Endometriosis Isn't Just "Too Much Oestrogen." Here's What's Really Happening

I wish we'd stop thinking about endometriosis as a purely hormonal condition, one where you simply have "too much oestrogen" and that's the end of the story. It's so much more complex than that.

Why blood tests don't show it

For a long time, endometriosis was considered an oestrogen dominant condition. But that raised an obvious question, if that's true, why doesn't it show up as raised oestrogen on a standard blood panel?

We now understand endometriosis is oestrogen driven, but the oestrogen problem isn't systemic. It's local. Endometriosis lesions actually produce their own oestrogen, right where they are, which changes oestrogen signalling in that specific tissue without necessarily raising your overall blood levels at all.

Why the lesions make their own oestrogen

Women with endometriosis appear to be predisposed to an upregulation of the enzyme that converts testosterone into oestrogen, alongside having less of the enzyme that would normally convert oestrogen into its weaker, less active form.

The result is more, and more potent, local oestrogen than there should be. That oestrogen then drives a compound called prostaglandin PGE2, which in turn stimulates even more of the enzyme making oestrogen in the first place. It's a loop, and once it starts, it keeps feeding itself.

Progesterone resistance, not low progesterone

That same PGE2 also helps the lesion grow and survive by suppressing the activity of progesterone, the hormone that would normally act as a natural brake, anti-inflammatory and oestrogen lowering.

This is progesterone resistance. It's not about how much progesterone you're producing, it's about your tissue no longer responding properly to the progesterone that's there. Progesterone resistance has been found in both the lesions themselves and the surrounding endometrial lining in women with endometriosis, and it's one reason implantation issues are so common when trying to conceive.

Crucially, this won't show up on a blood test. A normal progesterone reading doesn't rule this out, because the issue isn't supply, it's response.

That same PGE2 also helps the lesion build its own blood supply, which is part of how it survives and grows over time.

The receptor problem

There are two oestrogen receptors involved here, alpha and beta. In a healthy system, they work in balance, one drives activity, the other keeps it in check. In endometriosis, both become dysfunctional.

The alpha receptor ends up creating a more pro-inflammatory, pro-growth environment for the lesions. Normally, the beta receptor would step in and oppose that. But because it's dysfunctional too, it can't do its job, and the lesions are able to survive and keep fuelling the inflammatory fire the alpha receptor started.

It's a vicious cycle, and it's one that feeds itself long after it starts.

If this is the first time you're hearing your endometriosis described this way, you're not alone, most of the treatment conversation still focuses on hormones at a very surface level. Understanding the mechanism is often the first step to a plan that goes beyond "just take the pill."