Document Type : Original Article

Authors

• Satvinder K Dhaliwal ¹
• Dana Dabelea ²
• Angela E Lee-Winn ³
• Deborah H Glueck ²
• Greta Wilkening ⁴
• Wei Perng ¹

¹ Lifecourse Epidemiology of Adiposity and Diabetes (LEAD) Center, University of Colorado Denver Anschutz Medical Campus, Aurora CO, USA and Department of Epidemiology, Colorado School of Public Health, University of Colorado Denver Anschutz Medical Campus, CO, USA

² Lifecourse Epidemiology of Adiposity and Diabetes (LEAD) Center, University of Colorado Denver Anschutz Medical Campus, Aurora CO, USA and Department of Epidemiology, Colorado School of Public Health, University of Colorado Denver Anschutz Medical Campus, CO, USA and Department of Pediatrics, School of Medicine, University of Colorado Denver Anschutz Medical Campus, CO, USA

³ Department of Epidemiology, Colorado School of Public Health, University of Colorado Denver Anschutz Medical Campus, CO, USA

⁴ Lifecourse Epidemiology of Adiposity and Diabetes (LEAD) Center, University of Colorado Denver Anschutz Medical Campus, Aurora CO, USA

Abstract

Background: In utero exposure to increased inflammation caused by acute experiences may negatively impact on child neurodevelopment, but little is known about the effects of low-grade chronic inflammation. We wanted to investigate prenatal inflammation, as indicated by biomarkers of low-grade chronic inflammation, as an in utero programming method for neurodevelopment, and see how much of these associations are explained by perinatal factors.
 
Methods: We utilized linear regression to analyze the relationship between prenatal C-reactive protein, interleukin-6, and tumor necrosis factor-α and offspring Child Behavior Check List scores for total problems, externalizing and internalizing behaviors in 489 mother-offspring pairs from the Healthy Start cohort, based in Denver, Colorado,  USA. We made sequential adjustments for perinatal correlates. Model 1 considered maternal age, gestational age at blood draw, and child age. Model 2 included further adjustments for mother race/ethnicity, followed by household income in Model 3 and pre-pregnancy body mass index (BMI) in Model 4. Finally, we used the maternal Edinburgh Postnatal Depression Scale and Perceived Stress Scale scores as measures of psychosocial stress.
 
Results: In Model 1, children of mothers with C-reactive protein in the fourth quartile had a 3.82 (95% CI: 0.94, 6.70) unit higher t-score for total problems compared to those in the first to third quartiles. The inclusion of household income and pre-pregnancy BMI in the fully adjusted model reduced the impact estimate to 3.11 (-0.45, 6.67). We found a similar pattern in externalizing behavior and across models for interleukin 6.
 
Conclusions: Maternal inflammation is associated with worse neurobehavioral outcomes in children. This association was influenced by higher pre-pregnancy BMI and lower household income.

Keywords

• Prenatal inflammation
• Offspring neurobehavioral health
• Psychosocial stress
• in utero
• BMI
• IL-6
• CRP
• TNF-α
• Offspring Child Behavior Checklist scores
• Maternal inflammation
• USA

Main Subjects

• Epidemiology