Since the emergence of the concept of developmental origins of health and disease (DOHaD), suggested by Barker in the 1980s, numerous epidemiological studies in humans have confirmed the relationship between maternal obesity during pregnancy and the risk of offspring developing various chronic adult illnesses. These effects of intrauterine life are independent of inheritance of disease susceptibility genes and/or socio-economic factors. Regarding potential mechanisms, recent data from animal models suggests a role of insulin resistance early in development. Another potential mechanism, in the case of maternal obesity, is increased placental nutrient transfer. The DOHaD concept also includes fetal exposure to environmental endocrine disruptors (EEDs). A Danish group for the first time recently analyzed EED passage across the placenta in humans throughout pregnancy. This study showed different levels of bioaccumulation depending on the fetal organ, with greater vulnerability in male than female fetuses. Recent clinical studies suggested an association between fetal exposure to particular EEDs and precocious puberty, increased incidence of cryptorchidism and impaired sperm quality in adulthood. These modifications of the in-utero environment also appear to be responsible for epigenetic changes that are transmittable over several generations. A recent example of this is the demonstration of the transmission of polycystic ovary syndrome (PCOS) in mice. In summary, an increasing number of examples of the impact of intrauterine life on the health of offspring have appeared in recent years, illustrating the important role that endocrinologists can play in preventing particular pathologies in future generations.