The symposium reviews forming part of this issue of The Journal arose from a mini-symposium entitled Altered placental function as a cause of altered fetal growth held at a meeting of the Society for Gynecologic Investigation in March 2009, which was sponsored, in part, by The Journal of Physiology. The papers explore the concept that the phenotype of the placenta and its ability to support fetal growth are not set at conception, or even implantation, but continue to adapt throughout pregnancy in relation to the prevailing environmental conditions and the genetically determined nutrient demands of the fetus for growth. In particular, these papers consider the adaptations in placental morphology and function commonly associated with intrauterine growth restriction (IUGR) and other growth disorders and the extent to which they are the cause or the consequence of the abnormalities in fetal growth. The four papers cover different aspects of this theme. Professor Sibley's paper sets the scene by asking how the syncytiotrophoblast compares to other transporting epithelia and in what ways it can adapt to integrate maternal and fetal signals that influence fetal growth (Sibley, 2009). He summarises what is known about transport across the human syncytiotrophoblast and how this is related to maternal nutrition and fetal demand for nutrients. Professor Cetin's paper focuses on the inter-relationship between placental function and maternal diet in the supply of nutrients to the fetus with special emphasis on the long chain fatty acids and their role in fetal development in human IUGR and other growth disorders (Cetin et al. 2009). In particular, her paper highlights the role of the placenta per se in modifying the fatty acids delivered to the fetus by desaturation, elongation, differential transport and sequestration. Professor Nelson's paper addresses the role of morphological changes in the trophoblast as a cause of IUGR. He discusses the extent to which apoptosis of the syncytiotrophoblast exceeds cytotrophoblast differentiation to cause the dysregulated trophoblast development often associated with IUGR (Scifres & Nelson, 2009). More specifically, he examines the potential causes of this dysregulation through changes in cell signalling pathways, fibrin deposition and the oxidative damage associated with ischaemia–reperfusion injury of the human trophoblast. Professor Fowden's contribution extends the discussion to a wider range of species and considers the morphological and functional mechanisms by which environmental challenges alter the efficiency and nutrient transport capacity of the placenta to help maintain fetal growth when its growth potential is compromised. She concentrates on the role of key maternal and fetal hormones both as signals of the mismatch between placental supply and fetal demand and as effectors of the placental adaptations that help rectify the imbalance and optimise fetal growth in the prevailing condition in utero (Fowden et al. 2009). More rigorous assessment of placental phenotype may, therefore, provide new markers of the fetal growth trajectory and help develop therapeutic treatments for placental dysfunction in IUGR and other compromised pregnancies (Sibley, 2009; Scifres & Nelson, 2009). The overall objectives of this series of articles are threefold: firstly, to raise awareness of placental adaptability to clinicians and biomedical scientists, secondly to highlight the importance of placental phenotype in determining life history of the infant, and finally, to stimulate further research into placental biology. There is plenty to do!