THE BREAST: FUNCTIONAL CHANGES AND LACTATION
The maturational changes in hormones from the anterior pituitary gland and ovary are major factors in the development and functioning of the mammary gland. Follicle-stimulating and luteinizing hormones are indispensable for the production of ovarian estrogen and progesterone, which, in turn, control mammary gland development. These are necessary but not sufficient to prepare the breast for lactation.
The mammary gland of a nonpregnant
woman is inadequately prepared for secretory activity. Only during pregnancy do
those changes normally occur that make milk production possible. In the first
trimester of pregnancy, the terminal tubules sprouting from the mammary ducts
proliferate in order to provide a maximum number of epithelial elements for future
acinar formation. In the midtrimester, the reduplicated terminal tubules are grouped
together to form large lobules. Their lumina begin to dilate, and the acinar structures
thus formed are lined by cuboidal epithelium; occasional acini contain small
amounts of colostrum secretion. In the last third of pregnancy, the acini formed
in early and midpregnancy are progressively dilated. The high levels of
circulating estrogens and progesterone during pregnancy are responsible for these
alterations in the breast.
During pregnancy, as estrogen levels
increase, there is a parallel hypertrophy and hyperplasia of the pituitary
lactotrophs. An increase in prolactin occurs soon after implantation,
concomitant with the increase in circulating estrogen. Circulating levels of
prolactin steadily increase throughout pregnancy, peaking at about 200 ng/mL
during the third trimester. This rise is in parallel with the continued
increase in circulating estrogen levels over this time. Despite these elevated
prolactin levels, lactation does not occur because estrogen inhibits the action
of prolactin on the breast (most likely blocking interaction with the prolactin
receptor).
Following childbirth, active
secretion begins in the now maximally dilated acinar structures as a result of
the stimulation by prolactin from the anterior pituitary gland and by the
nursing of the infant. A day or two following delivery of the placenta, both
estrogen levels and prolactin levels decline rapidly and lactation is initiated.
Prolactin levels reach basal concentrations after 2 to 3 weeks in women who do
not breastfeed. In nursing women, basal levels of prolactin decline to the
nonpregnant range within 6 months after parturition; after each act of
suckling, prolactin increases markedly.
Lactation, starting 3 to 4 days
after delivery, is stimulated and maintained through the mechanical act of
sucking. In addition to prompting a pulse in prolactin, stimulation of the
areola causes the secretion of oxytocin, which is responsible for the letdown
reflex and ductal contraction that expels the milk. Therefore, it is through
these feedback mechanisms that suckling ensures further milk production.
Prolactin has not been shown to
affect the macro or microscopic changes in the gland. Its only function is to
stimulate milk secretion after the tissues have been previously adequately
prepared (by estrogen and progestin). During consistent breastfeeding,
follicular ripening and ovulation are suppressed for
approximately 6 months.
The secretion of true milk takes
place in the epithelial lining of the dilated acini by cuboidal or columnar
cells with nuclei at their bases or tips. This epithelium rests on a narrow
band of connective tissue that encloses thin-walled capillaries. Secretory
globules and desquamated epithelial cells distend the acini and their afferent
channels. During the height of lactation, milk secretion and its storage account for one-fifth to
one-third of the breast volume.
Nipple and breast stimulation can
also increase prolactin levels in the nonpregnant woman. Prolactin levels normally
rise following ingestion of the noonday meal and may increase in response to
exercise, sleep, and stress. For these reasons, prolactin levels normally fluctuate
throughout the day, with maximal levels observed during
night time sleep and in the early afternoon.
