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Childhood thyroid function may be determined by maternal TSH, free T4 during pregnancy
Maternal thyroid-stimulating hormone and free thyroxine levels, as well as thyroid-specific single nucleotide polymorphisms, may help determine childhood thyroid function, according to recent study findings published in The Journal of Clinical Endocrinology & Metabolism.
“In addition, higher maternal [free] T4 was also associated with more suppression of newborn TSH levels,” the researchers wrote. “Various stress-related factors were associated with newborn TSH and [free] T4, but these associations did not persist into childhood. We also show evidence that offspring thyroid function may differ according to the inherited [single nucleotide polymorphisms] that have been associated with thyroid function in adults.”
Tim Korevaar, MD, MSc, of Erasmus University Medical Center in Rotterdam, Netherlands, and colleagues evaluated data from the Generation R Study on 4,573 mother–child pairs with data on maternal gestational TSH and free T4 levels and newborn TSH or free T4 (n = 3,339; at birth) or childhood TSH or free T4 (n = 2,523; median age, 6 years) to determine the association between maternal and fetal characteristics with thyroid function in newborn and school-aged children.
Tim Korevaar
Maternal TSH and free T4 levels during pregnancy were strongly associated with newborn and childhood TSH and free T4 levels, respectively (P < .0001 for both). Further, maternal free T4 levels were associated with newborn TSH levels (P = .0009). Newborn TSH and free T4 were determined by birth weight, fetal distress, gestational age at birth and maternal parity (P < .0001); however, these relationships did not persist into childhood.
A genetic risk score for TSH was associated with newborn TSH and explained 0.8% to 1% of newborn TSH variability. Similarly, a genetic risk score for free T4 was associated with newborn free T4 and explained 0.2% to 0.3% of newborn free T4 variability. Genetic risk scores for TSH and free T4 explained variability for childhood TSH (5.3% to 5.5%) and T4 (1.9% to 3.6%).
In addition, genetic risk scores for TSH and free T4 based on the DNA of their offspring were associated with both maternal TSH and free T4. This suggests that the similarities in genetic variation between mother and their offspring may explain the associations between maternal and offspring thyroid function but further analyses showed that these were separate associations.
“Longer follow-up of children is needed, preferably until they start to develop thyroid disease, so that we can try to identify early markers of thyroid dysfunction, which could allow us to identify high-risk groups,” Korevaar told Endocrine Today. “Also, it will be very important that fetal programming studies, focusing on the effects of the maternal thyroid function during pregnancy and adverse child outcomes will take into account potential confounding or mediation due to the strong association between maternal and child thyroid function.” – by Amber Cox
Disclosure: The researchers report no relevant financial disclosures.
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