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Volume 132, Issue 5, Pages 768-776 (May 1998)


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Role of the prenatal environment in the development of obesity☆☆★★

Presented in part at a workshop entitled “Prevention and Treatment of Childhood Obesity: Research Directions,” sponsored by the National Institutes of Health, the National Task Force on Prevention and Treatment of Obesity, and the International Life Sciences Institute, Bethesda, Md., Sept. 11, 1995.

Robert C. Whitaker, MD, MPH, William H. Dietz, MD, PhD

Received 11 January 1996; received in revised form 3 January 1997, 27 March 1997 and 4 June 1997; accepted 6 June 1997.

Abstract 

Establishing that prenatal life is a critical or sensitive period for the development of obesity may focus basic research and clinical prevention efforts on this period. This review summarizes evidence that the intrauterine environment influences the risk of later obesity and considers the mechanisms by which this may occur. The association between birth weight and adult weight suggests that there are enduring effects of the intrauterine environment on later obesity risk. We examine whether the maternal factors of diabetes, obesity, and pregnancy weight gain alter the intrauterine environment and thereby increase the risk of later obesity in the offspring. Of these maternal factors, evidence is strongest for the role of maternal diabetes. No single mechanism explains how these maternal factors could change the intrauterine environment to increase obesity risk. How ever, all potential mechanisms involve an altered transfer of metabolic substrates between mother and fetus, which may influence the developing structure or function of the organs involved in energy metabolism. (J Pediatr 1998;132:768-76)

 From the Department of Pediatrics, Children's Hospital Medical Center and the University of Cincinnati College of Medicine, Cincinnati, Ohio, and the Department of Pediatrics, New England Medical Center, Boston, Massachusetts.

☆☆ Supported in part by the Generalist Physician Faculty Scholars Award from the Robert Wood Johnson Foundation, Princeton, N.J. (Dr. Whitaker), and by grants DK/HD 50537 and P30-DK46200 from the National Institutes of Health (Dr. Dietz).

 Reprint requests: Robert C. Whitaker, MD, MPH, Children's Hospital Medical Center, Division of General and Community Pediatrics, CH-1S, 3333 Burnet Avenue, Cincinnati, OH 45229-3039.

★★ 9/19/83970

PII: S0022-3476(98)70302-6


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