Fetal origins of adult disease: strength of effects and biological basis.

By D. Barker, J. Eriksson, T. Forsén, C. Osmond. International Journal of Epidemiology, 2002

2,048 citations recorded by the source corpus.

Subfields: Obstetrics and Gynecology, Pediatrics, Perinatology and Child Health

View Paper: https://www.semanticscholar.org/paper/60dd4e64898abc8c24ba00a828bd3f791e966de6

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In Obstetrics and Gynecology

In Pediatrics, Perinatology and Child Health

Citations in the corpus

Prenatal exposure to maternal depression and cortisol influences infant temperament. (2007, neutral): “Furthermore, neither maternal prenatal medical risk status ( r 247 = 0.06; p = .36) nor annual household income, used as an index of socioeconomic status ( r 247 = 0.05; p = .31), were correlated with infant temperament.”
Endocrine regulation of human fetal growth: the role of the mother, placenta, and fetus. (2006, background): “(388) found that adults from Helsinki who had been born small and had the largest body mass index in childhood were at greatest risk for type 2 diabetes, hypertension, and death or hospitalization due to coronary heart disease.”
Adult Consequences of Fetal Growth Restriction (2006, background): “Currently, the Helsinki studies are the main source of information.(26) Table 9 is based on the Helsinki cohort born between 1934 and 1944.”
Ten Putative Contributors to the Obesity Epidemic (2009, positive): “Elsewhere it has been argued that it is a major contributor to the risks of heart disease and diabetes (Barker et al., 2002).”
Early-childhood poverty and adult attainment, behavior, and health. (2010, background): “A pattern of small size at birth and low body mass index (BMI) at age 2, followed by rapid weight gain after age 2, is a risk factor for the development of insulin resistance and a disproportionately high fat mass in relation to muscle mass (Barker, Osmond, Forsén, Kajantie, & Eriksson, 2005; Barker”
Obesity: a chronic relapsing progressive disease process. A position statement of the World Obesity Federation (2017, background): “Individuals who were malnourished while in utero may be more prone to weight gain, insulin resistance, beta-cell failure and hence diabetes than those who are well nourished, a hypothesis known as the ‘Developmental Origin of Disease’ or the ‘Barker Hypothesis’ (77).”
Developmental origins of the metabolic syndrome: prediction, plasticity, and programming. (2005, neutral): “This latter point is important since the number requiring treatment decreases progressively with increasing birth weight (20, 132).”
Investing in Young Children: An Early Childhood Development Guide for Policy Dialogue and Project Preparation (2010, background): “This theory proposes that LBW and stunted growth in early childhood, followed by compensatory weight gain at later ages (after age 2), are associated with hypertension, increased serum cholesterol, higher susceptibility to type 2 diabetes, and increased risk of coronary heart disease in adulthood (B”