Lactation describes the secretion of milk from the mammary glands and the period of time that a mother lactates to feed her young.
The process of feeding milk is called nursing, and breastfeeding.
Newborn infants often produce some milk from their own breast tissue, known colloquially as witch’s milk.
Galactopoiesis is the maintenance of milk production, and requires prolactin.
Oxytocin is critical for the milk let-down reflex in response to suckling.
Galactorrhea is milk production unrelated to nursing.
Galactorrhea can occur in males and females of many mammal species as result of hormonal imbalances such as hyperprolactinaemia.
The main function of a lactation is to provide nutrition and immune protection to the young after birth.
Lactation induces a period of infertility, lactational amenorrhea, which serves to provide the optimal birth spacing for survival of the offspring.
From the eighteenth week of pregnancy a woman’s body produces hormones that stimulate the growth of the milk duct system in the breasts.
Progesterone influences the growth in size of alveoli and lobes.
High levels of progesterone and estrogen can inhibit lactation before birth.
Progesterone levels drop after birth; this triggers the onset of copious milk production.
Estrogen stimulates the milk duct system to grow and differentiate.
Estrogen levels also drop at delivery and remain low for the first several months of breastfeeding.
Breastfeeding mothers should avoid estrogens as a spike in estrogen levels may reduce a mother’s milk supply.
Prolactin contributes to the increased growth and differentiation of the alveoli, and also influences differentiation of ductal structures.
Elevated levels of prolactin during pregnancy and breastfeeding increase insulin resistance, increase growth factor levels (IGF-1) and modify lipid metabolism in preparation for breastfeeding.
During lactation, prolactin is the main factor maintaining tight junctions of the ductal epithelium and regulating milk production through osmotic balance.
From the second month of pregnancy, the placenta releases large amounts of Human placental lactogen (HPL).
This hormone is closely associated with prolactin and appears to be instrumental in breast, nipple, and areola growth before birth.
Follicle stimulating hormone (FSH), luteinizing hormone (LH), and human chorionic gonadotropin (hCG), through control of estrogen and progesterone production, and also, by extension, prolactin and growth hormone production, are essential.
Growth hormone (GH) is structurally very similar to prolactin and independently contributes to its galactopoiesis.
Adrenocorticotropic hormone (ACTH) and glucocorticoids such as cortisol have an important lactation inducing function.
Glucocorticoids play a complex regulating role in the maintenance of tight junctions.
Thyroid-stimulating hormone (TSH) and thyrotropin-releasing hormone (TRH) are very important galactopoietic hormones whose levels are naturally increased during pregnancy.
Oxytocin contracts the smooth muscle of the uterus during and after birth, and during orgasm(s).
After birth, oxytocin contracts the smooth muscle layer of band-like cells surrounding the alveoli to squeeze the newly produced milk into the duct system.
Oxytocin is necessary for the milk ejection reflex, or let-down, in response to suckling, to occur.
It is possible to induce lactation without pregnancy through combinations of birth control pills, galactagogues, and milk expression using a breast pump.
During the latter part of pregnancy, the woman’s breasts enter into the secretory differentiation stage, when the breasts make colostrum.
Colostrum is a thick, sometimes yellowish fluid.
During the latter part of pregnancy stage high levels of progesterone inhibit most milk production.
If a pregnant woman leaks any colostrum before her baby’s birth it is not a health concern, nor is it an indication of future milk production.
At birth, prolactin levels remain high.
At birth the delivery of the placenta results in a sudden drop in progesterone, estrogen, and HPL levels.
This abrupt withdrawal of progesterone at birth the presence of high prolactin levels stimulates the copious milk production of secretory activation.
With breast stimulation prolactin levels in the blood rise, peak in about 45 minutes, and return to the pre-breastfeeding state about three hours later.
Prolactin triggers the cells in the alveoli to make milk.
Prolactin also transfers to the breast milk.
Prolactin in milk is greater at times of higher milk production, and lower when breasts are fuller, and that the highest levels tend to occur between 2 a.m. and 6 a.m.
Secretory Activation begins about 30–40 hours after birth, but mothers do not typically begin feeling the sensation of milk coming in the breast until 50–73 hours or 2–3 days after birth.
Colostrum is the first milk a breastfed baby receives.
It contains higher amounts of white blood cells and antibodies than mature milk, and is especially high in immunoglobulin A (IgA), which coats the lining of the baby’s immature intestines, and helps to prevent pathogens from invading the baby’s system.
Secretory IgA also helps prevent food allergies.
Over the first two weeks after the birth, colostrum production slowly gives way to mature breast milk.
