The process whereby interactions between the genome and the environment, in utero and during infancy, produce structural and functional adaptations that alter susceptibility to common diseases (e.g., diabetes) in adult life. The fetal programming or fetal origins of adult disease hypothesis started with findings from retrospective epidemiological studies in the 1990s. It holds that prenatal insults arising from, for example, defects in the placental supply of nutrients or severe instances of hypermesis gravid (morning sickness) can lead to permanent effects on the structure, physiology, and metabolism of organ systems that become evident through susceptibility to a range of diseases and disorders in children and beyond. When first put forward, the hypothesis addressed cardiovascular and respiratory diseases, but it has since been extended to include cognitive and behavioral dysfunctions as a consequence of maternal anxiety or stress experienced during pregnancy, as shown in figure below. One criticism of the hypothesis is that is does not cater for what has been termed the ‘double-edged sword’: fetal stress, for example, in the form of pre-eclampsia, can result in the acceleration of both brain and lung maturation. It remains to be seen, however, if such seemingly counterintuitive effects are necessarily beneficial in the long term.
