How Does Endometriosis Actually Happen?
- laurenmc413
- Dec 30, 2025
- 5 min read
If you’ve already explored what endometriosis can look like — the symptoms, the unpredictability, the way it shows up differently in every body — the next natural question is why. This blog will tackle that bothersome question, explaining how and why endometriosis can occur.
Endometriosis isn’t about cells mysteriously “ending up in the wrong place” for no reason. Instead, research suggests that a combination of menstrual flow patterns, cellular behavior, immune function, hormones, inflammation, and gene expression all interact over time — creating the conditions that allow endometriosis to develop and persist. These processes unfold gradually, which helps explain why symptoms often worsen over years rather than appearing all at once.
Rather than one single cause, endometriosis is best understood as a multi-factorial process shaped by how multiple systems communicate (and sometimes miscommunicate) over time.
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Endo in Unexpected Places
Endometriosis isn’t limited to one predictable area. If you’ve already read the Endometriosis 101 blog, you may remember that it’s most commonly found within the pelvis, but that it can also be identified in areas farther from the reproductive organs — including the diaphragm, lungs, and even the brain.
Hearing that endometriosis can show up in
tissues such as the brain sounds impossible…
right? Like the cells are packing tiny suitcases and traveling cross-country. But there are actually several scientific theories that help explain how this happens. These theories focus less on physical distance and more on how cells respond to their biological environment.
Researchers don’t view these theories as competing explanations — many actually work together.
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What the Research Is Saying:
Retrograde Menstruation (the explanation that makes the most sense)
This is the idea that menstrual blood and endometrial cells flow backward through the fallopian tubes (2) into the pelvis instead of out through the cervix during menses. Those cells can then implant on nearby organs.
However, up to 90% of menstruators experience retrograde flow (3), and only a fraction develop endometriosis. This gap highlights the importance of immune, inflammatory, and hormonal factors that determine whether these cells are eliminated or allowed to persist. This tells us that retrograde menstruation alone isn’t enough — something else must allow those cells to survive, implant, and grow.
Coelomic Metaplasia (cell transformation)
This theory is based on the fact that the pelvic lining (peritoneum) and the uterine lining (endometrium) come from the same embryonic tissue — the coelomic epithelium (4). Because of this shared origin, these cells retain a degree of developmental flexibility.
Under certain conditions — hormonal imbalances, inflammation, immune dysfunction, environmental factors, and/or developmental factors — gene expression can be altered. This affects how cells behave and function.
This process is known as epigenetics (5) and may help explain why normal, healthy cells from the pelvic organs “decide” to become endometrial-like over time. These changes don’t alter DNA itself, but they do influence which genes are turned on or off in response to the environment.
Benign Metastasis (beyond the pelvis)
Benign metastasis helps explain how endometriosis can appear in areas far from the reproductive organs. According to this theory, endometrial-like cells may enter the bloodstream or lymphatic system and relocate to distant tissues (6), where they implant and respond to hormonal signals.
Although these cells are not cancerous, their ability to spread and establish blood supply resembles metastatic behavior. This mechanism is often used to explain endometriosis found in the lungs, diaphragm, or brain.
Immune Dysregulation (failure to clear misplaced cells)
Under typical circumstances, the immune system acts as a cleanup crew — identifying and removing endometrial cells that end up outside the uterus. In endometriosis, this surveillance system is altered.
Reduced natural killer (NK) cell activity and changes in macrophage signaling allow misplaced cells to escape destruction. Instead of clearing these cells, the immune system may unintentionally support their survival and implantation (6).
Hormonal Imbalance (estrogen dominance and progesterone resistance)
Hormones further shape how endometriosis develops and persists. Estrogen promotes the growth and survival of endometrial-like tissue, while progesterone — which normally helps regulate this growth — sends weaker signals in endometriosis (6).
Many lesions can also produce estrogen locally, reinforcing inflammation and creating a hormonal environment that supports their own growth.
For a better understanding of what hormonal imbalance is and why lesions in endometriosis aren't alarming, check out the Perimenopause (7) and Endometriosis 101 (1) blogs.
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Why Some Cells Implant — and Others Don’t
Misplaced endometrial cells don’t automatically become endometriosis. Many women+ experience retrograde menstruation, immune activity in the pelvis, and hormonal fluctuations — yet only some develop lesions. The difference isn’t the cells themselves, but the environment they encounter.
When immune signaling is altered, misplaced cells may escape normal clearance. At the same time, inflammation can make surrounding tissue more receptive to implantation (8) by increasing blood vessel growth and altering cell communication.
Over time, epigenetic changes influence how cells respond to these signals, affecting whether they attach, persist, or are eliminated from the body. Together, this helps explain why endometriosis isn’t caused by a single factor, but rather by multiple systems being slightly out of sync for long enough that implantation becomes possible (9).
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Bringing It All Together
So, if endometriosis doesn’t have just one cause, what does this actually mean for people living with it?
It means endometriosis isn’t random. And it certainly isn’t a personal failure of your body.
Instead, it develops when multiple systems stop communicating clearly over time. Menstrual flow patterns, immune surveillance, hormone signaling, inflammation, and gene expression all play their little roles — and when even a few of these systems are slightly off, the environment becomes more permissive for endometrial-like tissue to survive where it shouldn’t.
This also explains why endometriosis:
Can take years to diagnose
Can worsen gradually instead of appearing suddenly
Looks completely different from person to person
Doesn’t always respond the same way to treatment strategies
In other words, endometriosis isn’t just a reproductive condition — it’s a whole-body condition shaped by how adaptable (and sensitive) the body truly is.
Understanding these mechanisms doesn’t mean you need to memorize biology terms or “fix” everything all at once. However, it does offer something powerful: context. When you understand why symptoms behave the way they do, it becomes easier to approach with more compassion (and less self-blame).
And if you’re pondering what to focus on next:
For inflammation and gut-immune communication, revisit the Fermentation blog (10)
For estrogen metabolism and elimination, the Fiber-Hormone Connection (11) blog is a great next step
For hormonal transitions and why fluctuations don’t equal dysfunction, the Perimenopause blog (7) offers a helpful perspective
Endometriosis isn’t about your body turning against you. It’s about systems doing their best under complex conditions — and learning how to support those systems more gently, consistently, and realistically over time.
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Hyperlinks:
How Does Endometriosis Actually Happen?
What the Research Is Saying
What the Research Is Saying
Coelomic Metaplasia (cell transformation)
Coelomic Metaplasia (cell transformation)
Benign Metastasis (beyond the pelvis)
Hormonal Imbalance (estrogen dominance and progesterone resistance)
Why Some Cells Implant — and Others Don’t
Why Some Cells Implant — and Others Don’t
Bringing It All Together
Bringing It All Together
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