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Sleep-disordered breathing in pregnancy: a developmental origin of offspring obesity?

Published online by Cambridge University Press:  19 May 2020

Sarah S. Farabi Open the ORCID record for Sarah S. Farabi [Opens in a new window] ,
Linda A. Barbour  and
Teri L. Hernandez
Sarah S. Farabi*
Affiliation:
Goldfarb School of Nursing, Office of Nursing Research, St. Louis, MO, USA Center for Human Nutrition, Washington University St. Louis School of Medicine, St. Louis, MO, USA
Linda A. Barbour
Affiliation:
Department of Medicine, Division of Endocrinology, Metabolism, and Diabetes, University of Colorado Anschutz Medical Campus, Aurora, CO, USA Department of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, USA
Teri L. Hernandez
Affiliation:
Department of Medicine, Division of Endocrinology, Metabolism, and Diabetes, University of Colorado Anschutz Medical Campus, Aurora, CO, USA College of Nursing, University of Colorado Anschutz Medical Campus, Aurora, CO, USA
*
Address for correspondence: Sarah S. Farabi, Goldfarb School of Nursing, Office of Nursing Research, Mailstop 90-36-697, 4483 Duncan Avenue, St. Louis, MO, USA. Email: Sarah.Farabi@barnesjeswishcollege.edu
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Abstract

Sleep-disordered breathing (SDB) worsens over pregnancy, and obstructive sleep apnea is associated with serious maternal complications. Intrauterine exposures that provoke insulin resistance (IR), inflammation, or oxidative stress may have long-term offspring health consequences. In obesity, worsening maternal SDB appears to be an exposure that increases the risk for both small- or large-for-gestational-age (SGA, LGA, respectively), suggesting distinct outcomes linked to a common maternal phenotype. The aim of this paper is to systematically review and link data from both mechanistic rodent models and descriptive human studies to characterize the impact of maternal SDB on fetal development. A systematic review of the literature was conducted using PubMed, Embase, and CINAHL (01/2000–09/2019). Data from rodent (9 studies) and human models (48 studies, 5 meta-analyses) were included and reviewed using PRISMA guidelines. Evidence from rodent models suggests that intermittent maternal hypoxia results in mixed changes in birth weight (BW) followed by accelerated postnatal growth, while maternal sleep fragmentation results in normal BW followed by later metabolic derangement. Human studies support that maternal SDB is associated with both SGA and LGA, both of which may predispose offspring to later obesity. Evidence also suggests a link between SDB, inflammation, and oxidative stress that may impact maternal metabolism and/or placental function. SDB is common in pregnancy and affects fetal growth and development. Given that SDB has significant potential to adversely influence the intrauterine metabolic environment, larger, prospective studies in humans are urgently needed to fully elucidate the effects of this exposure on offspring metabolic risk.

Keywords

Sleep disordered breathingpregnancydevelopmental originsobesity
Type
Review
Information
Journal of Developmental Origins of Health and Disease , Volume 12 , Issue 2 , April 2021 , pp. 237 - 249
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Copyright
© Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2020

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