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14 - Perinatal influences on the endocrine and metabolic axes during childhood

Published online by Cambridge University Press:  08 August 2009

W. S. Cutfield
Affiliation:
University of Auckland
C. A. Jefferies
Affiliation:
University of Auckland
P. L. Hofman
Affiliation:
University of Auckland
Peter Gluckman
Affiliation:
University of Auckland
Mark Hanson
Affiliation:
University of Southampton
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Summary

Introduction

Over the past 15 to 20 years, David Barker and colleagues at the Southampton Epidemiology Unit have made a sequence of landmark epidemiological observations linking reduction in birthweight with increasing risk of diseases in late adult life that included type 2 diabetes mellitus, syndrome X, hypertension, cerebrovascular disease, coronary artery disease and chronic bronchitis (Barker et al. 1989a, 1989b, 1993, Hales et al. 1991, Hales and Baker 1992, Robinson et al. 1992, Martyn et al. 1996). These observations were possible due to the meticulous neonatal and infancy records kept across several places in England, including Hertfordshire and Preston from 1911 onwards. These initial studies led Barker to propose the fetal origins of adult disease hypothesis (also known as the Barker hypothesis). This hypothesis proposes that the origins of adult disease begin in utero. The observations made by the Southampton Epidemiology Unit linking reduction in birthweight with disordered glucose metabolism in adult life have been confirmed by other research groups across ethnicities and countries including the Netherlands, USA, Sweden and India (Valdez et al. 1994, Curhan et al. 1996, Lithell et al. 1996, McCance et al. 1996, Ravelli et al. 1998). Arguably, the most important of these studies was conducted on adult survivors of the Second World War Dutch famine, in whom 2-hour plasma glucose values following an oral glucose tolerance test were higher than in those born before or conceived after the famine (Ravelli et al. 1998).

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Publisher: Cambridge University Press
Print publication year: 2006

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