Marie Davis RN IBCLC
How the Breast Makes Milk
For a look at the internal structures of the breast see: Anatomy of the Breast
Lactogenesis (the beginning of milk production) occurs in three phases. Stage I occurs about 12 weeks before delivery. There are increases in lactose, total protein, immunoglobulins and decreases in sodium and chloride content along with the gathering of substrates for milk production in the breast (Lawrence and Lawrence 65-66). The initiation of Stage II Lactogenesis begins with the sudden withdrawal of pregnancy hormones at the delivery of the placenta. Stage II occurs at 2 to 3 days postpartum, paralleling the time when "the milk comes in." This stage includes increases in blood flow, oxygen, glucose and citrate in the breast. The breasts will begin to produce milk independent of infant suckling. Stage III, formally called galactopoiesis, is the establishment of a mature milk supply. (Lawrence and Lawrence 66) The breast is not merely a passive container of milk. It is an organ of active production. When the infant suckles a series of events takes place within the mother's body. Once Stage II Lactogenesis has begun, continued milk production is governed by the infant (Riordan and Auerbach 102).
Three major factors are necessary to maintain the milk supply:
Intact neuro-hormonal pathways
Suckling, breast stimulation,
Prolactin, often called the "mothering" hormone, is secreted in the anterior pituitary. During pregnancy prolactin is essential for complete lobular development in the breast. Prolactin levels rise from a non pregnant baseline of 10-25 ng/mL to 200-400 ng/mL at term (Riordan and Auerbach 98). Progesterone antagonism from the placenta enables the prolactin level to rise without subsequent milk production (Lawrence and Lawrence 65). Progesterone interferes with prolactin's activity on the cell receptor sites in the alveoli of the breast (Riordan and Auerbach 98). With the birth of the placenta, and the sudden drop in pregnancy hormones; progesterone and estrogen, the elevated prolactin level brings in the milk supply. Prolactin is released in pulses directly related to stimulation of the areola or breast. "For any hormone to exert its biologic effects, however, specific receptors for the hormone must be present in the target tissue (Lawrence and Lawrence 72)." Frequent feeding in the early days increases the number of prolactin receptor sites within the breast (Riordan and Auerbach 88). The implication from research is that "the controlling factor in breastmilk output is the number of prolactin receptors [in the breast] rather than the amount of serum prolactin (Riordan and Auerbach 101)." These prolactin receptors are laid down in the first 3 months postpartum. The prolactin receptors in the breast allow abundant milk production to continue when total baseline prolactin levels drop over the first 3 to 4 months. Even with more "normal" baseline levels, breast stimulation continues the doubling of the declining baseline prolactin levels into the second year (Lawrence and Lawrence 66- 70). The prolactin receptor site theory raises serious concern over progesterone laden birth control methods when started within days of the birth. Depo-Provera (medroxyprogesterone acetate) shots are often given immediately postpartum, while the mother is still in the hospital. If progesterone is an antagonist to prolactin, logic dictates that progesterone shots, implants and pills would inhibit early establishment of milk production (Lawrence and Lawrence 666). Elevated prolactin levels in the early days of lactation help milk and receptor site production. Each nursing produces a doubling in serum prolactin levels. Prolactin level naturally rises in sleep states (Lawrence and Lawrence 67). Night nursings help maintain an elevated baseline prolactin level. Thus, it is unwise for a mother to skip breastfeedings at night (having someone else give bottles) if she wants to develop a good milk supply. Frequent prolactin release inhibits follicle stimulating hormone (FSH) and luteinizing hormone (LH), causing lactational amenorrhea preventing the return of fertility (Lawrence and Lawrence 653). Prolactin is biologically potent for the infant. Milk prolactin levels are highest in colostrum and transitional milk. In mature milk the highest prolactin concentration is in the foremilk. In the infant gut, prolactin effects fluid and electrolyte exchange in particular, sodium, potassium, and calcium. (Riordan and Auerbach 100, Lawrence and Lawrence 67 68)
While prolactin is essential for initiating and maintaining lactation, oxytocin is keyed more closely to milk ejection. Oxytocin receptor sites in the breast gradually increase by 10 fold in pregnancy. Just before delivery the number of oxytocin receptor sites in the uterus increase dramatically and then suddenly disappear after the birth. Oxytocin is taken up by the uterus first to facilitate delivery, prevent postpartum hemorrhage by uterine contraction and then cause milk ejection. (Lawrence and Lawrence 76) The nipple becomes more sensitive to tactile stimulation in the 24 hours following birth. (Lawrence and Lawrence 74) Stretch receptors in the nipple stimulate the release of oxytocin from the posterior pituitary. Oxytocin causes the let-down reflex or milk ejection response.
