The human breast is formed early in fetal life from an invagination of the ectoderm. During the fourth week, a raised area can be seen in the developing fetus. Near term, 15-25 ducts form the fetal breast. Male and female breast tissue develop in the same fashion. The withdrawal of maternal hormones can cause breast engorgement in the newborn. Shortly after birth, a neonate's breasts may produce a small amount of milk called "witches' milk." Study of this neonatal milk shows that it greatly resembles the components of mother's milk (Pittard 294-298). Production in the neonatal breast quickly subsides and the glands become the mammary disk of childhood. "The human mammary gland is the only organ that is not fully developed at birth (Lawrence and Lawrence 35)." The mammary glands will remain inactive until puberty.
Organogenesis begins just before the onset of puberty in the female (age 10 or 12). The internal breast structures begin to expand rapidly under the influence of estrogen. Typically a girl's first period will begin about a year or two after her breasts begin to grow (Love and Lindsey 11) With every menstrual cycle a new phase of growth occurs which includes extensive branching of the ductal system and organization of the internal structures. Fat deposits in the breast give it a more adult, rounded appearance. The greatest changes occur by age 20 but the breast continues to develop until age 35 (Riordan and Auerbach 94). The breast is not considered fully mature until a woman gives birth and begins to produce milk (Love and Lindsey 15).
The breast tissue follows a teardrop shape. The top of the tear is located in axillary region and is called the "tail of Spence." The main body of the breast, the corpus mammae, is the bottom portion of the drop. Breast tissue and/or extra nipples may occur anywhere along the "milk line," a line extending downward from the inner arm toward the inner thigh. However, ectopic breast and/or nipple tissue can occur anywhere on the body. Hyperthelia or supernumerary nipples often resemble simple moles. Hyperadenia, (breast tissue without a nipple) or polymastia (breast tissue with a nipple) is difficult to detect except during pregnancy and lactation. The most commonly reported site for hyperadenia is in the axillary fold. Occasionally the extra tissue may also have an ill-defined nipple that mother assumes is a mole. In all the cases I have seen the condition is bilateral. Extra breast tissue in the axillary region is separate from the "tail of Spence." During pregnancy areas of hyperadenia and/or hyperthelia may become sensitive. Extra glandular tissue can be expected to experience growth during pregnancy. If a pregnant woman complains of a tender "mole" it should be examined to see if it is extra breast tissue. It may be appropriate to remove excess tissue if it causes pain, embarrassment, engorgement or mastitis as these areas are not fully functional breasts. (Lawrence and Lawrence 40-41 ) Breast tissue high in the axilla cannot be seen on mammography and is difficult to palpate on breast examination. Breast surgeons recommend removal of the extra tissue not only as a comfort measure but that the area is a potential site where breast cancer may hide.
The adult female breast is made up of glandular tissue, supportive and connective tissue, and protective fatty tissue. The stroma or supportive tissue of the breast contains connective tissue, fat, blood vessels, nerves and lymphatics. The breast is suspended by Cooper's ligaments. Breast sagging is not a result of breastfeeding, but the result of pregnancy hormones and gravity loosening the Cooper's ligaments. The stroma appears to keep the lobes from encroaching upon each other, maintaining an orderly structure within the breast.
The glandular tissue is composed of the lobi, lobuli, and alveoli and resembles a bunch of grapes. There between 15 and 25 lobes, arranged in a wheel spoke pattern in each breast. The lobuli are clusters of alveoli. The alveoli are the milk producing units of the breast. Individual alveoli empty into small lactiferous ducts that converge in each lobulus with several lobuli forming a lobe. The larger ducts of the lobe converge into a milk sinus under the areola and finally end at the nipple. There are 15-25 openings in the nipple corresponding to the internal lobes. [Tables] Occasionally, one or more of the ducts may end at the areola and may leak milk during pregnancy and lactation. This is a normal variation.
