The obesity epidemic, including a marked increase in the prevalence of obesity among pregnant women, represents a critical public health problem in the United States and throughout the world. Over the past two decades, it has been increasingly recognized that the risk of adult health disorders, particularly metabolic syndrome, can be markedly influenced by prenatal and infant environmental exposures (ie, developmental programming). Low birth weight, together with infant catch-up growth, is associated with a significant risk of adult obesity and cardiovascular disease, as well as adverse effects on pulmonary, renal, and cerebral function. Conversely, exposure to maternal obesity or high birth weight also represents an increased risk for childhood and adult obesity. In addition, fetal exposure to select chemicals (eg, phytoestrogens) or environmental pollutants (eg, tobacco smoke) may affect the predisposition to adult disease. Animal models have confirmed human epidemiologic findings and provided insight into putative programming mechanisms, including altered organ development, cellular signaling responses, and epigenetic modifications (ie, control of gene expression without modification of DNA sequence). Prenatal care is transitioning to incorporate goals of optimizing maternal, fetal, and neonatal health to prevent or reduce adult-onset diseases. Guidelines regarding optimal pregnancy nutrition and weight gain, management of low- and high-fetal-weight pregnancies, use of maternal glucocorticoids, and newborn feeding strategies, among others, have yet to fully integrate long-term consequences on adult health.
Because the risk of adult obesity is markedly influenced by neonatal birth weight and prenatal environmental exposures, optimal prenatal care may improve adult health significantly.
From the Toxicity Assessment Division, National Health and Environmental Effects Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina; and the Department of Obstetrics and Gynecology, Geffen School of Medicine at UCLA, Los Angeles, California; Harbor-UCLA Medical Center, Torrance, California.
This document has been reviewed in accordance with the U.S. Environmental Protection Agency policy and approved for publication. Approval does not signify that the contents reflect the views of the Agency, nor does mention of trade names or commercial products constitute endorsement or recommendation for use.
Corresponding author: Michael G. Ross, MD, MPH, Professor and Chairman, Department of Obstetrics and Gynecology, Harbor-UCLA Medical Center, 1000 W. Carson St, Box 3, Torrance, CA 90502; e-mail: firstname.lastname@example.org.
Financial Disclosure The author did not report any potential conflicts of interest.