The postpartum period and lactation physiology

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The postpartum period and lactation physiology

Ilana R. Azulay Chertok

The postpartum period is a time of restoration and return to the nonpregnant state. This period is generally defined as the 6- to 8-week postpartum period from the delivery of the placenta to the involution and return of the reproductive organs to their nonpregnant state. The postpartum period is characterized by significant anatomic, physiologic, and endocrinologic changes related to the involution and lactation processes. It is also a time of major psychologic and social change as the new mother bonds with her infant, assumes responsibility for, and incorporates her infant into the family system. The focus of this chapter is on the physiologic and endocrinologic changes associated with return of the reproductive system to its nonpregnant state and with the anatomic, physiologic, and endocrinologic changes associated with initiation and maintenance of lactation. The physiologic and anatomic changes within other body systems as they return to the nonpregnant state are described in Chapters 8 to 20.

Involution of the reproductive organs

The process of involution involves the gradual and progressive return of the reproductive system (i.e., uterus, cervix, vagina, and breasts in the nonlactating woman) to its nonpregnant state during the 6- to 8-week postpartum period.


Immediately following delivery of the placenta, the uterus weighs approximately 1000 g and lies with its anterior and posterior walls in close approximation in midline about halfway between the umbilicus and symphysis pubis. Over the next 12 hours the fundus of the uterus is located approximately at the level of the umbilicus. Involution of the uterus involves uterine contraction, autolysis of myometrial cells, and epithelial regeneration and proliferation. The height of the fundus continues to decrease by about 1 cm per day so that by 3 days the fundus lies 2 to 3 fingerbreadths below the umbilicus (or slightly higher in multiparous women). By 1 week, the uterus weighs about 500 g and is 4 to 5 fingerbreadths below the umbilicus. By 2 weeks, the uterus weighs about 300 g and has descended into the true pelvis and the fundus can no longer be palpated abdominally. The size of the uterus gradually decreases over the next month so that by 6 weeks the uterus has nearly returned to its nonpregnant location and size.69 Immediately following delivery of the infant, contractions of the uterine myometrium compress the blood vessels supplying the placental site, causing hemostasis and separation of the placenta from the uterine wall, leaving the basal portion of the decidua. Postpartum contractions (“afterpains”) during the first few days of postpartum may be strong, especially with increasing parity, gradually diminishing in intensity and frequency within the first week. Infant suckling also stimulates oxytocin release resulting in uterine contractions.17

Subinvolution, slowed, delayed, and/or incomplete involution, is usually due to a lack of effective uterine contraction related to various causes including uterine atony (most common), retained placental fragments, uterine inversion, lacerations, or infection, which are usually responsive to early diagnosis and treatment.17 There has been research indicating that uterine massage after placental delivery may prevent postpartum hemorrhage.31 Signs and symptoms of infection may include fever, abdominal tenderness, and foul-smelling lochia. Signs and symptoms of hemorrhage include tachycardia, low blood pressure, boggy uterus, and excessive uterine bleeding with clots, consisting of a blood loss over 500 mL post-vaginal delivery and 1000 mL or more post-cesarean delivery. Postpartum hemorrhage is most commonly associated with coagulation disorders, infection, and subinvolution and its causes, as well as other risk factors including retained placenta, failure to progress in the second stage of labor, placenta accrete, lacerations, instrumental delivery, large for gestational age infant, hypertensive disorders, induction of labor, and oxytocin-augmented labor.72 Assessment using the “four Ts” (tone of the uterus; trauma including lacerations, inversion, and rupture; tissue retention or invasion; and thrombin and coagulation disorders), along with prevention and early intervention are crucial. Management of uterine atony and hemorrhage is aimed at increasing uterine contractility by attempting bimanual uterine compression massage, and uterotonic medications such as uterotonic oxytocin, misoprostol, methylergonovine maleate, and other prostaglandins.5,83 If uterine atony and hemorrhage persist, uterine suture compression or surgical intervention may be necessary.17,37

