Barker hypothesis

Barker hypothesis

The proposition that a baby's nourishment in utero and during infancy determines the subsequent development of risk factors such as high blood pressure, blood clotting biochemistry and glucose intolerance and is thus a major determinant of coronary heart disease later in life.
References in periodicals archive ?
The high incidence of premature and small for gestational age (SGA) births in developing countries as a risk factor for kidney disease in adulthood, in the absence of evident kidney disease in early life, has been explained by the Barker hypothesis. [14,15] Steps need to be taken to decrease the premature birth rate by educating mothers to book early for antenatal screening, encourage proper nutrition and monitoring by health personnel on the progress of the pregnancy, thus preventing eventual hypertension, metabolic syndrome and possible type 2 diabetes mellitus.
His theory about how nutrition and growth before birth may affect cardiovascular health later on, as well as other adult chronic diseases and conditions, became known as the Barker Hypothesis.
Dover, "The Barker hypothesis: how pediatricans will diagnose and prevent common adult-onset diseases," Transactions of the American Clinical and Climatological Association, vol.
As leading proponents of the DOHaD hypothesis, Barker and colleagues have provided much of the impetus toward research of adverse influences during intrauterine development, so much so that this hypothesis is often referred to as the "Barker Hypothesis." While programming for other adult disease outcomes has been examined in the literature, this review will focus on the association with cardiovascular disease.
The paper is the first summary of prehistoric evidence for the Barker hypothesis - the idea that many adult diseases originate during fetal development and early childhood.
The "Barker Hypothesis" relates low birth weight to the emergence of cardiovascular and metabolic diseases later in life (Barker 2003), and thus our results suggest that this relationship may equally apply to adverse neurodevelopmental consequences after exposure to environmental toxicants.
Moore looked at obesity trends through the lens of the Barker Hypothesis, which got us thinking more than 3 decades ago about the role of intrauterine environment in short- and long-term health of offspring.
This proposal grew out of the Barker hypothesis which evolved into the Thrifty Phenotype hypothesis.
Some of these may have a direct influence on embryonic development, whereas others may exert their effects later in life, as predicted by the Barker hypothesis (Barker 1990).
Barker's hypothesis, known then as the "fetal origins hypothesis" but subsequently referred to as the "Barker hypothesis," was published.
Key words: Barker hypothesis, chlorpyrifos, cholesterol, diabetes mellitus type 2, insulin, organophosphates, triglycerides.