Fetal Origins of Adult Disease
By K. Calkins, Sherin U. Devaskar. Current Problems in Pediatric and Adolescent Health Care, 2011
887 citations recorded by the source corpus.
Dr. David Barker first popularized the concept of fetal origins of adult disease (FOAD). Since its inception, FOAD has received considerable attention. The FOAD hypothesis holds that events during early development have a profound impact on one’s risk for development of future adult disease. Low birth weight, a surrogate marker of poor fetal growth and nutrition, is linked to coronary artery disease, hypertension, obesity, and insulin resistance. Clues originally arose from large 20th century, European birth registries. Today, large, diverse human cohorts and various animal models have extensively replicated these original observations. This review will focus on the pathogenesis related to FOAD and examines Dr. David Barker’s landmark studies, along with additional human and animal model data. Implications of the FOAD extend beyond the low birth weight population and include babies exposed to stress, both nutritional and non-nutritional, during different critical periods of development, which ultimately result in a disease state. By understanding FOAD, health care professionals and policy makers will make this issue a high healthcare priority and implement preventative measures and treatment for those at higher risk for chronic diseases.
Subfields: Obstetrics and Gynecology, Pediatrics, Perinatology and Child Health
View Paper: https://www.semanticscholar.org/paper/e25983443f402ca765c99ad047f8683c2fb41d69
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In Obstetrics and Gynecology
In Pediatrics, Perinatology and Child Health
Citations in the corpus
- Bisphenol A and human health: a review of the literature. (2013, background): “There is, however, a large body of literature linking prenatal or early environmental exposures to adverse adult outcomes [102].”
- Antioxidant Role for Lipid Droplets in a Stem Cell Niche of Drosophila (2015, background): “It is also well described that neonatal brain size is highly protected or spared from the increased hypoxia and malnutrition that are experienced during intrauterine growth restriction (Barker, 1995; Gruenwald, 1963).”
- Social Determinants of Risk and Outcomes for Cardiovascular Disease: A Scientific Statement From the American Heart Association (2015, background): “Intrauterine growth retardation is associated with a reduced number and function of pancreatic β cells, resulting in decreased insulin production.(316) This alteration leads to abnormal muscle, liver, and adipocyte insulin signaling and eventually to the development of insulin resistance.”