normal thyroxine (4.4% and 6.5% respectively).

Iodine insufficiency is now a prominent issue in the UK and other European countries due to low intakes of dairy products and seafood (especially where iodine fortification is not in place). In the present study, we tested a commercially available encapsulated edible seaweed (Napiers Hebridean Seagreens®Ascophyllum nodosum species) for its acceptability to consumers and iodine bioavailability and investigated the impact of a 2-week daily seaweed supplementation on iodine concentrations and thyroid function. Healthy non-pregnant women of childbearing age, self-reporting low dairy product and seafood consumption, with no history of thyroid or gastrointestinal disease were recruited. Seaweed iodine (712 μg, in 1 g seaweed) was modestly bioavailable at 33 (interquartile range (IQR) 28–46) % of the ingested iodine dose compared with 59 (IQR 46–74) % of iodine from the KI supplement (n 22). After supplement ingestion (2 weeks, 0·5 g seaweed daily, n 42), urinary iodine excretion increased from 78 (IQR 39–114) to 140 (IQR 103–195) μg/l (P< 0·001). The concentrations of thyroid-stimulating hormone increased from 1·5 (IQR 1·2–2·2) to 2·1 (IQR 1·3–2·9) mIU/l (P< 0·001), with two participants having concentrations exceeding the normal range after supplement ingestion (but normal free thyroxine concentrations). There was no change in the concentrations of other thyroid hormones after supplement ingestion. The seaweed was palatable and acceptable to consumers as a whole food or as a food ingredient and effective as a source of iodine in an iodine-insufficient population. In conclusion, seaweed inclusion in staple foods would serve as an alternative to fortification of salt or other foods with KI.

Iodine deficiency affects an estimated 241 million school-aged children in the world. Little is known about iodine deficiency in relation to auditory function, except for the fact that deaf–mutism is one of the features of cretinism. In the present review, we documented the scientific knowledge on the role of iodine and hypothyroidism in the auditory system. We found that ear development and hearing function depend on thyroid hormones. Multiple pathways are involved in this, including both inner ear morphology as well as neurological processes. Conductive as well as sensorineural hearing loss is found in studies with animals that were rendered hypothyroidic. In humans, auditory impairment is reported frequently in relation to hypothyroidism, ranging from mild disturbances to severe handicap. Auditory impairment has been related more explicitly to congenital hypothyroidism than to acquired hypothyroidism. The critical period for thyroid function-related hearing maturation is the first and second trimesters of pregnancy. Although only a limited number of studies have directly investigated the relationship between iodine deficiency and auditory function, most studies point toward an association. However, evidence from good randomised controlled trials is lacking. Inclusion of auditory outcomes in iodine supplementation studies is therefore to be recommended, especially for trials in pregnancy. Hearing deficit is an invisible abnormality, but has major consequences for educational and social skills if not detected. In view of this, auditory impairment should be mapped in iodine-deficient areas in order to realistically estimate the magnitude of the problem.

The benefits of iodine supplements during pregnancy remain controversial in areas with a mild-to-moderate iodine deficiency. The aim of the present study was to determine the effect of improving iodine intakes, with iodised salt (IS) or iodine supplements, in pregnant Spanish women. A total of 131 pregnant women in their first trimester were randomly assigned to three groups: (1) IS in cooking and at the table, (2) 200 μg potassium iodide (KI)/d or (3) 300 μg KI/d. No differences were found in thyroid-stimulating hormone (TSH), free thyroxine (FT4), free triiodothyronine (FT3) or thyroid volume (TV) between the three groups. Regardless of the group in which women were included, those who had been taking IS for at least 1 year before becoming pregnant had a significantly lower TV in the third trimester (P= 0·01) and a significantly higher urinary iodine in the first (173·7 (sd 81·8) v. 113·8 (sd 79·6) μg/l, P= 0·001) and third trimesters (206·3 (sd 91·2) v. 160·4 (sd 87·7) μg/l, P= 0·03). Also, no differences were seen in TSH, FT4 or FT3. Children's neurological development was not significantly associated with the consumption of IS for at least 1 year before becoming pregnant and no differences were found according to the treatment group. In conclusion, in pregnant women with insufficient iodine intake, the intake of IS before becoming pregnant was associated with a better maternal thyroid function. The form of iodide intake was not associated with maternal thyroid function or children's neurological development.