Under the influence of estrogens, the myometrium undergoes hypertrophy and hyperplasia during pregnancy with increases in cell cytoplasm and size. Following delivery, excess intracellular proteins (especially actin and myosin) and cytoplasm within the myometrial cells are eliminated by autolysis with degradation by proteolytic enzymes and macrophages. As a result, the size of individual myometrial cells is markedly reduced without a significant reduction in the total number of cells. Initially the endometrium resembles a large desquamating wound. The upper portion of the spongy endometrial layer is sloughed off with delivery of the placenta.

Regeneration of the uterine epithelial lining begins 2 to 3 days postpartum with differentiation of the remaining decidua into two layers, a superficial layer and a basal layer. The superficial layer of granulation tissue, which provides a barrier to infection, is formed as leukocytes invade the remaining decidua. This layer gradually degenerates, becoming necrotic, and is sloughed off in lochia. The basal layer, containing residual endometrial glands, remains intact and contributes to the new endometrium. By about 2 to 3 weeks, the endometrium has been restored and is similar to the nonpregnant endometrium in the proliferative phase of the menstrual cycle except for remnants of hyalinized decidua with areas of leukocyte infiltration.69 Healing at the placental site takes longer with regeneration occurring gradually over 6 weeks. Following delivery, the placental site is a rough area 4 to 5 cm in diameter containing many thrombosed vessels. The large blood vessels that supplied the intervillous spaces are invaded by fibroblasts and their lumen is obscured. Some of these vessels recanalize later with smaller lumens. The placental site heals by decidual sloughing and exfoliation and by growth of endometrial tissue.69


The process of involution and restoration of the endometrium is reflected in the characteristics of lochia, the postpartum vaginal discharge. Lochia varies in amount and color as healing progresses. Three forms of lochia are observed, generally in the following pattern: rubra, serosa, and alba. Lochia rubra is red or red-brown with a fleshy odor and is seen during the first few days or through the first week postpartum. Lochia rubra contains blood from the placental site; pieces of amnion and chorion; and cellular elements from the decidua, vernix, lanugo, and meconium. Lochia serosa is a pinkish-brown discharge lasting approximately 2 to 3 weeks. Lochia serosa contains some blood, wound exudate, erythrocytes, leukocytes, cervical mucus, microorganisms, and shreds of decidual tissue. The lochia becomes progressively lighter in color. Lochia alba is whitish-yellow in color because it primarily contains leukocytes and decidual cells which may continue for another few weeks. Overall lochia duration may last 4 to 6 weeks postpartum, which is a longer duration than traditionally described, and may vary according to breastfeeding practice and parity.51,73,78

Cervix, vagina, and perineum

Immediately following a vaginal delivery, the cervix hangs into the vagina and is dilated, bruised, and edematous, with possible lacerations. During the first 12 to 18 hours, the cervix shortens and becomes firmer (“forming up”) and, as measured by magnetic resonance imaging, has a mean length of 5.6 cm by 30 hours (versus 2.9 cm by 6 months).81 By the second or third day, the cervix is dilated 2 to 3 cm and by 1 week the cervix is approximately 1 cm dilated. By 4 weeks the external os appears as a small transverse slit, characteristic of multiparous women. Even by 6 weeks, there may still be evidence of stromal edema and round cell infiltrates, which may persist until 3 to 4 months.69 Remodeling and involution of the cervix begin immediately postpartum and occurs rapidly with an increase in fibroblasts, which play a major role in remodelling, collagen, and proteoglycans. This process may be mediated by transforming growth factor-β (TGF-β) and other cytokines.79 This process works to restore the cervical structure altered during cervical ripening and delivery.

