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Author Notes:

Correspondence: K.Joseph.Hurt@ucdenver.edu

NC and KJH conceived of and designed the approach to the review and the manuscript summary.

NC conducted literature search with TLH (obesity metabolism) and KJH (labor mechanism).

NC drafted the manuscript with critical revision by TLH and KJH.

All authors read, revised, and approved the submitted version.

The authors acknowledge Dr. Nancy Lowe for her mentorship of NC through studies on labor dystocia, and David Carlson, for the original medical illustration.

Our appreciation to Drs. Thomas Jansson, Peggy Neville, Andy Bradford, Elizabeth Holt, Emily Su, Gosia Skaznik-Wikiel, and Nancy Lowe for discussions and helpful feedback on the manuscript.

The authors declare that they have no competing interests.


Research Funding:

NIH National Institute of Nursing Research, Grant # 1F31NR014061-01A1, March of Dimes Graduate Nursing Grant, and The University of Colorado School of Nursing ‘Touched by a Nurse’ Scholarship (NC); R01-DK101659 (TLH); and March of Dimes Basil O’Connor award, #5-FY12-37, NIH/NCATS Colorado CTSA Grant #UL1TR001082, and UCDenver WRHR #2K12HD001271 (KJH).


  • Cesarean section
  • Cholesterol
  • Dystocia
  • Labor
  • Leptin
  • Meta-inflammation
  • Myometrium
  • Pregnancy
  • Uterus

Parturition dysfunction in obesity: time to target the pathobiology


Journal Title:

Reproductive Biology and Endocrinology


Volume 13, Number 1


Type of Work:

Article | Final Publisher PDF


Over a third of women of childbearing age in the United States are obese, and during pregnancy they are at increased risk for delayed labor onset and slow labor progress that often results in unplanned cesarean delivery. The biology behind this dysfunctional parturition is not well understood. Studies of obesity-induced changes in parturition physiology may facilitate approaches to optimize labor in obese women. In this review, we summarize known and proposed biologic effects of obesity on labor preparation, contraction/synchronization, and endurance, drawing on both clinical observation and experimental data. We present evidence from human and animal studies of interactions between obesity and parturition signaling in all elements of the birth process, including: delayed cervical ripening, prostaglandin insensitivity, amniotic membrane strengthening, decreased myometrial oxytocin receptor expression, decreased myocyte action potential initiation and contractility, decreased myocyte gap junction formation, and impaired myocyte neutralization of reactive oxygen species. We found convincing clinical data on the effect of obesity on labor initiation and successful delivery, but few studies on the underlying pathobiology. We suggest research opportunities and therapeutic interventions based on plausible biologic mechanisms.

Copyright information:

© Carlson et al. 2015

This is an Open Access work distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/).

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