Little information is available as to whether doses of iodide similar to those recommended in clinical practice for the prevention of iodine deficiency in pregnant women affect thyroid function. The aim of the present study was to analyse whether doses of iodide can affect thyroid function in adults, and evaluate its effect on plasma markers of oxidative stress, inflammation and acute-phase proteins. A total of thirty healthy volunteers (ten men and twenty women) with normal thyroid function were randomly assigned to three groups (n 10). Each group received a daily dose of 100, 200 or 300 μg of iodide in the form of KI for 6 months. Free tetraiodothyronine (FT4) levels at day 60 of the study were higher in the groups treated with 200 and 300 μg (P = 0·01), and correlated with the increase in urinary iodine (r 0·50, P = 0·007). This correlation lost its significance after adjustment for the baseline FT4. The baseline urinary iodine and FT4 correlated positively with the baseline glutathione peroxidase. On day 60, urinary iodine correlated with C-reactive protein (r 0·461, P = 0·018), and free triiodothyronine correlated with IL-6 (r − 0·429, P = 0·025). On day 60, the changes produced in urinary iodine correlated significantly with the changes produced in α1-antitrypsin (r 0·475, P = 0·014) and ceruloplasmin (r 0·599, P = 0·001). The changes in thyroid-stimulating hormone correlated significantly with the changes in α1-antitrypsin (r − 0·521, P = 0·005) and ceruloplasmin (r − 0·459, P = 0·016). In conclusion, the administration of an iodide supplement between 100 and 300 μg/d did not modify thyroid function in a population with adequate iodine intake. The results also showed a slight anti-inflammatory and antioxidative action of iodide.

Two rapeseed (Brassica napus) meals, RM1 and RM2, with two levels of glucosinolates (GLS; 5 and 41 μmol/g DM respectively) were incorporated at the levels of 300 and 500 g/kg of the diets of juvenile rainbow trout (Oncorhynchus mykiss) in replacement of fish meal, and compared with a fish-meal-based diet. A decrease in the digestibility of the DM, protein, gross energy and P was observed with high-rapeseed meal (RM) incorporation. In trout fed on RM-based diets, growth performance was reduced even after only 3 weeks of feeding. Feed efficiency was adversely affected by RM and GLS intake. Protein and energy retention coefficients were significantly lower in fish fed on the diet containing the higher level of GLS. P retention was significantly lower with all the RM-based diets than with the fish-meal diet. Irrespective of the degree of growth inhibition, fish fed on RM-based diets exhibited similar typical features of hypothyroid condition due to GLS intake, expressed by lower plasma levels of triiodothyronine and especially thyroxine and a hyperactivity of the thyroid follicles. This hypothyroidal condition led to a strong adjustment of the deiodinase activities in the liver, the kidney and the brain. A significant increase of the outer ring deiodinase activities (deiodinases type I and II respectively) and a decrease of the inner ring deiodinase activity (deiodinase type III) were observed. It is concluded that the observed growth depression could be attributed to the concomitant presence of GLS, depressing the thyroid function, and of other antinutritional factors affecting digestibility and the metabolic utilization of dietary nutrients and energy.

The clinical and demographic features of 100 bipolar disorder patients, who were categorised into bipolar I, bipolar II, unipolar mania and rapid cycling groups, and who were further classified on the basis of the sequence of occurrence of the manic and depressive episodes within each cycle, are compared. Bipolar I (including unipolar manic) patients, 77% of whom had a sequence of moods where mania preceded depression (Mania-Depression – normothymic Interval: M.D.I.) constituted 69% of the total sample. Six per cent were classified as bipolar II and 25% has a rapid cycling disorder. Patients who had an M.D.I. sequence of moods, whether rapid or non-rapid cycling, had a younger age of onset, a higher male:female ratio and a stronger family history of bipolar disorder than patients whose depression preceded mania (D.M.I.). Unipolar manic patients, 12% of the sample, had a comparable age of onset, a greater family history of bipolarity and more frequent hospitalisations than the bipolar I-M.D.I. group. Rapid cycling patients had a lower mean serum thyroxine concentration than the non-rapid cycling bipolar disorder patients. This study supports the rationale for distinguishing bipolar patients with an M.D.I, sequence from those with a D.M.I, pattern and rapid cyclers from non-rapid cyclers.