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The aim of this systematic review and meta-analysis was, for the first time, to explore whether postpartum maternal iodine status or supplementation is associated with thyroid function after delivery. The MEDLINE/PubMed, Web of Science, Embase, and Scopus were searched up to December 2021 to identify relevant studies. The pooled mean thyroid stimulating hormone (TSH), free thyroxine (fT4), and thyroxine (T4) concentrations and 95% confidence intervals (CIs) were estimated based on maternal urinary iodine concentration (UIC) (< 50, 50–100, 100–200, and > 200 µg/L) or breast milk iodine concentration (BMIC) (< 100 µg/L vs. ≥ 100 µg/L) during postpartum. A fixed/random effects model was used based on the absence/presence of heterogeneity, respectively. The study is registered with PROSPERO, number CRD42022336145. A total of 2175 studies were identified, of which 18 were eligible for the meta-analysis. The pooled values for TSH, fT4, and T4 concentrations in all subgroups were within the normal range; however, except for TSH, comparing the 95% CI showed no statistically significant difference among different subgroups. The pooled mean for TSH concentration in women with UIC > 200 µg/L was 2.23 mIU/L, whereas the corresponding values in women with UIC < 50, 50–100 and 100–200 µg/L were 0.56, 0.56 and 0.95 mIU/L, respectively. Thyroid hormones in women with BMIC < 100 µg/L and ≥ 100 µg/L were within the normal range. Iodine supplementation during postpartum was not associated with any differences in thyroid parameters, compared to non-supplemented women. In conclusion, iodine status or supplementation had no effect on thyroid hormones in postpartum women. [ABSTRACT FROM AUTHOR]

Objective Examine the associations of maternal thyroid hormones, maternal dietary information, and newborn T.sub.4 levels with cognitive outcomes in mid-childhood. Methods We studied 921 children born 1999-2003 at gestational age [greater than or equal to] 34 weeks, who were participants in Project Viva, a prospective pre-birth cohort study in Massachusetts. We examined maternal dietary information, maternal thyroid hormone levels, and neonatal levels of T.sub.4. Research staff performed cognitive testing in mid-childhood (median age 7.7 years). Results We included 514 women with measured first trimester thyroid hormone concentrations (mean 10.2 weeks); 15% of women had a thyroid stimulating hormone (TSH) level [greater than or equal to] 2.5 mU/L, and 71% were college graduates. Newborn T.sub.4 was collected from 375 infants (mean 17.6 [mu]g/dl; SD 4.0), on day 2 (mean 1.9 days; SD 0.7) as part of the newborn screening program. Mean (SD) verbal and nonverbal IQ, memory, and motor scores of children were 113.2 (14.3), 107.1 (16.7), 17.1 (4.4), and 92.5 (16.6) points, respectively. In multivariable analysis, first trimester maternal thyroid function (total T.sub.3, total T.sub.4, free T.sub.4, thyroid stimulating hormone (TSH) or total thyroid peroxidase (TPO) antibody levels) or newborn T.sub.4 were not associated with any of the cognitive outcomes in mid-childhood after adjustment for sociodemographic and perinatal variables. Conclusions for Practice Maternal or neonatal thyroid hormone levels were not associated with cognitive outcomes in mid-childhood in this population with generally normal thyroid function. As we studied a highly educated cohort residing in an iodine-sufficient area, findings may not be generalizable., Author(s): Samantha J. Lain [sup.1] [sup.4] , Sheryl L. Rifas-Shiman [sup.2] , Elizabeth N. Pearce [sup.3] , Natasha Nassar [sup.1] , Emily Oken [sup.2] Author Affiliations: (1) grid.1013.3, 0000 0004 [...]

Background: Autism spectrum disorder (ASD) is a neurodevelopmental condition with unknown etiology. Both genetic and environmental factors have been associated with ASD. Environmental exposures during the prenatal period may play an important role in ASD development. This narrative review critically examines the evidence for a relationship between maternal thyroid dysfunction during pregnancy and ASD in the child. Summary: Studies that assessed the associations of hypothyroidism, hyperthyroidism, hypothyroxinemia, thyroid hormone concentrations, or autoimmune thyroid disease with ASD outcomes were included. Most research focused on the relationship between hypothyroidism and ASD. Multiple population-based studies found that maternal hypothyroidism was associated with higher likelihood of an ASD diagnosis in offspring. Associations with other forms of maternal thyroid dysfunction were less consistent. Findings may have been affected by misclassification bias, survival bias, or publication bias. Studies using medical records may have misclassified subclinical thyroid dysfunction as euthyroidism. Two studies that assessed children at early ages may have misclassified those with ASD as typically developing. Most studies adjusted for maternal body mass index (BMI) and/or mental illness, but not interpregnancy interval or pesticide exposure, all factors associated with fetal survival and ASD. Most studies reported a combination of null and statistically significant findings, although publication bias is still possible. Conclusions: Overall, evidence supported a positive association between maternal thyroid dysfunction during pregnancy and ASD outcomes in the child, especially for hypothyroidism. Future studies could reduce misclassification bias by using laboratory measures instead of medical records to ascertain thyroid dysfunction and evaluating children for ASD at an age when it can be reliably detected. Survival bias could be further mitigated by adjusting models for more factors associated with fetal survival and ASD. Additional research is needed to comprehensively understand the roles of maternal levothyroxine treatment, iodine deficiency, or exposure to thyroid-disrupting compounds in the relationship between maternal thyroid dysfunction and child ASD outcomes. [ABSTRACT FROM AUTHOR]

