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

TLDR

Low birthweight is consistently linked to coronary heart disease and its risk factors, with effects amplified by slow infant growth and rapid childhood weight gain. The study aims to quantify how fetal, infant, and childhood growth influence later life outcomes such as death, hospital treatment, and medication use for chronic disease. A longitudinal cohort of 13,517 Helsinki residents born 1924–1944 was followed, with recorded birth and childhood body sizes and documented deaths, hospital admissions, and chronic disease medication prescriptions. Small size at birth and infancy combined with accelerated weight gain from ages 3 to 11 predicts markedly higher cumulative incidence of coronary heart disease, type 2 diabetes, and hypertension, suggesting developmental plasticity and compensatory growth as underlying mechanisms.

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.