Milk Ejection Response (Let-down)
The surface tension in the breast is sustained so that milk does not freely move out of the breast. The milk ejection response (MER) is the action of oxytocin upon the smooth muscle of each alveolus at the microscopic level. Contraction of the alveoli actively push the milk into the ducts toward the nipple and finally to the infant. (Lawrence and Lawrence 74) As the baby continues to nurse additional MER's occur. In the early days of nursing, it may take five to eight minutes for the first let-down to occur. Oxytocin, like prolactin, is released in pulses. It has a very short life span in maternal serum. The first pulse begins before the baby is put to breast (triggered by mother thinking its time to feed or infant crying). Subsequent release is in response to nipple stretching. The uterus contracts from oxytocin release. In the early days of breastfeeding these "afterbirth pains" can be very uncomfortable. (Riordan and Auerbach 103) The higher the mother's parity the more intense the afterbirth pains. Mothers are very concerned when they cannot feel the let-down in the postpartum period. This lack of sensation is normal. The mother can be taught to observe the infant for bursts of swallowing, uterine cramping dripping milk, sleepiness and/or thirst as cues that a let down has occurred. After the first week or two, mother will usually begin to feel the let down. Most mothers state they only feel the first let-down in a feeding. This may be due to the distention of the ducts with foremilk. A few women are aware of each let-down. The let down reflex can be felt as a tingling sensation. Occasionally, women may describe the let down as a burning or painful sensation.
The manufacture of milk also requires several other hormones for milk synthesis at the alveolar level including: insulin, cortisol, thyroid, parathyroid and growth hormone.
Until very recently, it was believed that because there are no obvious cisterns or bladders the breast that most of the milk was made as it was demanded (during the feeding). Recent research by Daly and Hartmann indicates that each breast has its own individualized maximum storage capacity. This is not related to breast size. Mothers with a larger storage capacity were found to feed less frequently than those with smaller capacities. However, the mothers in the research group produced about the same amount of milk over a 24 hour period. The storage capacity studies show why cue feeding, rather than strict scheduling, is best for the baby and mom's milk supply (Marasco and Barger).
The breast never truly empties. "An empty breast is a misnomer and is physiologically untenable (Lawrence and Lawrence 265)." The greater the infant demand, the greater the milk production (Lawrence and Lawrence 70; Riordan and Auerbach 102). Thus the rate of production is dependent on milk removal: the more milk removed, the greater the production. Autocrine (local) control takes over at approximately 3 months postpartum. Milk is made at a local level dependent on the number of prolactin receptor sites laid down during the endocrine stage. If milk is not removed, a negative feedback loop occurs resulting in lower milk production.
Cellular Manufacture of Milk
Foremilk and hindmilk are oversimplified views of what is actually occurring in the breast. Essentially, foremilk is the mixture of non fat components that are produced constantly and some high fat components (either remaining from the last feeding or newly made at a much slower rate). Foremilk looks thin and bluish. Hindmilk is the fat rich milk made with each MER. Once the fat globules enter the milk, the milk becomes thicker and more white in color. As the baby nurses, the fat content of the milk increases with the duration of the feeding and the amount of milk removed. The fat content of the milk is also affected by the frequency of feedings due to elevations in prolactin levels that accompany suckling.
