Maternal inflammatory diet and adverse pregnancy outcomes: Circulating cytokines and genomic imprinting as potential regulators?

Journal Article (Journal Article)

Excessive inflammation during pregnancy alters homeostatic mechanisms of the developing fetus and has been linked to adverse pregnancy outcomes. An anti-inflammatory diet could be a promising avenue to combat the pro-inflammatory state of pregnancy, particularly in obese women, but we lack mechanistic data linking this dietary pattern during pregnancy to inflammation and birth outcomes. In an ethnically diverse cohort of 1057 mother-child pairs, we estimated the relationships between dietary inflammatory potential [measured via the energy-adjusted dietary inflammatory index (E-DII™)] and birth outcomes overall, as well as by offspring sex and maternal pre-pregnancy body mass index (BMI). In a subset of women, we also explored associations between E-DII, circulating cytokines (n = 105), and offspring methylation (n = 338) as potential modulators of these relationships using linear regression. Adjusted regression models revealed that women with pro-inflammatory diets had elevated rates of preterm birth among female offspring [β = -0.22, standard error (SE) = 0.07, P<0.01], but not male offspring (β=0.09, SE = 0.06, P<0.12) (Pinteraction = 0.003). Similarly, we observed pro-inflammatory diets were associated with higher rates of caesarean delivery among obese women (β = 0.17, SE = 0.08, P = 0.03), but not among women with BMI <25 kg/m2 (Pinteraction = 0.02). We observed consistent inverse associations between maternal inflammatory cytokine concentrations (IL-12, IL-17, IL-4, IL-6, and TNFα) and lower methylation at the MEG3 regulatory sequence (P<0.05); however, results did not support the link between maternal E-DII and circulating cytokines. We replicate work by others on the association between maternal inflammatory diet and adverse pregnancy outcomes and provide the first empirical evidence supporting the inverse association between circulating cytokine concentrations and offspring methylation.

Full Text

Duke Authors

Cited Authors

  • McCullough, LE; Miller, EE; Calderwood, LE; Shivappa, N; Steck, SE; Forman, MR; A Mendez, M; Maguire, R; Fuemmeler, BF; Kollins, SH; D Bilbo, S; Huang, Z; Murtha, AP; Murphy, SK; Hébert, JR; Hoyo, C

Published Date

  • August 2017

Published In

Volume / Issue

  • 12 / 8

Start / End Page

  • 688 - 697

PubMed ID

  • 28678596

Pubmed Central ID

  • PMC5687326

Electronic International Standard Serial Number (EISSN)

  • 1559-2308

Digital Object Identifier (DOI)

  • 10.1080/15592294.2017.1347241


  • eng

Conference Location

  • United States