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

• Published in: International journal of epidemiology Vol. 31; no. 6; pp. 1235 - 1239
• Main Authors: Barker, DJP, Eriksson, JG, Forsén, T, Osmond, C
• Format: Journal Article
• Language: English
• Published: Oxford Oxford University Press 01.12.2002; Oxford Publishing Limited (England)
• Subjects: Aged; Anthropometry; Biological and medical sciences; Birth Weight; Body Mass Index; Cardiology. Vascular system; Cardiovascular Diseases - embryology; childhood growth; Coronary Disease - embryology; Coronary Disease - epidemiology; Coronary heart disease; Diabetes Mellitus, Type 2 - embryology; Diabetes Mellitus, Type 2 - epidemiology; Embryonic and Fetal Development; Female; Fetal growth; Finland - epidemiology; Growth; Heart; Humans; hypertension; Hypertension - embryology; Hypertension - epidemiology; Incidence; Infant, Low Birth Weight; Infant, Newborn; Longitudinal Studies; Male; Medical sciences; Middle Aged; Odds Ratio; Pregnancy; Prenatal Exposure Delayed Effects; type 2 diabetes; Weight Gain; Finland; Endocrinopathy; Human; Hypertension; Fetal growth; Pregnancy disorders; Growth; Low birth weight; Cardiovascular disease; Coronary heart disease; Non insulin dependent diabetes; Epidemiology; Weight gain; Body mass index; Newborn diseases; type 2 diabetes; Prematurity; Risk factor; Adult; Fetus; childhood growth; Child; Public health
• ISSN: 0300-5771; 1464-3685
• DOI: 10.1093/ije/31.6.1235

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.