The Process of Engorgement
Mild engorgement is a signal that mother's "milk is in" (Stage II Lactogenesis). This is a normal expected event. The lack of breast fullness may indicate the breasts have not been signaled to produce milk or another problem. Women who do not experience breast fullness should be referred to a medical provider or lactation consultant for further evaluation (Lawrence and Lawrence 255). Painful engorgement often occurs when the feedings are infrequent and/or of a limited duration. The best management of engorgement is prevention. The process of painful engorgement is threefold: increased blood flow to the breasts causes tissue congestion, the ducts and alveoli become distended with milk, and edema secondary to swelling and obstruction of the lymphatic drainage system (Lawrence and Lawrence 255) If the breasts are not signaled by a suckling infant or breast stimulation within the first 24 to 48 hours postpartum the result is alveolar distention, tissue congestion and destruction of alveolar tissue. Distended lactational tissue and tissue congestion may prevent the appropriate hormones from reaching the breast and producing the desired effect of milk synthesis and milk ejection. Some mothers develop a fever if excessive engorgement occurs. A fever as high as 100°F accompanying engorgement, in the early postpartum period, can be mistaken for postpartum infection. Unrelieved engorgement and over distention of the alveoli can cause some alveoli to rupture, resulting in partial involution of the breast. Subsequently, complete involution of the breasts can occur in as little as six hours in unrelieved engorgement.
Colostrum, the first milk, should be viewed as concentrated milk. It is a mixture of residual cells in the breast and newly formed milk. Colostrum is yellow to orange in color, resembling melted butter. It is thick and sticky like maple syrup. Colostrum's yellow color is due to beta-carotene. Colostrum has a high ash content and higher concentrations of sodium, potassium, chloride, protein, fat soluble vitamins and minerals than mature milk. Colostrum contains approximately 58 Kcal per 100 cc compared to mature milk at 70 Kcal per 100 cc. Colostrum has an important laxative effect on the infant bowel that assists in the emptying of meconium. The retention of meconium can contribute to neonatal jaundice due to reabsorption of its bilirubin content. It is a common misconception that when the baby nurses in the first day or two, that he gets nothing. Luckily this is not true. It is however, difficult to convince some mothers of the need to nurse early and often when they believe that their "milk has not come in." In addition some cultures hold the belief that colostrum is "bad" milk and will not breastfeed until the mother's mature milk is in. Many women have to be engorged before they will believe that there is any milk for the baby. Likewise, if the mother is no longer engorged, she may falsely believe that her milk is gone. Expressing a drop or two of colostrum for the mother will give her a strong visual cue that her breasts are not empty. The mother produces small amounts of colostrum in the first 24 hours; ranging from 7 ml to 123 ml. The newborn takes 7-14 ml per feeding (Riordan and Auerbach, 124). A gradual increase occurs during the first day and a half followed by a dramatic increase in milk output by the second day that continues through day four. At 5 days postpartum milk production is approximately 500 ml/24 hours. This is evidence that mother nature intended the infant's gastrointestinal tract to start up slowly after birth.
Transitional milk follows colostrum. Transitional milk can appear as early as twelve hours after delivery and may continue for 7-14 days. Transitional milk retains some of the yellow color of colostrum. The concentrations of immunoglobulins, total calories and protein decrease while lactose and total fat increase.
Mature milk, seen as early as three days postpartum, becomes the predominant milk type by day nine. Mature milk supplies everything that baby needs including water. Breastmilk is greater than 87% water. Even on the hottest days, breastmilk provides sufficient water intake for the baby (Lawrence and Lawrence 106). Mature milk looks thin and slightly bluish in color if compared with formula or homogenized cows' milk. Formula is processed from cow milk or soybeans, which are thicker and have a different color than human milk. Mature milk provides all needed nutrients for normal growth and development. Breastmilk will meet all of the infant's nutritional needs for six months.
Lawrence and Lawrence state, "The biochemistry of human milk encompasses a mammoth supply of scientific data . . . Each report or study adds a tiny piece to the complex puzzle of the nutrients that make up human milk (95)." We now know that breastmilk also contains many nonnutritive, bioactive substances that have direct effects on the infant's physiology. Breastmilk "is not a uniform body fluid but a secretion of the mammary gland of changing composition (Lawrence and Lawrence 95)." No two samples of breastmilk are the same, even when taken from the same mother.