Breast Size
The size of the breast varies greatly depending on the amount
of adipose tissue present within the breast. Breast size bears
no relationship to the amount of milk produced. The rare exception
is a condition called Insufficient Glandular Development of the
Breast (Neifert, Seacat, Jobe, Lact Failure 823-828). In these
cases some or all of the lobes in the breast have not fully developed.
The breast with Insufficient Glandular Development can appear
long, thin and tube like, almost pointed at the areola and nipple
or it may appear pubescent: flat with little or no development
of the nipple and areola. [Many women with these types of Insufficient
Glandular Development may have breast augmentation surgery to
give the breast or breasts an adult, rounded appearance.] Occasionally
the breast may appear normal. Upon palpation, the breast feels
empty in the areas where insufficient development has occurred.
Little or no firm glandular tissue can be felt beneath the skin
in affected areas. The condition can affect one or both breasts
or it may only affect a portion of the breast(s). Definitive diagnosis
can be made with ultra sound or mammography.
External Anatomy
External structures of the breast are the nipple, areola and Montgomery
glands [Table]. The nipple functions as a nozzle for delivery
of the milk. The nipple is the most sensitive to tactile stimulation
and pain. The darker portion behind the nipple is called the areola
and can vary widely in size and color. The milk sinuses lie directly
below the areola. The compression of the milk sinuses beneath
the areola delivers milk to the nipple. The darkening of the areola
during pregnancy may serve to act as a visual target for the newborn.
Secondary areolar darkening or patchy pigmentation behind the
areolar rim can also occur in pregnancy. Surrounding the areola,
are areas that elevate during pregnancy called Montgomery glands.
It is widely believed that these sebaceous glands produce a waxy
substance that both lubricates and protects the nipple and areola
with an antibacterial action but no evidence of this function
exists (Riordan and Auerbach 96).
Breast Growth in Pregnancy
Pregnancy brings increased growth within the breast. By the time
the baby is born, the glandular tissue in the breast has completely
replaced the fatty tissue (Eiger and Olds 41). Before pregnancy
most of the glandular tissue in the breast looks like a fruit
tree in winter (branches and twigs). The first trimester of pregnancy
causes the internal structures to branch and sprout. Under the
influence of 10 to 20 fold increase in placental lactogen, colostrum
appears near the end of the second trimester. The breast will
produce colostrum if the fetus is born at 16 weeks. However, "the
division and differentiation of mammary epithelial cells and presecretory
alveolar cells into secretory milk-releasing alveolar cells (Lawrence
and Lawrence 55-56)," occur in the third trimester. Third trimester
changes may account in part for the difficulty reported by mothers
of premature infants (under 32 weeks) regarding maintaining a
milk supply when they are exclusively pumping long term, especially
in prima-paras.
Involution of the Lactating Breast
Following lactation, the breasts involute. If milk is not removed
from the breasts the glands become distended. This distention
interferes with the blood supply to the breasts and milk production
ceases. There is also evidence that an enzyme produced by the
unremoved milk decreases production. Milk remaining in the alveoli
is gradually reabsorbed and the alveoli collapse or rupture. Initially,
after weaning, the breasts may appear smaller then pre pregnancy
size. This is due to the lack of adipose tissue within the breast.
The adipose tissue gradually increases and the breast returns
to its resting state. Some residual growth of the glandular tissue
remains after lactation. Women can often express a drop or two
of milk for up to twelve months following weaning.
TYPES OF BREASTMILK
Colostrum
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
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
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.
MILK PRODUCTION
Lactogenesis
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:
Neuro-Endrocrine
Autocrine
Hormonal Controls of Lactation
Prolactin
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)
Oxytocin
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
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.
Supportive Hormones
The manufacture of milk also requires several other hormones for
milk synthesis at the alveolar level including: insulin, cortisol,
thyroid, parathyroid and growth hormone.
Storage Capacity
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 (or 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).
Autocrine Control
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.
A CLOSER LOOK AT THE COMPONENTS OF HUMAN MILK
Breastmilk Composition
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.
Protein
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
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).
Carbohydrates
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)
Minerals
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.
Vitamins
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.
Immunological Components
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: