Effect of Thyroid Function on Offspring Neurodevelopment in People Receiving ART Therapy: A Prospective Cohort Study

Adequate maternal thyroid hormone is vital for fetal neurodevelopment. Abnormal thyroid function can cause developmental defects in offspring from spontaneous pregnancies; however, research in assisted reproduction is lacking.

This work aimed to investigate the association between thyroid disorders and offspring neurodevelopment from assisted reproduction.

In this prospective and longitudinal birth cohort study (Jiangsu, China), we included 729 women who had their thyroid function tested before an assisted reproductive technology cycle and delivered liveborn babies between November 2015 and June 2020. Maternal thyroid function was assessed by measuring thyroid antibodies, free thyroxine, and serum thyrotropin. The third edition Bayley Scales of Infant and Toddler Development screening test (Bayley-III screening test) was used to assess infant neurodevelopment.

In multivariable-corrected linear regression analysis, infants of women with subclinical hypothyroidism (SCH) demonstrated a significantly lower receptive communication score (β = -.63; 95% CI, -1.12 to -0.14; P = .013), with stratified analysis showing a significant association among female offspring (β = -.87; 95% CI, -1.59 to -0.15; P = .018) but a null association among male offspring (β = -.44; 95% CI, -1.03 to 0.15; P = .145). No significant differences were found in the assisted pregnancy population with normal thyroid function and positive antibodies according to the diagnostic cutoffs applied to normal pregnant women.

SCH in assisted pregnancies correlates with lower communication scores in 1-year-olds, especially in girls. We recommend medication for SCH throughout, regardless of thyroid autoantibody status.