Maternal Thyroid Function during the Second Half of Pregnancy and Child Neurodevelopment at 6, 12, 24, and 60 Months of Age (original) (raw)
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Maternal thyroid hormones early in pregnancy and fetal brain development
Best Practice & Research Clinical Endocrinology & Metabolism, 2004
During the last few decades our understanding of the possible role of thyroid hormones during brain development has increased and contributed to resolve previously discordant hypotheses, although much remains to be clarified. Thyroid hormones of maternal origin are present in the fetal compartment, despite the very efficient uterine-placental 'barrier', necessary to avoid potentially toxic concentrations of free T4 and T3 from reaching fetal tissues before they are required for development. T3 remains low throughout pregnancy, whereas FT4 in fetal fluids increases rapidly to adult levels, and is determined by the maternal availability of T4. It is present in embryonic fluids 4 weeks after conception, with FT4 steadily increasing to biologically relevant values. T3, generated from T4 in the cerebral cortex, reaches adult values by mid-gestation and is partly bound to specific nuclear receptor isoforms. Iodothyronine deioidinases are important for the spatial and temporal regulation of T3 bioavailability, tailored to the differing and changing requirements of thyroid hormone-sensitive genes in different brain structures, but other regulatory mechanism(s) are likely to be involved. Maternal transfer constitutes a major fraction of fetal serum T4, even after onset of fetal thyroid secretion, and continues to have an important protective role in fetal neurodevelopment until birth.
Archives of Endocrinology and Metabolism
Clinical and subclinical hypothyroidism are the most common hormonal dysfunctions during pregnancy. Insufficient maternal thyroid hormones (THs) in the early stages of pregnancy can lead to severe impairments in the development of the central nervous system because THs are critical to central nervous system development. In the fetus and after birth, THs participate in neurogenic processes, cell differentiation, neuronal activation, axonal growth, dendritic arborization, synaptogenesis and myelination. Although treatment is simple and effective, approximately 30% of pregnant women in Brazil with access to prenatal care have their first consultation after the first trimester of pregnancy, and any delay in diagnosis and resulting treatment delay may lead to cognitive impairment in children. This review summarizes the effects of clinical and subclinical hypothyroidism on fetal neurodevelopment, behavior and cognition in humans and rodents.
Thyroxine Levels During Pregnancy in Healthy Women and Early Child Neurodevelopment
Epidemiology, 2013
The fetus depends on maternal thyroid hormones during pregnancy for normal brain development. Little is known about the effects of subclinical hypothyroidism and mild hypothyroxinemia during pregnancy on neurodevelopment of the child. Methods: We evaluated a population-based birth cohort in Spain. A total of 1761 children and their mothers were included in the main analyses. Serum levels of free thyroxine and thyrotropin were measured in pregnant women. Mental and psychomotor development of their children was assessed using the Bayley Scales of Infant Development during the second year of life. Results: Low free thyroxine levels (<5th percentile) and selfreported prepregnancy thyroid disorder without medical treatment were associated with a decrease of mental scores (Beta = −3.4 [95% confidence interval= −6.7 to −0.2]) and −5.5 [−8.9 to −2.0], respectively). No association between thyrotropin levels and mental scores or psychomotor scores was observed.
Thyroid, 2009
Background: Maternal hypothyroxinemia, due to gestational iodine deficiency, causes neurological dysfunctions in the progeny. Our aim was to determine the effects of delayed iodine supplementation (200 mg KI per day) to mildly hypothyroxinemic pregnant women at the beginning of gestation (i.e., having circulating free thyroxine [FT 4 ] within the 0th-10th percentile interval and normal thyrotropin [TSH]) on the neurobehavioral development of their children. Methods: Using the Brunet-Lézine scale, we evaluated the neurocognitive performance at 18 months of age in three groups of children. Group 1 included children of women with FT 4 above the 20th percentile at 4-6 gestational weeks and at full-term. Group 2 included children of mildly hypothyroxinemic women diagnosed during the first 12-14 gestational weeks and with FT 4 above the 20th percentile at full-term. Group 3 included children born to mildly hypothyroxinemic women at full-term, without iodine supplementation during gestation. Women of all groups were iodine supplemented from the day of enrollment until the end of lactation. Results: Before iodine supplementation, 33.0% of the women (114 out of 345) were hypothyroxinemic, with FT 4 below normal in 28 of them (8.1%). None were found to be hypothyroxinemic at full-term after supplementation. The mean (AESD) developmental quotient of children was 101.8 AE 9.7 in group 1 (n ¼ 13) vs. 87.5 AE 8.9 in group 3 (n ¼ 19; p < 0.001) and 92.2 AE 5.4 in group 2 (n ¼ 12; p < 0.05). The difference between groups 2 and 3 was not statistically significant. Delayed neurobehavioral performance was observed in 36.8% and 25.0% of children in groups 3 and 2, respectively, compared with no children in group 1. Differences (p < 0.001) were found on gross and fine motor coordination and socialization quotients. No statistically significant differences were found on language quotients. Conclusions: A delay of 6-10 weeks in iodine supplementation of hypothyroxinemic mothers at the beginning of gestation increases the risk of neurodevelopmental delay in the progeny. Public health programs should address the growing problem of iodine deficiency among women of gestational age in developing and industrialized nations.
