An adequate supply of thyroid hormone (TH) is essential for placental development and the increased metabolic demands of pregnancy as well as for normal fetal brain development. Since the fetal brain needs TH long before the fetal thyroid starts to function, maternal TH transferred via the placenta is the main source of hormone during pregnancy. Also iodine, a component substrate of TH, is essential for normal neurodevelopment and iodine deficiency can cause severe neurodevelopmental disorders. Furthermore, an expanding literature has identified a large number of environmental chemicals that can disrupt normal maternal thyroid function negatively affecting the pregnancy and offspring. Accumulating evidence now suggests that even mild maternal thyroid deficiency can have a negative impact on obstetric outcomes leading to premature delivery and abnormal birth weights and predisposing the offspring to adverse effects such as cognitive impairments, behavioral disorders (e.g., autism, ADHD), and atypical brain development. Surprisingly, recent attempts to treat women with mild thyroid dysfunction have failed to yield improvements in the offspring. Based on rodent data, it is now recognized that maternal TH transfer to specific fetal brain regions is far more complex than originally conceived and involves a number of diverse regulatory and compensatory mechanisms.
To better understand the pathophysiology and risk factors associated with maternal thyroid dysfunction and the consequent obstetric complications and adverse effects on the offspring throughout development, this call proposes a cross-disciplinary approach that integrates the most up-to-date basic and clinical data on these issues. It is hoped that this information can serve to identify new and effective therapies or subgroups benefiting most from current therapies as well as safer environments for optimizing pregnancy outcomes and child neurodevelopment.
An adequate supply of thyroid hormone (TH) is essential for placental development and the increased metabolic demands of pregnancy as well as for normal fetal brain development. Since the fetal brain needs TH long before the fetal thyroid starts to function, maternal TH transferred via the placenta is the main source of hormone during pregnancy. Also iodine, a component substrate of TH, is essential for normal neurodevelopment and iodine deficiency can cause severe neurodevelopmental disorders. Furthermore, an expanding literature has identified a large number of environmental chemicals that can disrupt normal maternal thyroid function negatively affecting the pregnancy and offspring. Accumulating evidence now suggests that even mild maternal thyroid deficiency can have a negative impact on obstetric outcomes leading to premature delivery and abnormal birth weights and predisposing the offspring to adverse effects such as cognitive impairments, behavioral disorders (e.g., autism, ADHD), and atypical brain development. Surprisingly, recent attempts to treat women with mild thyroid dysfunction have failed to yield improvements in the offspring. Based on rodent data, it is now recognized that maternal TH transfer to specific fetal brain regions is far more complex than originally conceived and involves a number of diverse regulatory and compensatory mechanisms.
To better understand the pathophysiology and risk factors associated with maternal thyroid dysfunction and the consequent obstetric complications and adverse effects on the offspring throughout development, this call proposes a cross-disciplinary approach that integrates the most up-to-date basic and clinical data on these issues. It is hoped that this information can serve to identify new and effective therapies or subgroups benefiting most from current therapies as well as safer environments for optimizing pregnancy outcomes and child neurodevelopment.