After vaginal delivery, the vagina is edematous and relaxed, with decreased tone and absence of rugae. The vagina gradually decreases in size and regains tone, although it does not fully return to its prepregnancy state. By 3 to 4 weeks, rugae have begun to reappear, and edema and vascularity have decreased. The vaginal epithelium is generally restored by 6 to 10 weeks postpartum.69 Decreased lubrication of the vagina during this period can lead to discomfort with sexual intercourse, especially in the lactating woman, as can perineal pain related to episiotomy, laceration, and trauma.17

The use of episiotomies has significantly decreased since the 1980s and 1990s when research documented risks associated with routine use and advocated for restrictive use of episiotomies. Systematic reviews have shown that restrictive use of episiotomies is associated with less severe perineal trauma, less suturing, fewer complications, and less pain.10,27 While initial healing occurs in 2 to 3 weeks, the episiotomy site may take 4 to 6 months to completely heal. A strategy that has been found to protect the perineum and decrease the risk for performing an episiotomy is prenatal perineal massage.6,19,20

Urinary function

Diuresis occurs during the postpartum period, reversing prenatal fluid retention. Overdistention of the bladder; prolonged labor; vulvar, urethral, or bladder trauma, may result in incomplete bladder emptying and urine retention, especially when analgesics were used in labor and delivery and following cesarean delivery.44,87 Management of maternal reports of urine retention in the early postpartum period include providing privacy, positioning, and immersing the woman’s hands in water, as least invasive measures, and catheterization and medication are more invasive options.87 Urinary incontinence is associated with pregnancy and trauma during the delivery process. Research has found that pelvic floor exercises can be effective in preventing and treating prenatal and postpartum urinary incontinence.28,39 Changes in postpartum urinary function are discussed further in Chapter 11.


The breasts or mammary glands undergo marked changes during pregnancy with development of alveolar tissue and ductal system in preparation for lactation. Following delivery, further anatomic and physiologic changes occur in breastfeeding women (see “Physiology of Lactation”).

In women who do not breastfeed, involution of the breasts occurs. Distention and stasis of the vascular and lymphatic circulation may result in primary engorgement by 2 to 4 days following delivery. The treatment of engorgement for nonlactating women includes abstaining from stimulation of milk production, abstaining from any breast stimulation, brief applications of cold compresses or cold packs, and administration of anti-inflammatory medication. Bromocriptine (Parlodel) is no longer approved by the Food and Drug Administration for lactation suppression due to numerous adverse maternal outcomes.25 Without stimulation by suckling and removal of milk, secretion of prolactin decreases and milk production ceases. Glandular tissue gradually returns to a resting state over the next few weeks, although breasts do not completely return to their prepregnant state, as new alveoli formed during pregnancy do not completely disappear.

Physical activity and sexual function

The postpartum period is often characterized by alterations in physical activity and function. Gradual resumption of safe physical exercise promotes postpartum maternal well-being, physically and psychologically, as well as facilitates postpartum weight management.4,63 Fatigue, postpartum anatomic and physiologic changes, lochia, perineal trauma, pain, decreased perineal tone, leaking or engorged breasts, the presence and stress of the new baby, adaptation to the demands of the new parental role, and psychologic factors can modify physical and sexual function. Reduced vaginal lubrication associated with the decreased estrogen levels in the postpartum period, especially in lactating women, may contribute to an alteration in sexuality and sexual discomfort.14 Masters and Johnson reported that orgasms in women for the first few months following birth tended to be shorter and less intense with greater latency of response and decreased vasocongestion of the labia majora and minora and decreased vaginal lubrication.52 The timing of resumption of sexual intercourse should depend on maternal physical restoration (cessation of bleeding and absence of discomfort) and the emotional and psychologic readiness of both partners, while accounting for traditional and cultural beliefs, attitudes, and preferences. Health care providers should be aware of, respectful of, and sensitive to cultural and religious practices associated with sexuality during the postpartum period. Interventions include education and counseling regarding postpartum physical and sexual function, contraception, use of vaginal lubricants, alternate forms of intimacy, and pelvic floor exercises to strengthen and tone the perineal muscles.

