Your milk production is downregulated by mechanical and immune processes

Your milk production is turned down by mechanical pressures which interact with your immune system

There are different theories about how your milk production is regulated. Most often you'll hear that your supply is turned down by various bioactive factors, and turned up by hormones. But if you look closely at the research used to support these theories, they don't really hold up. Here's what I think, drawing on the latest research from the field of mechanobiology.

The downregulation of milk secretion is controlled by a complex system of inflammatory signalling networks. The mechanical pressure that is created as milk accumulates inside your milk glands and ducts interacts with your immune system to form an important part of your lactating breasts’ daily protective functions.

Here's how it seems to work.

High milk backpressures trigger an inflammatory or wound-healing response

Lactocytes take up the shape of plump little triangles when the lumen is empty, or perhaps as rectangles or columns if there is a little milk inside. Lactocytes join together at what we call a tight junction. As the alveolus fills with milk, the lactocytes stretch horizontally, becoming more and more flattened and thinned.

Eventually, as the amount of milk in the lumen increases, and the lactocytes are as stretched as they can be, the high pressure inside the gland strains at the tight junctions. This strain triggers networks of chemical signals which warn your immune system of early cell and tissue damage.

The immune system launches a healing or protective response. A cascade of inflammatory signals dilates up the capillaries and venules in the area, increasing the blood flow. Both the inflammatory signalling and increased blood flow bring in lots of [white cells] (neutrophils and macrophages) and other protective factors.

Milk supply is downregulated when enough alveoli break apart

As the amount of milk inside the lumen continues to increase, the tight junctions between the lactocytes stretch. At this stage, some lactocytes may even be shed into the milk. Eventually, the tight junctions break, and the basement membrane surrounding the milk gland or alveolus breaks too, so that the alveolus ruptures. This creates a microscopic puddle of broken cellular pieces and other debris, which is quickly mopped up by white cells and other protective inflammatory factors. You can see why this is often referred to as a ‘wound-healing’ response.

The same process might happen within the milk ducts too, if milk pressures stretch the epithelial cells enough. Again, their tight junctions break, basement membranes rupture and a wound-healing inflammatory process gets underway.

You won’t be aware of any of this, because it is happening all the time on a microscopic level throughout your breast when you are making milk, especially if you are going through a period when your production is exceeding what baby is taking from your breast, so that there is a rise in backpressures of milk, and your supply is in the process of downregulating. The decreased numbers of alveoli will mean less milk production overall in your breast.

• If it happens to enough of the alveoli in your breasts, then the number of glands available to secrete milk decreases and you will have less milk. That may be a good and necessary thing if you are producing milk beyond what your baby needs. It may also be upsetting if you aren’t producing enough milk for your baby’s needs.

• If it happens to a lot of alveoli in the one area of your breast, you may develop visible and painful inflammation.

Recommended resources

Mechanical pressures are the engine room of breastfeeding and lactation

Selected references

Stewart TA, Hughes K, Stevenson AJ, Marino N, Ju AL, Morehead M, et al. Mammary mechanobiology - investigating roles for mechanically activated ion channels in lactation and involution. Journal of Cell Science. 2021;134:doi:10.124/jcs.248849.

Jindal S, Narasimhan J, Vorges VF, Schedin P. Characterization of weaning-induced breast involution in women: implications for young women's breast cancer. Breast Cancer. 2020;6(55):https://doi.org/10.1038/s41523-41020-00196-41523.

Ivanova E, Le Guillou S, Hue-Beauvais C, Le Provost F. Epigenetics: new insights into mammary gland biology. Genes. 2021;12:https://doi.org/10.d3390/genes12020231.

Weaver SR, Hernandez LL. Autocrine-paracrine regulation of the mammary gland. Journal of Dairy Science. 2016;99:842-853.

Hartmann PE, Atwood CS, Cox DB, Daly SEJ. Endocrine and autocrine strategies for the control of lactation in women and sows. In: Press P, editor. Intercellular signalling in the mammary gland. New York 1995.

Douglas PS. Re-thinking benign inflammation of the lactating breast: a mechanobiological model. Women's Health. 2022;18:https://doi.org/10.1177/17455065221075907.

Zaragoza R, Garcia-Trevijano ER, Lluch A, Ribas G, Vina JR. Involvement of different networks in the mammary gland involution after the pregnancy/lactation cycle: implications in breast cancer. International Union of Biochemistry and Molecular Biology. 2015;67(4):227-238.

Ivanova E, Le Guillou S, Hue-Beauvais C, Le Provost F. Epigenetics: new insights into mammary gland biology. Genes. 2021;12:https://doi.org/10.d3390/genes12020231.