[Truncated abstract] There is a large body of evidence describing the benefits and risks, to the human fetus, of antenatal glucocorticoid treatment, but no published research on the effects on lactation. The withdrawal of progesterone, in the presence of high levels of endogenous glucocorticoids and prolactin, triggers the onset of copious milk secretion (lactogenesis II) at the end of pregnancy. The alteration of lactogenesis II by exogenous glucocorticoids could potentially have adverse impacts on postnatal nutrition in both term and preterm infants. I aimed to determine the effects of maternal antenatal glucocorticoid treatment on lactogenesis II in both ewes and women. I found profound adverse effects on lactation in ewes, and similar but more subtle effects on lactation in women . . . This thesis represents the first investigation of the effects of antenatal glucocorticoid treatment on lactogenesis II in both ewes and women. I found that, in ewes, antenatal glucocorticoid treatment stimulated premature lactogenesis II, and this was caused by disruptions to hormonal regulation during pregnancy. This event was followed by profound delays in lactogenesis II after term parturition. More subtle effects in women suggest that antenatal glucocorticoid treatment did not have a major, prolonged impact on postnatal lactogenesis II. Very preterm gestational age strongly predicted delays in lactogenesis II stressing the importance of assistance for these mothers when they are establishing lactation.