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After Breastfeeding Is Over, Your Boobs Start To Eat Themselves

Becoming a mom for the first time comes with a lot of weird, wonderful and often uncomfortable physical changes. The most remarkable change for a woman is the transition of their breasts from ordinary lumps of tissue to a 24/7 milk factory, and then back to normal just as fast.

This transition has become very tough for biologists to explain, but a recent study has finally provided some answers.

Researchers and scientists have identified a cellular process that confirms that breasts transition from providing milk to becoming straight up cannibals. Read on to learn more about this new finding!

Under normal circumstances, when the body has a lot of junk to clean up such as bacteria or dying red blood cells – other cells called phagocytes come in and ingest them. This clears away any unwanted build-up or harmful infections.

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But when a woman stops breastfeeding, cells called “epithelial cells” begin to form small milk-secreting sacs called alveoli begin to self-destruct in large numbers which allows the breasts to regain their regular state.

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This is where scientists have a hard time explaining how the phagocytes could clean this mess up without an ounce of pain being felt.

shutterstock_569323669 MatejKastelic/

Scientists explain that if phagocytes were solely responsible for clearing away all the dead cells and milk that is left once breastfeeding is over, it would be a very uncomfortable experience for new mothers.

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The body’s immune cells usually remove dying cells through a process called phagocytosis. The amount of material that cells consume is so heavy that you’d expect severe inflammation, tissue damage and pain. But this tends to not occur once the breastfeeding phase is over.

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So with no clear answer to how this process was so painless, a team of researchers from the University of Sheffield decided to investigate it.


The investigation was focused on one protein called Rac1, which plays an essential role in milk production and the phagocytosis process.

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So the team bred mice that were unable to produce the Rac1 protein and observed what would happen when they had pups. The first litter of pups survived, but they were a lot smaller than normal. The rest of the litter did not survive.

shutterstock_250743292 RudmerZwerver/

The results from the study helped the team discover that the dead cells and excess milk from the first pregnancy clogged up the breast tissue, which caused severe inflammation and swelling so the mice were unable to produce enough milk.

shutterstock_54260662 SebastianKaulitzki/

Without the Rac1 protein, dead cells and milk flooded the breast ducts which caused the chronic inflammation. Because of that, the bloated breast ducts are unable to produce milk for future pregnancies, which is why the second litter of mice all died.

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This breakthrough that demonstrated that the Rac1 protein is not just involved the phagocytic activity – it’s responsible for the whole thing.

shutterstock_622995446 Timonina/

It turns out that when Rac1 facilitates phagocytosis, it also appears to keep dead or dying epithelial cells that are attached to the alveoli for longer, and this could encourage them to eat each other instead of getting the immune cells involved.

shutterstock_355766561 KaterynaKon/

By doing this, it keeps the phagocytes at bay by allowing the epithelial cells to do all of the heavy lifting. By allowing this, it prevents pain and inflammation from breastfeeding.

shutterstock_192415883 Gazlast/

Despite the positivity and clarification that come with these findings, there are also consequences in the development of breast cancer.

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Despite research linking prolonged breastfeeding to a reduced risk of cancer for women, women actually have an increased risk of developing breast cancer for the first 5 to 10 years following pregnancy.

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One theory is that the inflammation that develops during the period of remodeling following breastfeeding may actually fuel cancer growth. Unfortunately this is all just theory, no definitive evidence has been identified.

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