Endocrine changes

Postpartum endocrine changes primarily occur secondary to fetoplacental hormonal withdrawal related to delivery of the infant and placenta and to increased production of prolactin. In general, most peptide hormones, enzymes, and other circulating proteins of placental origin reach nonpregnant levels by 6 weeks postpartum. Removal of placental hormones alters the physiologic function of many body systems, thus initiating return of those systems to their nonpregnant state. The rate at which placental hormones disappear from the maternal system depends on the half-life phases of the particular substance in maternal blood. There are two phases. The first half-life, which is relatively short, involves hormonal removal from the intravascular system; the second half-life involves the slower removal from extravascular and intracellular space.77 For example, human placental lactogen (hPL) has a short second half-life and generally disappears by 1 to 2 days, whereas human chorionic gonadotropin (hCG) has a longer second half-life and can be detected for 3 to 4 weeks.77 Substances of fetoplacental origin, such as pregnancy-associated proteins, also disappear soon after delivery, whereas other proteins such as alpha-fetoprotein, derived from both placental and maternal sources, are present in maternal plasma for several weeks postpartum.77 Endocrine changes related to mammary development in lactating and nonlactating women are summarized in Figure 5-1.

Estrogens and progesterone

During pregnancy, estrogen promotes development of the mammary ductal system and progesterone promotes lobular and alveolar growth. The elevated levels of these hormones inhibit prolactin action thereby inhibiting lactation. Because the placenta is the major source of estrogens and progesterone, these hormones disappear rapidly following delivery. Plasma estradiol (with a first half-life of 20 minutes and second half-life of 6 to 7 hours) reaches levels that are less than 2% of pregnancy values by 24 hours. By 1 to 3 days, estradiol levels are similar to those found during the follicular phase of the menstrual cycle (less than 100 pg/mL [367 pmol/L]), and unconjugated estriol is undetectable. Although the first and second half-lives of progesterone are short, progesterone levels do not fall as rapidly as estradiol levels because the corpus luteum continues progesterone secretion during the first days following delivery. Generally progesterone falls to levels similar to the luteal phase of the menstrual cycle (2 to 25 ng/mL [6.4 to 79.5 pmol/L]) by 24 to 48 hours and to the follicular phase (less than 1 ng/mL [3.2 pmol/L]) by 3 to 7 days.77 Ovarian production of estrogens and progesterone is low during the first 2 weeks postpartum and gradually increases with resumption of gonadotropin secretion.

Pituitary gonadotropin

The pituitary-hypothalamic-ovarian axis (see Chapter 2), along with production of pituitary gonadotropin, follicle-stimulating hormone (FSH), and luteinizing hormone (LH), is suppressed during pregnancy. Serum levels of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) remain very low during the first 2 weeks postpartum in both lactating and nonlactating women, gradually increasing with resumption of pituitary function by 4 to 6 weeks. The basis for the initially sluggish pituitary response is unknown. Tulchinsky suggests that this phenomenon may be related to (1) suppression of the pituitary-hypothalamic-ovarian axis by the high levels of circulating estrogens during pregnancy, (2) need for time to reestablish adequate stores of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) leading to a delay in secretion of gonadotropin-releasing hormone (GnRH) by the hypothalamus, and (3) possibly inhibition of luteinizing hormone (LH) release by human chorionic gonadotropin (hCG) and prolactin.77


