Minireview Maternal inflammation, growth retardation, and preterm birth: Insights into adult cardiovascular disease Lynette K. Rogers a , Markus Velten a, b, ⁎ a The Center for Perinatal Research, The Research Institute at Nationwide Children's Hospital, The Ohio State University, Columbus, Ohio, United States b Department of Anesthesiology and Intensive Care Medicine, University Hospital Bonn, Germany abstract article info Article history: Received 8 June 2011 Accepted 16 July 2011 Keywords: Fetal origin adult diseases Barker hypothesis Cardiovascular disease Maternal inflammation Fetal programming The “fetal origin of adult disease Hypothesis” originally described by Barker et al. identified the relationship between impaired in utero growth and adult cardiovascular disease risk and death. Since then, numerous clinical and experimental studies have confirmed that early developmental influences can lead to cardiovascular, pulmonary, metabolic, and psychological diseases during adulthood with and without alterations in birth weight. This so called “fetal programming” includes developmental disruption, immediate adaptation, or predictive adaptation and can lead to epigenetic changes affecting a specific organ or overall health. The intrauterine environment is dramatically impacted by the overall maternal health. Both premature birth or low birth weight can result from a variety of maternal conditions including undernutrition or dysnutrition, metabolic diseases, chronic maternal stresses induced by infections and inflammation, as well as hypercholesterolemia and smoking. Numerous animal studies have supported the importance of both maternal health and maternal environment on the long term outcomes of the offspring. With increasing rates of obesity and diabetes and survival of preterm infants born at early gestational ages, the need to elucidate mechanisms responsible for programming of adult cardiovascular disease is essential for the treatment of upcoming generations. © 2011 Elsevier Inc. All rights reserved. Contents Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 417 Cardiovascular risks and low birth weight; the “Barker hypothesis” . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 418 Preterm birth and fetal programming . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 418 Fetal programming and epigenetics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 419 Maternal influences on fetal programming . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 419 Animal studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 419 Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 420 Conflict of interest statement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 420 Acknowledgements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 420 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 420 Introduction The “fetal origin of adult disease” hypothesis was introduced by Barker et al. almost 25 years ago and addresses the influence of the intrauterine and early postnatal environment on the development of adult diseases (Barker and Osmond, 1986; Barker, 1997a, 1997b, 2004a, 2004b). Based on epidemiological data, Barker and coworkers described low weight at birth as highly correlated with increased risk for the development of cardiovascular complications (Barker et al., 1989). Numerous retrospective and prospective clinical studies have revealed significant associations between low weight at birth and the development of cardiovascular diseases (CVD) during adulthood (Eriksson et al., 1999; Frankel et al., 1996; Stein et al., 1996). Further Life Sciences 89 (2011) 417–421 ⁎ Corresponding author at: Department of Anesthesiology and Intensive Care Medicine, University Hospital Bonn, Germany, Sigmund-Freud-Straße 25, 53105 Bonn, Germany. Tel.: +49 228 287 14114; fax: +49 228 287 14125. E-mail address: Markus.Velten@UKB.uni-bonn.de (M. Velten). 0024-3205/$ – see front matter © 2011 Elsevier Inc. All rights reserved. doi:10.1016/j.lfs.2011.07.017 Contents lists available at ScienceDirect Life Sciences journal homepage: www.elsevier.com/locate/lifescie