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Clinical Review State of the Art Review

Obesity and pregnancy: mechanisms of short term and long term adverse consequences for mother and child

BMJ 2017; 356 doi: (Published 08 February 2017) Cite this as: BMJ 2017;356:j1
  1. Patrick M Catalano, professor and director1 2,
  2. Kartik Shankar, associate professor3 4
  1. 1Department of Obstetrics and Gynecology, Center for Reproductive Health/MetroHealth Medical Center, Cleveland, Ohio, USA
  2. 2Case Western Reserve University, Cleveland, Ohio, USA
  3. 3Arkansas Children’s Nutrition Center, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA
  4. 4Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA
  1. Correspondence to: P M Catalano pcatalano{at}
  • Accepted 5 December 2016


Obesity is the most common medical condition in women of reproductive age. Obesity during pregnancy has short term and long term adverse consequences for both mother and child. Obesity causes problems with infertility, and in early gestation it causes spontaneous pregnancy loss and congenital anomalies. Metabolically, obese women have increased insulin resistance in early pregnancy, which becomes manifest clinically in late gestation as glucose intolerance and fetal overgrowth. At term, the risk of cesarean delivery and wound complications is increased. Postpartum, obese women have an increased risk of venous thromboembolism, depression, and difficulty with breast feeding. Because 50-60% of overweight or obese women gain more than recommended by Institute of Medicine gestational weight guidelines, postpartum weight retention increases future cardiometabolic risks and prepregnancy obesity in subsequent pregnancies. Neonates of obese women have increased body fat at birth, which increases the risk of childhood obesity. Although there is no unifying mechanism responsible for the adverse perinatal outcomes associated with maternal obesity, on the basis of the available data, increased prepregnancy maternal insulin resistance and accompanying hyperinsulinemia, inflammation, and oxidative stress seem to contribute to early placental and fetal dysfunction. We will review the pathophysiology underlying these data and try to shed light on the specific underlying mechanisms.


  • The authors are supported in part by the following grants: Eunice Kennedy Shriver National Institute of Child Health and development HD-11089-19 (PMC) and USDA Agricultural Research Service CRIS 6251-51000-010-05S (KS).

  • Contributors: PMC and KS both performed the literature search, wrote the draft article, and revised the manuscript. They are both guarantors.

  • Competing interests: The authors have read and understood BMJ policy on declaration of interests and have no conflicts to declare.

  • Provenance and peer review: Commissioned; externally peer reviewed.

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