Prolactin is a single-chain peptide hormone secreted in pulses by the anterior pituitary gland. Serum levels of prolactin dramatically increase during pregnancy (from 10 ng/mL to 200 ng/mL [434.8 to 8695.6 pmol/L]), working synergistically with other hormones to promote mammary development including lobular, alveolar, and nipple growth. Throughout pregnancy, secretion of prolactin by the anterior pituitary is controlled by hypothalamic prolactin-inhibiting factor (PIF), mainly dopamine.55 A placental hormone, probably progesterone, inhibits the direct influence of prolactin on the breast during pregnancy, thereby suppressing lactation. With the expulsion of the placenta at delivery, and the significant drop in progesterone, lactogenesis II (copious milk secretion) is initiated.61 Delayed lactogenesis may result from retained placental fragments with the potential to secrete progesterone.61 Postpartum prolactin levels remain elevated due to frequent infant suckling and nipple stimulation.55 In nonlactating women, prolactin levels fall into the high end of the nonpregnant range by 7 to 14 days.77 Breastfeeding women experience a gradual decreasing trend in serum prolactin surges after 6 weeks postpartum, even with continued breastfeeding. Patterns of prolactin secretion associated with lactation are described in “Physiology of Lactation.”

Resumption of menstruation and ovulation

The early postpartum period tends to be a period of relative infertility for many women. Resumption of menstruation and ovulation varies among individual women regardless of whether or not the woman is lactating, although there is a greater tendency for exclusively breastfeeding women to experience a longer period of anovulation and amenorrhea. Menstruation usually resumes by 6 weeks postpartum in nonlactating women, although research has found even earlier resumption of menstruation.35 The first postpartum menstrual cycle may be anovulatory, although nearly a third of these cycles are preceded by ovulation. That first cycle may also have inadequate luteal function, thereby decreasing fertility in the early postpartum period.35 Considering the possibility of resumption of ovulation in the early postpartum period, discussion of contraceptive options should be initiated prenatally or immediately postpartum.

Lactation is associated with a delay in resumption of menstruation and ovulation. In response to infant suckling during breastfeeding, there is a disruption in the normal pattern of gonadotropin-releasing hormone (GnRH) secretion from the hypothalamus, resulting in lower levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH).54 This relationship was demonstrated by a study whereby gonadotropin-releasing hormone (GnRH) infused every 90 minutes into amenorrheic lactating women resulted in stimulation of normal follicular growth.88 Although pulsatile secretion of luteinizing hormone (LH) is seen by 8 weeks postpartum, levels are low and of variable frequency with no preovulatory surge. With regular suckling, luteinizing hormone (LH) remains suppressed.58 With decreased lactation frequency, gonadotropin-releasing hormone (GnRH) secretion returns to normal and follicle-stimulating hormone (FSH) stimulates follicular growth, which in turn increases estradiol and results in luteinizing hormone (LH) release, causing follicular rupture, egg release, and formation of the corpus luteum.54 Health care providers should discuss contraceptive options with lactating women, explaining the relationship between frequency of breastfeeding and fertility, in anticipation of contraceptive needs.

The duration of lactation-suppressed ovulation, known as lactational amenorrhea, depends upon the duration and frequency of breastfeeding and milk expression, with some evidence of longer duration in women who exclusively breastfeed than in those who partially breastfeed.76 Therefore exclusive and frequent breastfeeding (often referred to as on-demand), at least 8 to 12 times per day with no supplementation, is a relatively reliable method for preventing pregnancy for the first 6 months postpartum, assuming the woman has not begun to menstruate. This method of family planning is called the lactational amenorrhea method (LAM) and has been studied and supported by research conducted since the 1988 Bellagio Consensus.42,86