The proteins in human milk are specific to human mammary production and are not found elsewhere in nature. Protein synthesis is under the genetic control of RNA. (Lawrence and Lawrence 86) Breastmilk composition is relatively stable throughout the world (Riordan and Auerbach 126). Cows' milk proteins and proteins from other sources are different in structure, quantity and quality and can cause allergic responses (Akre 25). Mature breastmilk is approximately 0.8 % to 0.9% protein and provides the infant's protein requirements in a way that changes as the infant matures. Some human milk protein is not nutritionally available but serves immunological needs. The protein content in colostrum is relatively high. The level declines as milk matures and stabilizes by the end of the third month. The protein levels in human milk are more than adequate for optimal growth and provide an appropriately low renal solute load for the baby (Akre 26). The casein group of proteins in human milk is a species specific composition of amino acids. Casein is 20 to 40% of total milk protein. Whey proteins are 60 to 80% of total milk protein and consist of alpha-lactalbumin, lactoferrin and secretory IgA (sIgA). The whey casein ratio of human milk is 80:20. Whereas the whey casein ratio in ABM ranges from 18:82 to 60:40. Infants fed ABM have high blood urea levels a causing additional stress on the kidneys. (Akre 26: Lawrence and Lawrence 116)
Lipids provide 50% of the energy content in human milk. The fat content of mature milk is 3.8%. Fat content varies from feeding to feeding and within individual feedings. Maternal diet affects the constituents of the lipids but not the total fat content. When a mother's caloric intake is poor, fat is mobilized from maternal fat stores (primarily in the hips and thighs). The cholesterol level of breastmilk will remain constant despite manipulation of the mother's cholesterol intake. Lipase in human milk complements the low level of pancreatic lipase in infants. Lipase activity is stable at a pH level of 3.5 at 37°C for one hour. Just long enough to be effective for fat digestion at the level of the infant's small intestine (Garza 19).
Lactose is a sugar present only in milk. In human milk the level of lactose is quite high. Other sugars are present but lactose is the driver sugar in breastmilk and provides approximately 50% of the caloric content. Lactose assists with the establishment of Lactobacillus bifidus flora in the infant bowel. Lactobacillus limits colonization by other bacteria by occupying the limited number of binding sites along the intestinal wall. Lactose enhances infant absorption of calcium from breastmilk. Alpha-Lactalbumin concentration is 2.6 grams per liter in human milk. Alpha-Lactalbumin is a specific protein required for lactose synthesis. Lactose is responsible in part for milk volume and mother needs an adequate source of carbohydrates in her diet. Excessive use of sugar substitutes may affect maternal milk volume. (Lawrence and Lawrence 126) There has been concern over lactose intolerance in infants lately. Primarily fueled by a new lactose free ABM. Since human milk is so high in lactose it seems unlikely that lactose intolerance in infancy would be compatible with life. (Riordan and Auerbach 129) The problem may be one of feed management rather than true intolerance. (see Protocol: Over Supply Syndrome)
The mineral content of milk is species specific. The type and amount of minerals present in milk reflect the growth rate and bone density of the offspring (Lawrence and Lawrence 126). The mineral content of cow or elephant milk therefore is higher than in human milk because of the animal's larger bone mass. The constituents in breastmilk are more readily available for the baby's use than those in vitamin and mineral supplements or in formula. Sodium levels in cows' milk based formula is more than three times that of human milk. Even in infants high sodium intakes can lead to hypertension. The calcium in breastmilk is in a highly absorbable form suited to the human infant. The iron in breastmilk is 49% available whereas only 4% in iron fortified formulas is absorbed. Breastfed infants are not at risk for iron deficiency anemia. Zinc, phosphorus, magnesium, copper and other trace elements are also present in breastmilk. The mineral content of breastmilk remains consistent despite changes in the maternal diet.
