The most frequent “great obstetrical syndromes” are fetal growth restriction, preeclampsia, and gestational diabetes mellitus. The placenta plays a prominent role for the development of these, or at least for some subtypes. In particular, the first trimester of pregnancy appears to be the key period in which a range of biological processes occurs, which are essential for proper placental development and maternal adaptation to pregnancy. At this very early stage, placental development comprises invasion of placenta-derived trophoblasts into the uterine wall to convert maternal spiral arteries into flaccid conduits, enabling adaption of the uteroplacental blood flow to ongoing pregnancy. Dysregulation of trophoblast invasion and inadequate spiral artery remodeling are at the root of preeclampsia and fetal growth restriction. Placental hormones and peptides provide stimuli for maternal insulin sensitivity and structural and functional adaptation in pregnancy, and they have been implicated in the development of gestational diabetes mellitus. Fetal adiposity, the essential phenotype of diabetic pregnancies, is likely the result of enhanced transplacental transfer of insulin secretagogues early in pregnancy and the subsequent glucose steal phenomenon. Later in pregnancy, once placental function is well developed, it mainly serves to protect the fetus in response to fetal signals.