Physiology and Endocrinology: Making and Moving Milk
Two hormones, two jobs
Lactogenesis I (secretory differentiation) begins mid-pregnancy: alveolar cells make colostrum, but copious secretion is held back by progesterone. Lactogenesis II (secretory activation) follows delivery of the placenta; progesterone withdrawal plus a prolactin surge switches the gland to copious milk production, usually 30–72 hours postpartum. Signs include fullness and a change in milk appearance. Lactogenesis III is autocrine: milk contains a feedback inhibitor of lactation (FIL), so the gland's output depends on how completely and how often milk is removed.
Prolactin, from the anterior pituitary, is the "make milk" hormone; it rises with nipple stimulation, is higher at night (supporting night feeds), and is suppressed by dopamine. Oxytocin, from the posterior pituitary, is the "move milk" hormone: it contracts myoepithelial cells and produces the milk ejection reflex. Pain, stress and embarrassment can inhibit oxytocin release even when prolactin is adequate; uterine cramping and drowsiness during feeds are signs it is working.
Milk synthesis runs at roughly 25–30 mL/hour in established lactation, and composition changes within a feed (fat rises toward the end) - the "foremilk/hindmilk" framing is a trap; there are not two separate milks.
Rule of thumb: if the breasts feel full but milk does not flow, think ejection (oxytocin); if supply is low, think removal frequency (FIL).