Anatomy of the mammary glands

The breasts or mammary glands are modified exocrine glands consisting of epithelial glandular tissue with an extensive system of branching ducts surrounded by adipose tissue and supported by the pectoralis major muscles and the fibrous bands of the Cooper’s ligaments. Cooper’s ligaments are suspensory and support the shape of the breast. The breasts are highly innervated with rich vascular and lymphatic systems. Each breast has been found to contain a range of 4 to 18 primary milk ducts arranged in a complex network and which converge at the nipple.68 The basic glandular unit is a lobe consisting of 4 to 18 lobules, each containing clusters of alveoli that are connected to fine ducts that merge into larger ducts that merge into a primary milk duct and lead to the nipple. The alveolus is the site of milk synthesis and secretion and consists of clusters of mammary epithelial secretory cells (lactocytes) surrounded by myoepithelial cells to form smooth muscle contractile units responsible for ejecting milk into the ducts from the lumen of the alveoli.67 The ducts and alveoli are surrounded by a stroma of fibroblasts, adipocytes, blood vessels, plasma cells (B lymphocytes capable of producing immunoglobulins, especially secretory immunoglobulin A), and a few nerves.58 Research using ultrasound imaging demonstrated that there are not lactiferous sinuses under the areola rather that some women experience temporary duct dilation with milk ejection which subsides with milk flow.67,68 Ducts serve to transport milk from the alveoli toward the nipple. The anterior and posterior medical branches of the internal mammary artery and the mammary branch of the lateral thoracic artery supply most of the blood to the breast. The internal thoracic, axillary, and cephalic veins drain the breast. Lymphatic drainage is conducted through the axillary and internal mammary nodes. The 2nd through 6th intercostal nerves innervate the breast. The structure of milk production and ejection portions of the mammary glands is illustrated in Figure 5-2. Figure 5-3 illustrates the mammary alveolus. The breast may be divided into four quadrants (lower inner, upper inner, lower outer, and upper outer quadrant with the adjacent Tail of Spence) for purposes of mapping and descriptive location.

The nipple is surrounded by the areola. Both the nipple and areola are elastic and darker in pigmentation than the rest of the breast, and become even darker during pregnancy and lactation, possibly providing a visual signal for the infant to latch. When not washed off, the mother’s nipple and areola also attract the newborn infant immediately after delivery through the senses of taste and smell.80 With suckling, the nipple and much of the areola are drawn into the infant’s mouth, forming a teat. Milk is removed by the stripping action of the infant’s tongue against the hard palate along with the infant’s application of vacuum on the breast and the maternal milk ejection response.23 Smooth muscle and elastic fibers in the areola and nipple form a sphincter to prevent milk loss when the infant is not suckling.58

Montgomery tubercles are sebaceous and lactiferous glands located around the areola. They are enlarged and elevated during pregnancy and lactation as they provide lubrication and antisepsis. Washing the nipples with soap or antiseptic is usually contraindicated as such action can remove the protective secretions of the Montgomery tubercles, leading to drying and cracking of the nipples and increasing the risk of infection.

Physiology of lactation

Human milk is species-specific and promotes proper growth and development of nearly all infants. Lactation is a complex physiologic process involving integration of neuronal and endocrine mechanisms. Mammary development and lactation can be divided into phases: embryogenesis, mammogenesis (mammary growth during puberty and pregnancy), lactogenesis (I and II, initiation of milk secretion), lactogenesis III (maintenance of established milk secretion), and involution (cessation of lactation).43,58 These phases are summarized in Table 5-1. Hormonal influences on lactation are summarized in Figure 5-4 andTable 5-2.

Table 5-1

Stages of Mammary Development

Embryogenesis Unknown Fat pad necessary for ductal extension Epithelial bud develops in 18- to 19-week fetus, extending a short distance into mammary fat pad with blind ducts that become canalized; some milk secretion may be present at birth
Pubertal development prior to onset of menses Estrogen, GH IGF-1, HGF, TGF-β, unknown Ductal extension into the mammary fat pad; branching morphogenesis
Pubertal development after onset of menses Estrogen, progesterone, possibly PRL   Lobular development with formation of TDLU
Development in pregnancy Progesterone, PRL, hPL Herrugulin, unknown Alveolus formation; partial cellular differentiation
Transition: lactogenesis Progesterone withdrawal, PRL, glucocorticoid Unknown Onset of milk secretion: Stage I: Mid-pregnancy; Stage II: Parturition
Lactation PRL, oxytocin FIL, stretch Ongoing milk secretion, milk ejection
Involution Withdrawal of prolactin Milk stasis, FIL Alveolar epithelium undergoes apoptosis and remodeling and gland reverts to pre-pregnant state


FIL, Feedback inhibitor of lactation; GH, growth hormone; HGF, hyperglycemic glyconeolytic factor; hPL, human placental lactogen; IGF, insulin-like growth factor; TDLU, terminal duct lobular unit.