Relation of Severity of Maternal Hypothyroidism to Cognitive Development of Offspring
Obstetrical and Gynecological Survey, 2001
Background-An association between maternal subclinical hypothyroidism and low intelligence quotient (IQ) in the oVspring has recently been shown. Objective-To provide evidence for the causality of the association by testing the hypothesis that severity of maternal hypothyroidism correlates inversely with IQ of the oVspring. Methods-IQ scores were compared among 8 year old oVspring of 124 control mothers whose thyroid stimulating hormone (TSH) concentrations were < 98th percentile of a cohort of 25 000 mothers at 17 weeks gestation, of 28 untreated hypothyroid women whose TSH was between the 98th and 99.85th percentiles, and of 20 untreated women whose TSH concentration was > 99.85th percentile.
2018
Introduction: The focus of the present study was the importance of the mother's thyroid function for foetal development in the first trimester, when the baby is totally dependent on the mother for thyroid hormones. Materials and methods: The study consisted of testing the intellectual performance of children with both euthyroid and thyroid-dysfunction mothers. The experimental group comprised 60 children of mothers with an untreated thyroid disorder in the first trimester of pregnancy (TSH ≥ 3.5 mlU/L [standard 0.15-3.5] and/or TPO-Ab ≥ 20 lU/L [standard < 20]). The control group contained 132 children whose mothers showed no symptoms of a thyroid disorder either before or during pregnancy/postpartum. Both groups of children were administered the Wechsler Intelligence Scale for Children-Third Edition (WISC-III), whereby the intellectual performance of the experimental-group children was compared with that of the control-group children. The comparison included the percentage of children with IQ ≤ 85 and SLD and/or ADD risks. Our research is a follow-up to a blanket thyroid screening of 1649 pregnant women conducted during 2004-2006 in the region around Havlíčkův Brod. Results: The research found no significant difference between the two groups of children with respect to their intellectual abilities, either regarding their overall IQ (p = 0.67), verbal IQ (p = 0.81), performance IQ (p = 0.41), or the individual scores (VCI: p = 0.85; POI: p = 0.54, FDI: p = 0.57; PSI: p = 0.13), nor did the experimental group show a significantly higher occurrence of children with IQ ≤ 85 than the control group (p = 0.66). However, the experimental group did exhibit a statistically significant increase in the percentage of children with a suspected SLD or clinically significant attention issues (p = 0.05). Conclusion: Untreated thyroid disorders in the first trimester of pregnancy can increase the risk of the child developing attention or learning issues.
Journal of Epidemiology and Community Health, 2020
BackgroundMaternal thyroid hormones’ supply is crucial for fetal neurodevelopment; however, the role of maternal mild thyroid dysfunction is not clear. We aimed to assess the association of maternal mild thyroid dysfunction with child neuropsychological development from infancy to early childhood.MethodsWe included 757 mother–child pairs from the prospective ‘Rhea’ cohort on Crete, Greece. Maternal thyroid functioning was assessed by quantitative analysis of serum thyroid-stimulating hormone, free thyroxine, thyroid peroxidase antibodies and thyroglobulin antibodies at early gestation (mean=14 weeks). Neuropsychological assessment was based on Bayley Scales of Infant Development (18 months of age), McCarthy Scales of Children’s Abilities (4 years of age), Raven’s Coloured Progressive Matrices, Trail Making Test and Finger Tapping Test (6 years of age).ResultsIn multivariate adjusted linear regression analyses, maternal hypothyroxinemia was associated with decreased verbal scores at ...