Poster #20 - Nutritional Choline Intake During Pregnancy Buffers the Impact of Prenatal Stress on Infant Cortisol Reactivity

• In Event: 1-115 - Poster Session 03
  In Poster Session: PS 03 Section - Biological Processes: Psychophysiology

Integrative Statement

Objective: Exposure to elevated maternal stress hormones (i.e., cortisol) during pregnancy, has been associated with a number of child developmental outcomes including elevated cortisol reactivity to stress in early infancy. Preliminary evidence suggests that choline (an essential nutrient found in eggs, dairy products, and meat) may have protective effects on fetal development by reducing the amount of maternal cortisol that passes through the placental barrier. Despite convincing animal evidence that nutrient exposures can attenuate the effects of stress on offspring development, there is a paucity of human studies assessing stress-nutrient co-exposures. The aim of the current study, therefore, was to examine whether nutritional choline intake buffers the effect of prenatal maternal cortisol exposure on infant cortisol reactivity to stress at 3 months of age.
Methods: Participants were 236 mother-child dyads enrolled in a longitudinal pregnancy cohort study (the Alberta Pregnancy Outcomes and Nutrition Study). During pregnancy, maternal choline intake was estimated utilizing repeated 24-hour dietary recalls and prenatal stress was assessed via salivary cortisol samples collected over the course of two consecutive days in early (mean = 16 weeks) and late (mean = 32 weeks) pregnancy. At 3 months postnatal, infant stress reactivity was assessed via salivary cortisol samples at baseline and 20 minutes post laboratory stressor.
Results: Prenatal choline intake by itself did not moderate the association between maternal cortisol levels during pregnancy and infant cortisol reactivity to stress at 3 months. However, adding sex to the model revealed a moderator effect for choline. There were significant and opposite interaction effects between prenatal choline intake and maternal cortisol levels to predict male, β = .0007, p = .002, and female, β = -.0005, p = .047, infant cortisol reactivity (Figure 1). When maternal choline intake was low, there was a positive association between maternal cortisol and infant cortisol reactivity for female infants, whereas there was a negative association for male infants. When maternal choline intake was high, male and female infant cortisol reactivity profiles became more similar regardless of maternal cortisol exposures during pregnancy.
Conclusion: Higher estimated prenatal choline intake reduced the impact of prenatal maternal cortisol exposure on the developing fetal stress reactivity system. However, when choline intake was low, maternal cortisol exposure had sex-specific effects on infant cortisol reactivity. Choline may represent a novel dietary intervention to offset the impact of prenatal stress on child development.

Authors

• Jenna C Thomas-Argyriou, University of Calgary
  Presenting Author

• Catherine J Field, University of Alberta
  Non-Presenting Author

• Erin D Lewis, Tufts University
  Non-Presenting Author

• Nicole Letourneau, University of Calgary
  Non-Presenting Author

• Tavis Campbell, University of Calgary
  Non-Presenting Author

• Gerald F Giesbrecht, University of Calgary
  Non-Presenting Author