The emerging story of the physiology of human birth is full of unexpected twists and turns. As the morula diverges into the trophectoderm and epiblast and forms the blastocyst, this critical developmental event sends these two sets of cells on two very different trajectories. The epiblast will form the fetus with every prospect of a future 90 years long. In contrast, the trophectoderm will play a key role as a type of booster rocket for the fetus, but is doomed to be jettisoned after just 9 months. New data indicates that the placenta’s short trajectory is initiated by chromosomal changes that allow expression of endogenous retroviruses. The formation of the human placenta requires the participation of the endogenous retrovirus coat protein, Syncytin 1. Syncytin 1 promotes the formation of the syncytiotrophoblast layer that is characteristic of the placenta. Syncytin 1 even has an immunosuppressive domain that may play a key role in the immune tolerance of the fetal allograft. The placenta then assumes the role of fetal guardian, immunological barrier, nutrient transporter, an agent of the father manipulating the metabolism and perhaps behaviour of the mother to improve the prospects for the fetus. During early pregnancy trophoblast tissue secretes hCG that maintains ovarian progesterone production. Together, hCG and progesterone suppress uterine contractility, allowing the blastocyst to remain within the uterus and preparing the endometrium for implantation. Syncytin-mediated pathways promote cytotrophoblast fusion into syncytiotrophoblast and increase the production of a variety of placental hormones including corticotrophin releasing hormone (CRH). CRH is released into the maternal circulation and is one of the hormones promoting increased cAMP, protein kinase A activation and myometrial relaxation. Increased uterine relaxation is required as pregnancy progresses and the size of the fetus increases within this smooth muscular organ with a proclivity to contraction. The placenta assumes more of this relaxatory role by becoming the major source of progesterone production. CRH is also released into the fetal circulation. Within the fetus, CRH stimulates fetal adrenal zone production of the steroid DHEAs. Fetal adrenal DHEA is a substrate for fetal liver 16 hydroxylase and the 16 hydroxylated steroid is converted in the placenta to estriol. Oestriol is therefore almost exclusively formed from fetal precursors. Meanwhile the placenta synthesises oestradiol from predominantly maternally derived DHEA. Why have two oestrogens produced in large amounts in this way? One potential explanation is that the oestriol-oestradiol occupancy of oestrogen receptor alpha inhibits transactivation at oestrogen responsive genes. This mechanism may prevent synthesis of pro-contractile proteins such as connexin 43. Late in pregnancy increasing CRH concentrations drive further increases in eostriol production. This allows formation of oestriol homodimers which cause transactivation of oestrogen responsive genes, leading to increased connexin 43 expression and consequent linkage of myometrial cells. The changes in the oestrogenic environment likely leads to use of an alternate promoter for the progesterone receptor gene leading to the formation of progesterone receptor A which blocks normal progesterone action. Progesterone action is also reduced by increased production of 20 alpha hydroxysteroid dehydrogenase. Changes in splicing of the oestrogen receptor alpha gene enhance the oestrogenic environment. Together these changes remove the relaxatory brake on the myometrium, and increase myometrial excitability by reducing potassium channels. The growing and maturing fetus participates in the onset of labour by creating the steroid precursor for placental oestriol leading to myometrial cell excitability and connectivity. Increased excitability and connectivity lead to increased synchrony of contractile behaviour of individual myometrial cells, increased intrauterine pressure, cervical dilatation and birth. The fetus and placenta are interdependent in human pregnancy, a well-matched developmental program for the partners is essential for a successful outcome that sets the fetus on a trajectory for a healthy life, leaving a senescent placenta in its wake.