For a long time it was assumed that the risk for diseases such as coronary heart disease (CHD) or insulin resistance, for example, develops from the genetic potential of the parents and is amplified by environmental influences such as an unfavorable lifestyle. This view has been completely overturned in the last two decades by the concept of fetal programming. The concept implies that a stimulus or insult during a sensitive period of fetal development produces permanent changes in structure, physiology, and metabolism, determining later risk for chronic diseases such as CHD and insulin resistance, as well as allergies, an impaired stress response, and many others in adulthood. The concept of Fetal Origins of Adult Disease (FOAD) was introduced by the British epidemiologist David Barker more than 20 years ago and has been the subject of intensive research ever since. The current research approaches aim to identify the biological mechanisms by which a prenatal stimulus or insult alters fetal development, the time lag between prenatal stimulus/insult and later disease, and the multiple factors that contribute to disease risk throughout the lifespan.