摘要：

Over the last decade, a series of epidemiological studies has begun to change the way in which we think about fetal growth restriction. Whereas previous attention was mainly focused on timing and mode of delivery, evidence now exists that this may represent one facet of a much broader spectrum of care. The 'Fetal Origins of Adult Disease' or 'Barker' hypothesis postulates that perturbed growth in utero may cause permanent physiological changes (programming) within the fetus. This is thought to increase susceptibility to chronic disease during adult life, such as hypertension, coronary heart disease and type 2 diabetes. In essence, a fetus subjected to adverse conditions in utero undergoes a series of adaptations. These prime it for a postnatal life in which similar adverse conditions, such as scarcity of food, are anticipated. For those born into societies with calorie-rich diets, food is abundant rather than scarce, and adaptations made to anticipate harsh conditions now become a burden. The term 'programming' is used to describe the mechanisms which determine fetal adaptation. Such changes are thought to follow gene–environment interaction during specific periods of fetal development. This review outlines the evidence for the Barker hypothesis, summarizing possible long-term consequences of the influence of the intra-uterine environment for both children and adults.

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