Maternal Obesity and Fatty Acids During Pregnancy Predict Infant Sleep and Cognition

• In Event: 1-021 - Maternal Obesity and Nutrition during Pregnancy: Effects on Offspring Neurobehavioral Development

Integrative Statement

Maternal obesity during pregnancy is linked to several negative outcomes in offspring, including psychopathology (Sanchez et al., 2017). Mechanistically, obesity contributes to increased inflammation, which in turn negatively impacts fetal brain development (van der Burg et al., 2016). Similarly, prenatal consumption of omega-3 (n3) and omega-6 (n6) fatty acids has been shown to predict alterations in infant central nervous system (CNS) functioning (Cheruku et al., 2002). These nutrients also have pro-inflammatory (n6) and anti-inflammatory (n3) properties. Therefore, there is reason to believe that maternal obesity and diet during pregnancy may jointly influence infant neurodevelopment, with maternal fatty acid levels possibly attenuating (n3) or exacerbating (n6) the negative impacts of prenatal obesity. The current study tests these hypotheses using infant sleep and cognition as two markers of neurodevelopment.

Data are from a longitudinal study of sleep development in African-American infants. 35 families participated in a 3rd trimester blood draw and a 6-month home visit, which included cognitive tasks and a week-long sleep assessment.

Plasma samples were assayed for fatty acids. Effects of alpha-linolenic acid (18:3n-3; LNA), docosahexaenoic acid (22:6n-3; DHA), linoleic acid (18:2n-6; LA), and arachidonic acid (20:4n-6; ARA) were originally investigated. However, as no results were found for DHA or LA, only LNA and ARA are discussed. At 3 months, mothers self-reported their height and weight, which were converted to BMI and used as a proxy for maternal prenatal obesity (BMI > 30; nobese = 24). Infant sleep was measured using seven nights of actigraphy monitoring. The longest continuous sleep period (LSP) and number of night wakings (NW) were averaged across all nights of data collection. Longer LSPs and fewer NWs indicate better sleep quality. Infant general cognitive ability was measured via the Bayley Scales of Infant Development (BSID-III; Bayley, 2006). Regression models tested direct and interactive effects of maternal obesity and fatty acids on infant LSP, NW, and BSID scores, controlling for maternal education and prenatal caloric intake. Non-significant interaction terms were trimmed before interpreting model coefficients.

Results indicated a significant main effect of maternal obesity on infant BSID scores (β = -.40, p < .05), but no main effects or interactions with LNA or ARA. As shown in Figure 1, there was a significant main effect of LNA on infant LSP (β = .44, p = .05), but no main effects of maternal obesity, ARA, or any significant interactions. Finally, we found a significant main effect of ARA on infant NW (β = .96, p < .01), as well as a significant interaction between maternal obesity and ARA (β = -.79, p < .05). Simple slopes analyses revealed a positive relationship between ARA and NW (b = 2.20, p < .001), but only for dyads where mothers were non-obese (Figure 2).

Our findings confirm that proinflammatory factors (obesity, n6) predict worse neurodevelopmental outcomes, whereas anti-inflammatory factors (n3) predict better outcomes. We also show preliminary evidence that prenatal obesity and diet may interact to predict child outcomes. Subsequent analyses will incorporate biomarkers of maternal prenatal inflammation (e.g., CRP, IL-6).

Authors

• Marie Camerota, UNC-Chapel Hill
  Presenting Author

• Carol L Cheatham, University of North Carolina at Chapel Hill
  Non-Presenting Author

• Cathi Propper, University of North Carolina at Chapel Hill
  Non-Presenting Author