During the last 15 years, a number of long-term health risks associated with reduced fetal growth have been identified, including cardiovascular diseases and the insulin-resistance syndrome or one of its components: hypertension, dyslipidemia, impaired glucose tolerance or Type 2 diabetes. A common feature of these conditions is the presence of high insulin levels, which are thought to play a pathogenic role. However, despite abundant data in the literature, it is still difficult to trace the pathway by which fetal events, environmental or not, may lead to the increased morbidity later in life. To explain this association, several hypotheses have been proposed pointing to the critical role of either a detrimental fetal environment or a genetic susceptibility, or indicating interaction of both. Clearly, not all subjects born small for gestational age are at the same risk of developing these complications. It appears that individuals at particular risk are those who were thin at birth and had a subsequent catch-up in body mass index, irrespective of the degree of adiposity in adulthood. It is suggested that this particular dynamic change in adiposity has a critical role in the development of long-term metabolic complications. Therefore, it is important to consider the relative impact of early postnatal events in relation to fetal growth to the diseases risk throughout life in forming health policy strategies towards eventual early interventions.