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Beyond birthweight: the maternal and placental origins of chronic disease

Published online by Cambridge University Press:  10 June 2010

D. J. P. Barker ,
K. L. Thornburg ,
C. Osmond ,
E. Kajantie  and
J. G. Eriksson
D. J. P. Barker*
Affiliation:
MRC Epidemiology Resource Centre, Southampton General Hospital, University of Southampton, Southampton, UK Heart Research Center, Oregon Health and Science University, Portland, OR, USA Fetal Programming Research Chair, King Saud University, Saudi Arabia
K. L. Thornburg
Affiliation:
Heart Research Center, Oregon Health and Science University, Portland, OR, USA
C. Osmond
Affiliation:
MRC Epidemiology Resource Centre, Southampton General Hospital, University of Southampton, Southampton, UK
E. Kajantie
Affiliation:
Department of Chronic Disease Prevention, National Institute for Health and Welfare, Helsinki, Finland Hospital for Children and Adolescents, Helsinki University Central Hospital, Helsinki, Finland
J. G. Eriksson
Affiliation:
Department of Chronic Disease Prevention, National Institute for Health and Welfare, Helsinki, Finland Department of General Practice and Primary Health Care, University of Helsinki, Helsinginyliopisto, Finland Vasa Central Hospital, Sandviksgatan 2–4, Vasa, Finland Folkhälsan Research Centre, Helsinki, Helsingfors Universitet, Finland Unit of General Practice, Helsinki University Central Hospital, Finland
*
*Address for correspondence: Prof. D. J. P. Barker, MRC Epidemiology Resource Centre, Southampton General Hospital, University of Southampton, Southampton, SO16 6YD, UK. (Email [email protected])
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Abstract

New findings on the maternal and placental programming of chronic disease lead to four conclusions: (1) Growth of the placental surface is polarized from the time of implantation, so that growth along the major axis, the length, is qualitatively different from growth along the minor axis, the breadth. (2) The human fetus may attempt to compensate for undernutrition by expansion of the placental surface along its minor axis. This only occurs if the mother was well nourished before conception, and may have long-term costs that include hypertension. (3) The effects of placental size on long-term health are conditioned by the mother’s nutritional state, as indicated by her socio-economic status, height and body mass index. (4) The maternal–placental programming of chronic disease differs in boys and girls. Boys invest less than girls in placental growth but more readily expand the placental surface if they become undernourished in mid-late gestation. Boys are more responsive to their mothers’ current diets while girls respond more to their mothers’ lifetime nutrition and metabolism.

Keywords

placental sizematernal body sizechronic disease
Type
Reviews
Information
Journal of Developmental Origins of Health and Disease , Volume 1 , Issue 6 , December 2010 , pp. 360 - 364
Copyright
Copyright © Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2010

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