Both fat soluble and water soluble vitamins are present in breastmilk. There is twice as much vitamin A in colostrum as in mature milk. Vitamin D is present in both fat and water soluble forms. Vitamin D only becomes a concern in populations with no maternal or infant exposure to sunlight. Vitamin E concentrations are adequate for term infants but may too low for premature infants.
Colostrum facilitates the establishment of bifidus flora in the infant gut that forms a coating on the lining of the intestine, protecting the baby from harmful bacteria. Once the infant is given anything other than breastmilk, the infant primarily has gram negative, potentially pathogenic colonization of bacteria in the intestines (Lawrence and Lawrence 184). Allergies are reactions to foreign protein. Allergic responses may be reduced or eliminated by delaying the introduction of foreign proteins for at least six months. Delaying the introduction of foods other than breastmilk until six months, when the infant's own immune system is more functional, can reduce hospital admissions for asthma and gastrointestinal problems. (Lawrence and Lawrence 617-632) Protection through passive immunity continues for as long as the infant is breastfed. An infant's immune response is not fully developed until age five. (Newman 76)
The immunoglobulin found in highest concentration in human milk is IgA. The secretory form of IgA (sIgA) lines the gut and respiratory system in adults. sIgA is the major component conferring passive immunity to the breastfed infant. sIgA is very stable in breastmilk and is not degraded by gastric acid or digestive enzymes. sIgA provides local immunity by building a lining on the walls of the intestinal tract, the oral pharynx and the urinary tract. Thus, sIgA protects the infant from infection by preventing invasion of organisms through the mucosa. sIgA fights disease without causing inflammation. IgA protects the infant from invasion, but does not fully line the gut until six months of age. It may take months before an infant can manufacturer his own IgA. "Infants who are bottle fed have few means for battling ingested pathogens until they begin making IgA on their own. (Newman 77)."
The transfer of sensitized plasma cells (immunoproteins) to breastmilk is mediated by the lactogenic hormones. Immunoproteins provide substantial protection when breastmilk is the majority of infant's nutritional intake.
sIgA is active against E. Coli. and cholera, Respiratory Syncytial Virus, polio virus, rhino virus, influenza virus, B encephalitis, and other respiratory and intestinal viruses. IgA prevents the absorption of protein macromolecules protecting the infant from allergic responses. The specificity of IgA response is related to the mother's antigenic exposure (Garza 17). By this mechanism, breastmilk is not only species specific but infant specific and may be environmentally specific as well. (See Enhancing Human Milk for Enteral Feedings)
Rotovirus binds to milk mucin inhibiting its replication. Nucleotides are a part of the immune system defending against bacteria, viruses, parasites and malignancies (Lawrence and Lawrence 123).
Breastmilk assists with the low phagocytic function of newborn blood cells. Living leukocytes are present in human milk. Macrophages comprise 90% of the leukocytes in breastmilk (Lawrence and Lawrence 162). Macrophages in breastmilk manufacture lysozyme, which destroys the cell walls of bacteria. Lysozyme destroys Enterobacteriaceae and gram positive bacteria. Lysozyme also helps develop and maintain the intestinal flora.
Lactoferrin is the iron-binding protein in human milk. Lactoferrin's role is to isolate external iron, not transport iron for infant metabolism. Iron transport for infant metabolism is through milk casein and lipids. At one week, lactoferrin concentration is approximately 5 grams per liter and stabilizes by twelve weeks at 1.7 grams per liter. Lactoferrin levels remain constant for the next two years of lactation. Lactoferrin inhibits the growth of iron dependent bacteria. Giving breastfed infants iron supplements inactivates the lactoferrin by saturating it with iron (Lawrence and Lawrence 175 ). Staphylococci and E. Coli are iron dependent bacteria. Lactoferrin also inhibits the growth of C. albicans.
Numerous authors have given more specific information on the known contents of breastmilk. The subject is far too complex to be given any more than a brief overview here. It is strongly suggested that the reader refer to these texts, if more information is desired.
Copyright Marie Davis, RN, IBCLC 1999
Last Reviewed: Sunday, May 17, 2015