Fetal nutrition and adult disease

• Published in: The American journal of clinical nutrition Vol. 71; no. 5; pp. S1344 - S1352
• Main Authors: GODFREY, K. M, BARKER, D. J
• Format: Conference Proceeding Journal Article
• Language: English
• Published: Bethesda, MD American Society for Clinical Nutrition 01.05.2000; American Society for Clinical Nutrition, Inc
• Subjects: Adult; Biological and medical sciences; Birth Weight; Cardiovascular disease; Coronary Disease - etiology; Diabetes Mellitus, Type 2 - etiology; Disease; Diseases of mother, fetus and pregnancy; Female; Fetal Growth Retardation - complications; Gynecology. Andrology. Obstetrics; Humans; Hypertension; Hypertension - etiology; Infant, Newborn; Male; Medical sciences; Mothers; Nutrition; Nutritional Physiological Phenomena; Polycystic Ovary Syndrome - etiology; Pregnancy; Pregnancy. Fetus. Placenta; Prenatal development; Endocrinopathy; Human; Hypertension; Intrauterine growth retardation; Pregnancy disorders; Disease; Cardiovascular disease; Female sterility; Polycystic ovary; Fetomaternal relation; Coronary heart disease; Non insulin dependent diabetes; Body composition; Female genital diseases; Feeding; Ovarian diseases; Fetal diseases; Fetal development; Cyst; Adult; Benign neoplasm
• ISSN: 0002-9165; 1938-3207
• DOI: 10.1093/ajcn/71.5.1344s

Recent research suggests that several of the major diseases of later life, including coronary heart disease, hypertension, and type 2 diabetes, originate in impaired intrauterine growth and development. These diseases may be consequences of "programming," whereby a stimulus or insult at a critical, sensitive period of early life has permanent effects on structure, physiology, and metabolism. Evidence that coronary heart disease, hypertension, and diabetes are programmed came from longitudinal studies of 25,000 UK men and women in which size at birth was related to the occurrence of the disease in middle age. People who were small or disproportionate (thin or short) at birth had high rates of coronary heart disease, high blood pressure, high cholesterol concentrations, and abnormal glucose-insulin metabolism. These relations were independent of the length of gestation, suggesting that cardiovascular disease is linked to fetal growth restriction rather than to premature birth. Replication of the UK findings has led to wide acceptance that low rates of fetal growth are associated with cardiovascular disease in later life. Impaired growth and development in utero seem to be widespread in the population, affecting many babies whose birth weights are within the normal range. Although the influences that impair fetal development and program adult cardiovascular disease remain to be defined, there are strong pointers to the importance of the fetal adaptations invoked when the maternoplacental nutrient supply fails to match the fetal nutrient demand.