The developmental origins of adult disease

By L. Joss-Moore, R. Lane. Current opinion in pediatrics, 2009

1,410 citations recorded by the source corpus.

Subfields: Endocrinology, Diabetes and Metabolism, Molecular Biology, Pediatrics, Perinatology and Child Health

View Paper: https://www.semanticscholar.org/paper/529573c10dc162d46c4fc531041f07722d28da05

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In Endocrinology, Diabetes and Metabolism

In Molecular Biology

In Pediatrics, Perinatology and Child Health

Citations in the corpus

Prenatal Stress, Glucocorticoids and the Programming of Adult Disease (2009, background): “…metabolic programming, numerous studies in both humans and animal models have shown that a poor intrauterine environment followed by postnatal overnutrition promotes the development of diseases including hypertension, insulin resistance, central obesity and type 2 diabetes (Gluckman et al., 2005).”
Endocrine-disrupting chemicals: an Endocrine Society scientific statement. (2009, background): “In fact, the field of endocrine disruption has embraced the terminology “the fetal basis of adult disease” (8) to describe observations that the environment of a developing organism, which includes the maternal environment (eutherian mammals), the egg (other vertebrates), and the external environmen”
Instrumental Variable Estimation of the Causal Effect of Hunger Early in Life on Health Later in Life (2016, neutral): “Gluckman et al. (2005) and Barker (2007) give overviews of the underlying © 2015 Royal Economic Society. medical mechanisms.”
Cell Biology of Ischemia/Reperfusion Injury (2012, background): “It is now clear that the response of the fetus to a broad range of environmental cues (hemodynamic effects, growth factors, cocaine and tobacco smoke exposure, oxygen and nutrient availability) increases the susceptibility to later development of cardiovascular disease (Langley-Evans and McMullen, 2”
Nutrition and epigenetics: An interplay of dietary methyl donors, one-carbon metabolism, and DNA methylation (2012, positive): “The study of nutri-epigenomics is particularly timely in the context of the developmental origins of health and disease (DOHaD) hypothesis [18], which posits that increased susceptibility to disease following early life experiences is shaped by epigenetic modifications such as DNA methylation and ch”
Mechanisms of Disease: glucocorticoids, their placental metabolism and fetal 'programming' of adult pathophysiology (2007, background): “Data from populations in Europe, Asia, Africa, Australia and North America have shown that low birth weight (a marker, however blunt, of an adverse intrauterine environment) predisposes affected individuals to hypertension, dyslipidemia, insulin resistance, type 2 diabetes, obesity and death from is”
11β-hydroxysteroid dehydrogenases: intracellular gate-keepers of tissue glucocorticoid action. (2013, background): “Indeed, in many mammalian species, maternal undernutrition (total calorie or protein deficiency) (56) or exposure to stress/glucocorticoid excess (625) reduce birth weight and cause persisting hypertension, hyperglycemia, affective dysfunction, and neuroendocrine abnormalities in the offspring.”
Prenatal environmental exposures, epigenetics, and disease (2011, positive): “Hajkova P, Erhardt S, Lane N, Haaf T, El-Maarri O, Reik W, et al. Epigenetic reprogramming in mouse primordial germ cells.”
Fetal Origins of Adult Disease (2011, neutral): “The Helsinki and Hertfordshire cohorts from the 1930s and 1940s, which comprised over 20,000 subjects collectively, linked poor fetal growth with CAD, hypertension, and insulin resistance in adult men and women.(1,2,9) Differential mortality rates have been associated”
EDC-2: The Endocrine Society's Second Scientific Statement on Endocrine-Disrupting Chemicals. (2015, background): “This reprogramming process is best appreciated within the framework of the developmental origins of health and disease (DOHaD) hypothesis, which posits that an adverse environment experienced by a developing individual can increase the risk of disease later in life (62, 63).”
Antenatal maternal stress and long-term effects on child neurodevelopment: how and why? (2007, background): “…Publishing, 9600 Garsington Road, Oxford OX4 2DQ, UK and 350 Main Street, Malden, MA 02148, USA been shown to place individuals at risk for developing features of cardiovascular disease and metabolic disorders such as diabetes, in adulthood (Barker, 2002, 2004, 2005; Barker & Hanson, 2004).”