title: Fetal programming of adult disease: implications for prenatal care.
abstract: 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.
authors.affiliation: 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.
authors.forename: Christopher
authors.initials: C
authors.lastname: Lau
authors.forename: John M
authors.initials: JM
authors.lastname: Rogers
authors.forename: Mina
authors.initials: M
authors.lastname: Desai
authors.forename: Michael G
authors.initials: MG
authors.lastname: Ross
mesh_terms: D000328:Adult; D001724:Birth Weight / Q000235:genetics; D005260:Female; D047109:Fetal Development / Q000235:genetics*; D006801:Humans; D007231:Infant, Newborn; D008429:Maternal Welfare; D024821:Metabolic Syndrome / Q000453:epidemiology / Q000235:genetics / Q000517:prevention & control*; D020380:Needs Assessment; D009765:Obesity / Q000235:genetics / Q000517:prevention & control*; D010353:Patient Education as Topic / Q000458:organization & administration*; D011247:Pregnancy; D011256:Pregnancy Outcome; D011295:Prenatal Care / Q000458:organization & administration*; D011297:Prenatal Exposure Delayed Effects / Q000453:epidemiology / Q000235:genetics; D016730:Program Development; D015397:Program Evaluation; D018570:Risk Assessment; D014481:United States