Maternal Prenatal Cortisol and Breastfeeding Predict Infant Growth.

Nicki L Aubuchon-Endsley,Nicole Douthit,Hillary E Swann-Thomsen

doi:10.3390/ijerph17218233

Nicki L Aubuchon-Endsley, Nicole Douthit + Show 1 more

Open Access

https://doi.org/10.3390/ijerph17218233

Copy DOI

Abstract

Fetal/infant growth affects adult obesity and morbidities/mortality and has been associated with prenatal exposure to cortisol. Bidirectional relations between maternal stress and breastfeeding suggest that they interact to influence offspring growth. No models have tested this hypothesis, particularly regarding longer-term offspring outcomes. We used a subset of the IDAHO Mom Study (n = 19–95) to examine associations among maternal prenatal cortisol (cortisol awakening response (CAR) and area under the curve), and standardized weight-for-length (WLZ) and length-for-age (LAZ) z-scores from birth-18 months, and main and interactive effects of prenatal cortisol and breastfeeding on infant growth from birth-6 months. CAR was negatively associated with LAZ at birth (r = −0.247, p = 0.039) but positively associated at 13–14 months (r = 0.378, p = 0.033), suggesting infant catch-up growth with lower birth weights, likely related to elevated cortisol exposure, continues beyond early infancy. A negative correlation between breastfeeding and 10-month WLZ (r = −0.344, p = 0.037) and LAZ (r = −0.468, p = 0.005) suggests that breastfeeding assists in managing infant growth. WLZ and LAZ increased from birth to 6 months (ps < 0.01), though this was unrelated to interactions between prenatal cortisol and breastfeeding (i.e., no significant moderation), suggesting that other factors played a role, which should be further investigated. Findings add to our understanding of the predictors of infant growth.

Highlights

Fetal and infant growth influence the risk of obesity, morbidity, and mortality across the lifespan [1]
The current study proposed to fill a gap in the existing literature on how maternal prenatal cortisol and breastfeeding influence growth outcomes in later infancy, as previous research has primarily focused on growth outcomes at birth [2]
We hypothesized that maternal prenatal cortisol would be negatively correlated with infant growth across infancy, we found limited statistically significant associations among maternal prenatal cortisol and infant growth outcomes

Summary

Introduction

Fetal and infant growth influence the risk of obesity, morbidity, (e.g., diabetes mellitus, cardiovascular disease, hypertension, sleep apnea, kidney and liver disease, infertility, gastroesophageal reflux disease, and certain cancers), and mortality across the lifespan [1]. Early biopsychosocial risk factors influencing fetal/infant growth are still not well understood. Additional research is needed to investigate maternal perinatal factors, which influence early offspring growth to identify early targets for obesity prevention and intervention. While literature supports two such factors, in utero glucocorticoid exposure and breastfeeding, no known studies have investigated an interaction between these factors in relation to offspring growth trajectories over infancy, which is the focus of the current project. Maternal cortisol is regulated by the placenta, uterine decidua, and fetal membrane, in addition to the hypothalamic–pituitary–adrenal (HPA) axis [2]. Public Health 2020, 17, 8233; doi:10.3390/ijerph17218233 www.mdpi.com/journal/ijerph

Methods

Discussion

Conclusion