Fetal programming of coronary heart disease.
People who develop coronary heart disease grow differently from other people both in utero and during childhood. Slow growth during fetal life and infancy is followed by accelerated weight gain in childhood. Two disorders that predispose to coronary heart disease, type 2 diabetes and hypertension, are preceded by similar paths of growth. Mechanisms underlying this are thought to include the development of insulin resistance in utero, reduced numbers of nephrons associated with small body size at birth and altered programming of the micro-architecture and function of the liver. Slow fetal growth might also heighten the body's stress responses and increase vulnerability to poor living conditions in later life. Coronary heart disease appears to be a developmental disorder that originates through two widespread biological phenomena, developmental plasticity and compensatory growth.
D001724:Birth Weight; D015992:Body Mass Index; D002648:Child; D003327:Coronary Disease / Q000453:epidemiology / Q000209:etiology*; D003924:Diabetes Mellitus, Type 2 / Q000453:epidemiology; D005314:Embryonic and Fetal Development; D005260:Female; D005317:Fetal Growth Retardation / Q000150:complications / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000453:epidemiology; D007223:Infant; D007230:Infant, Low Birth Weight; D007231:Infant, Newborn; D008297:Male; D011203:Poverty; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D015430:Weight Gain