Programming of infant neurodevelopment by maternal obesity: potential role of maternal inflammation and insulin
Mira Dewi1,2, Susan E Carlson2, Kathleen M Gustafson3
1Department of Dietetics and Nutrition, School of Health Professions, University of Kansas Medical Center, Kansas City, KS, USA.
Insights
Maternal insulin resistance and inflammation were not linked to fetal heart rate variability, a measure of neurodevelopment. Further research with larger sample sizes is required to confirm these findings on fetal development.
Area of Science:
- Perinatal Medicine
- Neurodevelopmental Biology
- Maternal-Fetal Health
Background:
- Maternal obesity is linked to adverse offspring neurodevelopmental outcomes.
- Intrauterine exposure to inflammation and insulin resistance (IR) may mediate this association.
- Fetal heart rate variability (HRV) serves as an indicator of fetal cardiac autonomic nervous system development.
Purpose of the Study:
- To investigate the association between maternal IR and inflammation with fetal neurodevelopment, assessed via fetal HRV.
- To determine if maternal metabolic and inflammatory markers correlate with fetal autonomic nervous system development.
Main Methods:
- Analysis of 44 healthy maternal-fetal pairs with varying maternal pre-pregnancy BMI.
- Assessment of maternal inflammation (IL-6, TNF-α) and IR (HOMA index).
- Measurement of fetal HRV (SD1, SD2) using fetal magnetocardiogram at 36 weeks gestation.
Main Results:
- No significant correlations were found between maternal IR or inflammation markers (IL-6, TNF-α) and fetal HRV components (SD1, SD2).
- A trend towards a negative association between maternal TNF-α and fetal SD2 approached significance (p=0.07).
Conclusions:
- Maternal IR and inflammation were not associated with fetal cardiac autonomic nervous system development in this cohort.
- Larger studies incorporating additional inflammatory markers are needed to fully elucidate these relationships.
Background And Objectives:
Recent studies show that maternal obesity is associated with impaired offspring neurodevelopmental outcomes. The mechanism underlying the association is unclear. However, there is evidence to suggest a role for intra-uterine exposure to inflammation and insulin resistance (IR). We aimed to determine if maternal IR and inflammation were associated to fetal neurodevelopment as indicated by fetal heart rate variability (HRV), an index of fetal cardiac autonomic nervous system development.
Methods And Study Design:
A total of 44 healthy maternal-fetal pairs (maternal pre-pregnancy BMI distribution: n=20 normal weight, 8 overweight, 16 obese) were analyzed. We assessed maternal inflammation (plasma IL-6 and TNF-α) and IR (HOMA index). Fetal HRV, a proxy for fetal neurodevelopment, was assessed using fetal magnetocardiogram at the 36th week of pregnancy. The relationships between maternal inflammation and IR with fetal HRV (SD1 and SD2) were estimated individually by Pearson bivariate correlations.
Results:
No correlations were observed between the fetal HRV components with maternal HOMA-IR and maternal plasma levels of IL-6 and TNF-α (all p<0.05). However, the negative association between maternal TNF-α level and fetal SD2 approached significance (correlation coefficient=-0.29, 95% confidence interval=-0.62,-0.03, p=0.07).
Conclusion:
Maternal IR and inflammation during pregnancy were not associated with fetal cardiac autonomic nervous system development. Further studies with a larger sample size and more maternal inflammatory indicators are needed to explore these relationships.
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