International Journal of Epidemiology 2002;31:1235-1239
© International Epidemiological Association 2002
Fetal Origins |
Fetal origins of adult disease: strength of effects and biological basis
a Medical Research Council Environmental Epidemiology Unit, Southampton SO16 6YD, UK.
b National Public Health Institute, Department of Epidemiology and Health Promotion, Diabetes and Genetic Epidemiology Unit, Mannerheimintie 166, Helsinki, Finland.
c University of Helsinki, Department of Public Health, 00014 Helsinki, Finland.
Correspondence: Professor DJP Barker, MRC Environmental Epidemiology Unit, University of Southampton, Southampton General Hospital, Southampton SO16 6YD, UK. E-mail: djpb{at}mrc.soton.ac.uk
Abstract
Background Low birthweight has been consistently shown to be associated with coronary heart disease (CHD) and its biological risk factors. The effects of low birthweight are increased by slow infant growth and rapid weight gain in childhood. To quantify the importance of developmental processes in the genesis of CHD it is necessary to establish the impact of fetal, infant and childhood growth on major pathological events in later life—death, hospital treatment and the need for medication.
Methods Longitudinal study of 13 517 men and women who were born in Helsinki University Hospital during 1924–1944, whose body sizes at birth and during childhood were recorded, and in whom deaths, hospital admissions, and prescription of medication for chronic disease are documented.
Results The combination of small size at birth and during infancy, followed by accelerated weight gain from age 3 to 11 years, predicts large differences in the cumulative incidence of CHD, type 2 diabetes and hypertension.
Conclusions Coronary heart disease and type 2 diabetes may originate through two widespread biological phenomena—developmental plasticity and compensatory growth.
Keywords Fetal growth, childhood growth, type 2 diabetes, hypertension, coronary heart disease
Accepted 11 June 2002
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