The hormonal endocrine system drives milk production during pregnancy and the first few days after the birth.
Subsequently, when the milk supply is more firmly established, local control system begins.
With local control stage the more that milk is removed from the breasts, the more the breast will produce milk.
Draining the breasts more fully also increases the rate of milk production.
The milk supply is strongly influenced by how often the baby feeds and how well it is able to transfer milk from the breast.
Low milksupply can often be traced to:
not feeding or pumping often enough
inability of the infant to transfer milk effectively caused by, among other things:
jaw or mouth structure deficits
poor latching technique
premature birth
drowsiness in the baby, due to illness,
medication or recovery from medical procedures
rare maternal endocrine disorders
hypoplastic breast tissue
inadequate calorie intake or malnutrition of the mother
Milk ejection reflex is the mechanism by which milk is transported from the breast alveoli to the nipple.
Suckling by the baby stimulates the paraventricular nuclei and supraoptic nucleus in the hypothalamus, which signals to the posterior pituitary gland to produce oxytocin.
Oxytocin stimulates contraction of the myoepithelial cells surrounding the alveoli, which already hold milk.
The increased pressure causes milk to flow through the duct system and be released through the nipple.
This response can be conditioned by the cry of the baby.
Milk ejection is therefore initiated in the mother’s breast by the act of suckling by the baby.
The milk ejection reflex is also called let-down reflex.
The milk ejection reflex is not always consistent, especially at first.
After being conditioned to nursing, let-down can be triggered by a variety of stimuli: sound of any baby, thinking about breastfeeding, can stimulate this reflex, causing unwanted leakage, or both breasts may give out milk when an infant is feeding from one breast.
Stress or anxiety can cause difficulties with breastfeeding.
The release of the hormone oxytocin leads to the milk ejection or let-down reflex.
Oxytocin stimulates the muscles surrounding the breast to squeeze out the milk.
Breastfeeding mothers describe varying sensation; tingling, pressure or slight pain/discomfort, and still others do not feel anything different.
A minority of mothers experience a dysphoric milk ejection reflex immediately before let-down.
It may be associated with anxiety, anger or nausea for up to a few minutes per feed.
A poor milk ejection reflex can be due to sore or cracked nipples, separation from the infant, a history of breast surgery, or tissue damage from prior breast trauma.
Milk ejection reflex mechanism is the mechanism by which milk is transported from the breast alveoli to the nipple.
Suckling by the baby innervates slowly-mechanoreceptors that are densely packed around the areolar region.
The electrical impulse follows the spinothalamic tract, which begins by innervation of fourth intercostal nerves.
The electrical impulse then ascends the posterolateral tract for one or two vertebral levels and synapses with second-order neurons, in the posterior dorsal horn.
The tract cells then decussate and ascend to the supraoptic nucleus and paraventricular nucleus in the hypothalamus, where they synapse with oxytocinergic third-order neurons.
The cell bodies of these neurons are located in the hypothalamus, but their axon and axon terminals are located in the infundibulum and pars nervosa of the posterior pituitary, respectively.
The oxytocin is produced in the neuron’s of the supraoptic and paraventricular nuclei, and is then transported down the infundibulum via the hypothalamo-neurohypophyseal tract with the help of the carrier protein, neurophysin I, to the pars nervosa of the posterior pituitary, and then stored in Herring bodies, where they are stored until the synapse between second- and third-order neurons.
Following the electrical impulse, oxytocin is released into the bloodstream, and makes its way to myoepithelial cells, which lie between the extracellular matrix and luminal epithelial cells that also make up the alveoli in breast tissue.
When oxytocin binds to the myoepithelial cells, they contract,
increasing intra-alveolar pressure that forces milk into the lactiferous sinuses, into the lactiferous ducts and then out the nipple.
A surge of oxytocin causes the uterus to contract, and during breastfeeding, mothers may feel these contractions as afterpains.
After pains may range from period-like cramps to strong labour-like contractions and can be more severe with second and subsequent babies.
In humans, induced lactation and relactation have been observed with varying success in adoptive mothers and wet nurses.
Lactation can be induced by a combination of physical and psychological stimulation, by drugs, or by a combination of those methods.
Several protocols for inducing lactation were developed and called the Newman-Goldfarb protocols.
The Newman-Goldfarb protocols involves the use of birth control pills to mimic the hormone levels of pregnancy with domperidone to stimulate milk production, followed by discontinuing the birth control and the introducing use of a double electric breast pump to induce milk production.
Domperidone is a drug that can induce lactation.