The human male and female fetus exhibit different strategies for survival to an adverse maternal environment. In pregnancies complicated by asthma we have identified that females reduce growth while males institute strategies to continue to grow. If a secondary event arises such as an asthma exacerbation, the female fetus does not change its smaller growth trajectory and survives to term. Conversely the male fetus is more at risk of growth restriction, preterm delivery or stillbirth in the presence of an exacerbation. These data suggest females adjust growth in response to an adverse maternal environment to survive any further reductions in oxygen or nutrients while males continue to grow normally at risk of a poor outcome if another adverse event occurs. We hypothesise that this sexually dimorphic response is the result of differences in sensitivity of the placenta to glucocorticoids which have downstream effects on pathways associated with growth. Our current research focuses on identifying the mechanism by which glucocorticoids confer a sex specific difference. Female placentae modulate intracellular cortisol concentrations by adjusting cortisol metabolism in response to maternal glucocorticoid concentrations relative to male placentae. We have identified sex differences in placental glucocorticoid receptor (GR) expression, function and regulation in human placentae of both term and preterm pregnancies. GR gene expression may be regulated by differential microRNA expression between the sexes. Different isoforms of the GR and their localisation in the cytoplasm and the nucleus vary between the sexes. In combination these findings suggest the male fetus institutes a state of glucocorticoid resistance in order to continue to grow in an adverse maternal environment via differential expression and localisation of the GR while the female fetus tightly regulates glucocorticoid responses via modulating cortisol metabolism and GR isoform interactions.