Adapted from Neville, M.C. (2001). Anatomy and Physiology of lactation. Pediatr Clin North Am, 48, 16.

Table 5-2

Hormonal Contributions to Breast Development

Prolactin (PRL) Anterior pituitary Serum levels rise but estrogen suppresses its effect during pregnancy Stimulates alveolar cells to produce milk; important in initiating and maintaining lactation; may also cause lactation infertility by suppressing release of FSH and LH from pituitary or by causing ovaries to be unresponsive to various psychogenic factors, stress, an esthesia, surgery, high serum osmolality, exercise, nipple stimulation, and sexual intercourse
Prolactin-inhibiting factor (PIF) Hypothalamus Suppresses release of PRL into blood; release stimulated by dopaminergic impulses (i.e., catecholamines) Suppresses release of PRL from anterior pituitary; agents that increase PRL by decreasing catecholamines and thus prolactin-inhibiting factor (PIF) include phenothiazides and reserpine
Oxytocin Posterior pituitary Generally no effect on mammary function; sensitivity of myoepithelial cells to oxytocin increases during pregnancy Causes myoepithelial cells to contract, leading to milk ejection; release is inhibited by stresses such as fear, anxiety, embarrassment, distraction; also causes uterine contraction and postpartum involution of the uterus
Estrogen Ovary and placenta Stimulates proliferation of glandular tissue and ducts in breast; probably stimulates pituitary to secrete PRL but inhibits PRL effects on breasts Blood level drops at parturition, which aids in initiating lactation; not important to lactation thereafter
Progesterone Ovary and placenta With estrogen, stimulates proliferation of glandular tissue and ducts in breast; inhibits milk secretion Blood level drops at parturition, which aids in initiating lactation; probably unimportant to lactation thereafter
Growth hormone Anterior pituitary   May act with PRL in initiating lactation but appears to be most important in maintaining established lactation
Adrenocorticotropic hormone (ACTH) Anterior pituitary Blood levels gradually increase during pregnancy; stimulates adrenal to release corticosteroids High level is believed necessary for maintenance of lactation
Human placental lactogen (hPL) Placenta Like growth hormone in structure; stimulates mammary growth; associated with mobilization of free fatty acids and inhibition of peripheral glucose utilization and lactogenic action  
Thyroxine Thyroid Normally no direct effect on lactation Appears to be important in maintaining lactation either through some direct effect on the mammary glands or by control of metabolism
Thyrotropin-releasing hormone Hypothalamus Normally no effect on lactation Stimulates release of PRL; can be used to maintain established lactation


FSH, Follicle-stimulating hormone; LH, luteinizing hormone.

Adapted from Worthington-Roberts, B.S. & Williams, S.R. (1997). Nutrition in pregnancy and lactation (6th ed.). Madison, WI: Brown & Benchmark.


Mammary growth begins with development of the mammary band and streak in the fourth week of embryonic development, which progresses into the mammary ridge by the fifth week. The ectoderm continues to proliferate and undergo inward growth into the underlying mesoderm as the mammary bud is formed. From the sixth week, mammary glands, milk ducts, and lobular branching gradually develop throughout the continued embryonic growth. The continued proliferation of ingrowing ectodermal cells leads to the development of the branching mammary duct system. By 18 to 19 weeks, a bulb-shaped mammary bud is evident and extends into the mesenchyme, where fat pads are developing. The bud forms secondary buds, which will form the duct system in the mature breast. The secondary buds elongate and invade the fat pads, then branch and canalize to form the rudimentary ductal system.59 Occasionally the newborn may have transient secretions from the breast in the first few days after birth, probably due to maternal hormonal levels.