Breastmilk production begins in pregnancy. From very early in pregnancy, the breasts undergo changes as they prepare for milk production. Montgomery’s tubercles, small sebaceous glands form on the areola in early pregnancy, they may be the first sign of a first pregnancy. They secrete oil which lubricates the nipple and can also have antibacterial effects. In the second half of pregnancy, the breasts increase in size as more breast tissue is formed, this can lead to breast tenderness. The areola often becomes darker and increased blood supply to the breasts can cause the veins of the breast to become more prominent. These are physiological changes of pregnancy.

Production of colostrum in late pregnancy is hormonally driven

Production of colostrum is triggered in the latter half of pregnancy by the hormone prolactin, but high levels of progesterone prevent mature milk production. The production of colostrum in pregnancy is called Lactogenesis I and is hormonally driven, so barring any medical conditions affecting hormone production, all mothers will produce colostrum at the latter stages of pregnancy. If cleared by her doctor or midwife, mothers who wish to hand express small amounts of colostrum can do so after the pregnancy has reached term and store this safely for her infant in preparation for the first feed.

After the baby is born, separation of the placenta from the wall of the uterus precipitates a sudden drop in oestrogen and progesterone which results in high levels of prolactin unopposed by progesterone, which triggers copious milk production, known as Lactogenesis II. Other hormones such as thyroxine, cortisol and insulin are thought to be involved in Lactogenesis II, however their role is not fully understood at present. Although mothers typically feel their ‘milk coming in’ around 2-3 days post partum, however biochemically it appears that Lactogenesis II occurs between 30 and 40 hours post birth.

It is important to reassure mothers, that Lactogenesis II or ‘milk coming in’ is triggered by the separation of the placenta from the uterine wall, which occurs in all births regardless of the mode of delivery

A common myth about breastfeeding is that mothers who have a Caesarean Section are less likely to be able to breastfeed as their milk takes longer to ‘come in’ due to not being influenced by the hormones of parturition or labour. It is important to reassure mothers, especially those whom are planned to give birth by Caesarean Section, that the hormonal shift that results in Lactogenesis II or ‘milk coming in’ is triggered by the separation of the placenta from the uterine wall, which occurs in all births regardless of the mode of delivery, and as such, they should expect to be able to breastfeed as normal.

The production of colostrum during pregnancy and increased milk production following the delivery of the placenta, Lactogenesis I and II are hormonally driven and, barring any medical conditions affecting the endocrine system, eg Sheehan’s Syndrome will occur in all mothers whether they breastfeed their infant or not.

Following Lactogenesis II, the next stage is locally, rather than hormonally driven. It is regulated by the emptying of the breasts and centres around milk release to the infant- a supply and demand system in its simplest terms. As soon as the baby begins to feed, there is a surge in oxytocin, which triggers the milk ejection reflex, also known as ‘let down’ which moves milk from the alveoli to the milk ducts. Mothers will be able to feel the milk ejection reflex as a specific sensation as they become familiar with breastfeeding. When the alveoli are emptied, the prolactin receptor sites on the walls of the alveoli are available to be activated by prolactin. This triggers production of more milk. As the alveoli must be emptied to allow priming of prolactin receptor sites to trigger further milk production, milk production is dependent on frequency of breastfeeding which is controlled by baby’s appetite. The research to date suggests that this is a dynamic process with more prolactin receptor sites available for priming as each alveolus empties of milk, resulting in an increase in milk production directly proportional to the degree of breast emptying. This prolactin receptor theory suggests that frequent emptying of the breasts in the early weeks of establishing lactation results in a higher number of prolactin receptor sites, which in turn results in a higher capability for breastmilk production overall.

Following Lactogenesis II, the next stage is locally, rather than hormonally driven. It is regulated by the emptying of the breasts and centres around milk release to the infant- a supply and demand system in its simplest terms. As soon as the baby begins to feed, there is a surge in oxytocin, which triggers the milk ejection reflex, also known as ‘let down’ which moves milk from the alveoli to the milk ducts. Mothers will be able to feel the milk ejection reflex as a specific sensation as they become familiar with breastfeeding. When the alveoli are emptied, the prolactin receptor sites on the walls of the alveoli are available to be activated by prolactin. This triggers production of more milk. As the alveoli must be emptied to allow priming of prolactin receptor sites to trigger further milk production, milk production is dependent on frequency of breastfeeding which is controlled by baby’s appetite. The research to date suggests that this is a dynamic process with more prolactin receptor sites available for priming as each alveolus empties of milk, resulting in an increase in milk production directly proportional to the degree of breast emptying. This prolactin receptor theory suggests that frequent emptying of the breasts in the early weeks of establishing lactation results in a higher number of prolactin receptor sites, which in turn results in a higher capability for breastmilk production overall.