During pregnancy, a rise in hormones such as progesterone and prolactin stimulates the growth of breast tissue, and the breasts increase by an average of one to two cup sizes. This outward growth is one indicator that the breasts are undergoing the inward growth necessary to support lactation, including the transition of mammary glands (modified sweat glands) into secretory cells, extensive branching of the milk ducts, and enlargement of the Montgomery glands (sebaceous glands in the areola surrounding the nipple).[1]
By 16 to 20 weeks of pregnancy, the breasts are fully ready to make milk. This marks the first stage of lactation: lactogenesis I. The end result is the formation of colostrum (“first milk”), the secretion and production of which is held in check by high levels of circulating progesterone.[2] Colostrum is rich in immunological components (especially the antibody immunoglobulin A) and developmental factors (like epidermal growth factor). It serves as the infant’s food for the first few days of life.[3] It also has a laxative effect in infants, helping the newborn expel meconium (the first stool).
After childbirth and expulsion of the placenta, progesterone drops and prolactin rises, cueing the second stage of milk production: lactogenesis II. This stage is known for copious milk production and begins by the fourth day postpartum with the production of around 500 mL of breast milk (called transitional milk). If lactogenesis II does not occur by four days postpartum, it is considered “delayed”. Approximately 20% to 30% of lactating parents have delayed lactogenesis II, and although the causes vary (e.g., obesity, primiparous parent/first-time parent, stress during delivery), the experience alone is associated with cessation of breastfeeding by four weeks postpartum.[4] Appropriate clinical support of these parents is necessary.
The milk produced during lactogenesis II is different from colostrum. It contains less sodium and chloride and more lactose as the closing of tight junctions in the mammary epithelial cells alters what passes into the milk.[2] While the milk production is still under endocrine control, frequent breastfeeding is important if the parent intends to continue breastfeeding. At around ten days postpartum, there is a switch from endocrine control to autocrine (or local) control of milk production. This ushers in the maintenance stage: lactogenesis III.
During lactogenesis III, the primary driver for increased milk supply is increased demand via milk removal. The breasts will make milk indefinitely as long as the milk is removed and there are no underlying lactation issues. (This explains how wet nurses maintained their occupation in lieu of repeated personal pregnancies.) Consequently, the role of systemic hormones in milk production and infant feeding is much smaller but not absent. For example, the hormone oxytocin is released from the posterior pituitary gland and is involved in the milk letdown reflex, and the hormone prolactin is released from the anterior pituitary gland and is involved in milk production. Stimulation of the nerve endings in the nipple by infant suckling or breast pumps is what triggers the release of these two hormones. [1]
By the end of the first month, the milk is considered fully mature and offers the infant approximately 0.9 to 1.2 grams of protein/dL, 3.2 to 3.6 grams of fat/dL, and 6.7 to 7.8 grams of lactose/dL.[5] The exact macronutrient ratio does vary, especially when comparing milk from mothers of preterm infants to milk from mothers of term infants, and it also changes with time.[5] When the mother begins to wean her infant and the local signals for milk production decrease, involution begins. Involution is the process by which the milk-producing cells are removed through apoptosis (programmed cell death) and replaced with fat cells. It may take up to 12 months for all lactating cells to be replaced.[3]
References
- ^Lee S, Kelleher SLBiological underpinnings of breastfeeding challenges: the role of genetics, diet, and environment on lactation physiology.Am J Physiol Endocrinol Metab.(2016-Aug-01)
- ^Neville MC, Morton J, Umemura SLactogenesis. The transition from pregnancy to lactation.Pediatr Clin North Am.(2001-Feb)
- ^Pang WW, Hartmann PEInitiation of human lactation: secretory differentiation and secretory activation.J Mammary Gland Biol Neoplasia.(2007-Dec)
- ^Brownell E, Howard CR, Lawrence RA, Dozier AMDelayed onset lactogenesis II predicts the cessation of any or exclusive breastfeeding.J Pediatr.(2012-Oct)
- ^Ballard O, Morrow ALHuman milk composition: nutrients and bioactive factors.Pediatr Clin North Am.(2013-Feb)