Importance: Overt hyperthyroidism, defined as suppressed thyrotropin (previously thyroid-stimulating hormone) and high concentration of triiodothyronine (T3) and/or free thyroxine (FT4), affects approximately 0.2% to 1.4% of people worldwide. Subclinical hyperthyroidism, defined as low concentrations of thyrotropin and normal concentrations of T3 and FT4, affects approximately 0.7% to 1.4% of people worldwide. Untreated hyperthyroidism can cause cardiac arrhythmias, heart failure, osteoporosis, and adverse pregnancy outcomes. It may lead to unintentional weight loss and is associated with increased mortality. Observations: The most common cause of hyperthyroidism is Graves disease, with a global prevalence of 2% in women and 0.5% in men. Other causes of hyperthyroidism and thyrotoxicosis include toxic nodules and the thyrotoxic phase of thyroiditis. Common symptoms of thyrotoxicosis include anxiety, insomnia, palpitations, unintentional weight loss, diarrhea, and heat intolerance. Patients with Graves disease may have a diffusely enlarged thyroid gland, stare, or exophthalmos on examination. Patients with toxic nodules (ie, in which thyroid nodules develop autonomous function) may have symptoms from local compression of structures in the neck by the thyroid gland, such as dysphagia, orthopnea, or voice changes. Etiology can typically be established based on clinical presentation, thyroid function tests, and thyrotropin-receptor antibody status. Thyroid scintigraphy is recommended if thyroid nodules are present or the etiology is unclear. Thyrotoxicosis from thyroiditis may be observed if symptomatic or treated with supportive care. Treatment options for overt hyperthyroidism from autonomous thyroid nodules or Graves disease include antithyroid drugs, radioactive iodine ablation, and surgery. Treatment for subclinical hyperthyroidism is recommended for patients at highest risk of osteoporosis and cardiovascular disease, such as those older than 65 years or with persistent serum thyrotropin level less than 0.1 mIU/L. Conclusions and Relevance: Hyperthyroidism affects 2.5% of adults worldwide and is associated with osteoporosis, heart disease, and increased mortality. First-line treatments are antithyroid drugs, thyroid surgery, and radioactive iodine treatment. Treatment choices should be individualized and patient centered. This review summarizes current evidence regarding the pathophysiology, clinical presentation, and treatment of hyperthyroidism, focusing on the management of Graves disease and toxic nodular disease. [ABSTRACT FROM AUTHOR]

Author(s): Elizabeth N. Pearce [sup.1] Author Affiliations: (1) Section of Endocrinology, Diabetes, and Nutrition, Boston University School of Medicine, Boston, USA Basics in clinical nutrition: what is already known? Iodine [...]

Background: We aimed to assess the long-term effects of the transition in iodine status on the incidence of thyroid disorders over 20 years of follow-up. Methods: The original prospective cohort study, started in 1999 (n = 3761), classified three regions in north China based on iodine status (insufficient iodine, more than adequate iodine, and excessive iodine, respectively) for 5 years. Subsequently, participants were followed for up to another 15 years to assess the long-term effects of shifts to adequate iodine on the incidence of thyroid disorders. Panshan transitioned from insufficient to adequate iodine, and Huanghua transitioned from excessive to more than adequate iodine. Both regions were compared with Zhangwu, in which iodine status changed from more than adequate to adequate iodine (from 214 to 167.2 μg/L). A cluster sampling method was used to select participants in the three regions. Participants completed questionnaires and underwent thyroid ultrasonography. Urinary iodine concentrations (UICs), serum thyroid hormone concentration, and thyroid antibodies were measured. Results: When the iodine status changed from insufficient to adequate (with the median UIC increasing from 88 to 141.9 μg/L), the incidence density of subclinical hyperthyroidism, positive thyroperoxidase antibody, positive thyroglobulin antibody (TgAb), and goiter decreased significantly (p < 0.05 for all). Additionally, the cumulative incidence of subclinical hypothyroidism was significantly lower compared with the region where the iodine status changed from being more than adequate to adequate (1.9% vs. 6.0%, p < 0.001). When the iodine status changed from excessive to more than adequate (median UIC from 634 to 266.7 μg/L), a significant decrease in the incidence density of subclinical hyperthyroidism, positive thyroid antibodies, positive TgAb, and goiter (p < 0.05 for all) were also found. However, an increase in thyroid nodule incidence density (17.26 vs. 28.25 per 1000 person-years, p < 0.001) was seen. Conclusions: The incidence of thyroid disorders (except for thyroid nodules) stabilized or decreased among adults in the three communities from year 5 to year 15 of follow-up. Appropriate iodine fortification is safe and effective over the long term. Restoring urinary iodine to appropriate levels reduces population risk for thyroid disorders. [ABSTRACT FROM AUTHOR]