Interpregnancy interval and early neurodevelopment in offspring: A
Prospective Birth Cohort Study
Abstract
Objective This study aimed to determine the correlation between
interpregnancy interval (IPI) and neurodevelopmental delay in infants
and to explore the potential mediating role of maternal-fetal glucose
metabolism. Design Population based cohort study. Setting China
Participants A total of 2559 mother-infant pairs between 2018 and 2022.
Methods The prospective birth cohort study included 2559 mother-infant
pairs. The IPI is calculated by subtracting the gestational age of the
current pregnancy from the interval at the end of the previous
pregnancy. Maternal fasting venous blood collection at 24-28 weeks and
cord blood collection at delivery. The association between IPI and
neurodevelopment was determined by logistic regression. Main outcome
measures Neurodevelopmental outcomes at 12 months in offspring were
assessed by the Ages and Stages Questionnaire Edition 3 (ASQ-3). Results
In our cohort, 14.0% had an IPI <12 months. IPI <12
months increased the failure of the communication domain, fine motor
domain, and personal social domain of the ASQ [relative risks (RRs)
with 95% confidence interval (CI): 1.75(1.13, 2.72); 1.77(1.13, 2.77);
1.51(1.01, 2.28)]. Maternal homeostasis model assessment of insulin
resistance (HOMA-IR) and cord blood C-peptide was significantly
associated with failure in the communication domain [RRs with 95% CI:
1.15(1.02, 1.31); 2.15(1.26, 3.67)]. The proportion of the association
between IPI and failure of the communication domain risk mediated by
maternal HOMA-IR and cord blood C-peptide was 14.4%. Conclusions IPI
<12 months was associated with failing the communication
domain in offspring. Maternal-fetal glucose metabolism abnormality may
partially explain the neurodevelopmental delay caused by short IPI.