There is evidence that an abnormal intrauterine environment has consequences for later life. Intrauterine growth retardation is associated with low insulin secretion during fetal life and probably a reduced development of insulin receptors. In later life these alterations can induce insulin resistance. Macrosomia is associated with an increased insulin secretion during fetal life and exhaustion of the insulin producing B cells. In later life a reduced insulin secretion is found. The working mechanisms have been explored in experimental studies. Normalisation of the diabetic intrauterine milieu can prevent consequences in later life. There are also indications that vascular changes in later life can be reduced by anti-oxidantia. In the human intrauterine growth retardation is related in later life with insulin resistance, vascular diseases and preeclampsia; macrosomia is related with gestational diabetes and breastcarcinoma.