Clinical associations of maternal thyroid function with foetal brain development: Epidemiological interpretation and overview of available evidence

Abstract

Thyroid hormone is an important regulator of early brain development, particularly during early stages of gestation during which foetal thyroid hormone availability depends on the maternal transfer of thyroid hormones. There is a wide range of experimental studies showing that low maternal thyroid hormone availability is associated with suboptimal brain development parameters. While few clinical studies have shown that overt maternal hypothyroidism is associated with lower child IQ, the question whether more subclinical changes in maternal thyroid function could also lead to suboptimal foetal brain development. In this review, we put the latter studies in perspective and discuss their interpretation from an epidemiological and clinical perspective. Furthermore, we extend this discussion to also include future perspective and identify important knowledge gaps in the field.

Thyroid hormone regulation of neural stem cell fate: From development to ageing

“…Moreover, a large cohort study recently showed that both mild hypo‐ and hyperthyroidism in the first trimester of prenatal brain development altered grey/white matter ratios in the progeny, suggesting that lineage specification was altered in embryonic development . Other neurological disorders including attention‐deficit hyperactivity disorder (ADHD), autism spectrum disorder (ASD) and schizophrenia, characterized by abnormal neuronal numbers and networks, are also suspected to have a developmental aetiology of which suboptimal TH levels might be one of the underlying causes . Lastly, a histological analysis of the brain of an MCT8‐deficient foetus showed loss of some neuronal subtypes, and a hypomyelinated state, suggesting similar problems in NSC biology and specification caused by insufficient TH uptake during early development .…”

Management for women with subclinical hypothyroidism in pregnancy

“…Meta-analysis of three studies shows that maternal SCH has a negative effect on subsequent intelligence score in the offspring, but these data are uncorrected for parental educational level and economic status 23. Practically, all studies that demonstrate a positive association between thyroid function and child neurodevelopment find the association between maternal T4 levels rather than TSH 24. This is consistent with known gestational physiology as it is T4, not TSH, which crosses the placental barrier and is required for neuronal migration in the fetus.…”

Maternal lithium chloride exposure alters the neuroendocrine‐cytokine axis in neonatal albino rats

“…This stability is vital for the developing brain (Ahmed, 2011;Ahmed et al, 2010;Aszalós, 2007;Coccini et al, 2007). Normal levels of THs regulate the neurogenesis process during development (Bernal, 2017;Fanibunda, Desouza, Kapoor, Vaidya, & Vaidya, 2018;Korevaar, Tiemeier, & Peeters, 2018;Moog et al, 2017;Richard & Flamant, 2018). Alternatively, THs can control the monoaminergic system via their receptors on the NE, E and DA-ergic fibers (Aszalós, 2007).…”