Abhishek Mahajan (narrator / author)

But this too suffers from similar issues.

If this transformation can happen anywhere there is coelomic epithelium, why is it almost always clustered in the same anatomical zones, and how can it appear elsewhere?

And there are so many more theories beyond this.

Still others blame it on immune dysfunction, entirely somatic mutations, and even bacterial contamination.

So, which one is true?

Unfortunately, as is often the case with biology, the answer may very well be a combination of all of them.

As you go from papers from the 2010s to the 2020s, there is increasingly more and more hesitance in ascribing a single cause to the condition.

Instead, it is likely that endometriosis itself results from a general process of heterogeneous events.

I'll give the general take I'm seeing people swirl around.

There isn't a great paper covering the following few paragraphs, but rest assured that it isn't mine, but rather a synthesis of multiple review papers I've gone through.

First, there must be a seed.

A founding cell with latent endometrial potential.

This can be embryonic stem cells that never completed malarian migration or circulating multipotent stem cells, which accounts for cis men, non-menstruating women cases, but, more often than not, it will be likely be endometrial stem cells found in menstruation blood, accounts for cis women.

Next, the seed must reach the correct soil for growth to occur?

Retrograde menstruation would deposit endometrial stem cells in the ideal place.

the pelvic peritoneum, which is barfed in the estrogen-laden menstrual fluid that pushed the seed there in the first place.

That's right, we're back to the retrograde menstruation theory.

But unlike that theory, embryonic stem cells or circulating multipotent stem cells also have the opportunity to result in endometriosis, but they only develop into lesions under unusual conditions, such as hormonal therapy or chronic inflammation, for example cesarean scars.

This explains a lot of things.

the rarity and the distribution of extrapelvic endometriosis, why increased rates of retrograde menstruation lead to a higher risk for endometriosis, and why high estrogenic conditions usually co-occur alongside endometriosis in people who theoretically shouldn't develop the disease.