A Surprising Cause Of Endometriosis Could Lead To Cure

Summary

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Short Wave – "A Surprising Cause Of Endometriosis Could Lead To Cure"

Podcast: Short Wave (NPR)
Episode Date: September 26, 2025
Host: Regina Barber
Guests: Katie Burns (endometriosis researcher), Meredith Wadman (science journalist)

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Episode Overview

This episode explores groundbreaking research shifting our understanding of endometriosis—a common, debilitating gynecological disease—from hormonal causes to the critical involvement of the immune system. Through the story of researcher Katie Burns and insight from science journalist Meredith Wadman, listeners learn about recent scientific advances, the limitations of existing treatments, and a hopeful path towards more effective therapies and diagnostics.

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Key Discussion Points & Insights

1. Katie Burns’ Personal Journey with Endometriosis

• (00:28-01:22) Katie recounts a childhood filled with illness and severe pain, often dismissed by adults and attributed to "growing pains."
  • Quote: “You would get your period and it would hurt and you move on with life. And that's what I did. I don't know if they understood the magnitude of the pain.” — Katie Burns (01:29)
• She describes missing out on normal teenage experiences due to pain and fatigue.

2. From Patient to Researcher

• (01:39-02:12) Burning curiosity and the drive to find relief led Katie to become a researcher, focusing her work on endometriosis after finding few effective therapies.
• Her research garnered attention, especially from MIT’s Linda Griffith, and soon, science reporter Meredith Wadman.

3. Challenging the Hormonal Model of Endometriosis

• (02:28-04:43) Early theories blamed hormones—particularly estrogen—for driving endometriosis. Hormonal treatments, however, only alleviate symptoms without curing the disease.
  • Quote: “You can quiet disease, but you don't cure it, you don't get rid of it.” — Katie Burns (02:45)
• Katie’s experiments with mice lacking key estrogen receptors showed endometriosis lesions could still develop, even in the near absence of estrogen:
  • Quote: "Something is helping these get established that does not have to do with estrogen." — Meredith Wadman on Katie’s discovery (07:32)

4. The Immune System: A New Suspect

• (06:21-08:55) Burns found that immune cells, not hormones, were the critical factor in lesion formation in the earliest stage.
  • Details:
    • Innate immune cells (neutrophils and macrophages) flooded the pelvic cavity, seemingly nurturing rather than eradicating the misplaced tissue.
    • Only after 72 hours did estrogen become necessary for lesions to thrive.
• Quote: “It really showed that the immune system seems to be that important starting piece and not the hormone receptors.” — Katie Burns (03:04)

5. Supporting Research into Immune Dysfunction

• (09:02-10:21) Wadman explains that subsequent research supports the immune involvement:
  • Natural killer cells that should destroy “errant” tissue are too few or inactive.
  • Neutrophils and macrophages contribute to chronic inflammation and help endometriosis tissue establish itself.
  • Genetics may account for about half of endometriosis cases, but there’s no single gene.
• Quote: “Neutrophils are hanging around the scene and getting, being inflammatory instead of quick zooming in and doing their hoovering up function and disappearing.” — Meredith Wadman (09:34)

6. Therapeutic Implications: Moving Beyond Hormones

• (10:21-11:54) New treatments could target the immune system:
  • Antibody therapies may block inflammatory immune substances (cytokines), reducing pain and disease progression.
  • University of Edinburgh is preparing human trials of “nibrozetone,” a drug to improve macrophage function in cleaning up misplaced tissue.
  • Recognizes individual variability: endometriosis is not the same in every patient, so personalized immune-based treatments may be more effective.

7. Prospects for Early, Non-Invasive Diagnosis

• (11:54-12:43) Scientists are developing diagnostic tests using menstrual fluid, which could replace surgical diagnosis:
  • The Feinstein Institutes pioneered this research despite initial skepticism.
  • Quote: “Right now, the only way you can get an ironclad diagnosis of endometriosis is by having surgery and having it visualized. And that really needs to change.” — Meredith Wadman (12:17)

8. The Funding Gap and Future Outlook

• (12:57-14:28) Despite scientific progress, research is underfunded:
  • The National Institutes of Health allocated only 0.03% of its 2024 budget to endometriosis.
  • Quote: “The uncertainty with NIH is palpable. I have never felt such stress from everybody around me. If I don't get grants approved, then the lab shuts down... for the sake of the young girls that are trying to avoid living the life that I did. That's what drives me.” — Katie Burns (13:54)
• Meredith Wadman points out that a cure will require sustained funding and attention.

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Notable Quotes & Memorable Moments

• Katie Burns’ frustration and motivation:
  • “I didn't live, I don't think as a normal teenager.” (01:16)
  • “If I don't get grants approved, then the lab shuts down for the sake of endometriosis... That's what drives me.” (13:54)
• Scientific breakthrough:
  • “These mice developed rudimentary endometriosis lesions... something is helping these get established that does not have to do with estrogen.” — Meredith Wadman (07:49)

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Important Timestamps

| Time | Segment / Topic | |-----------|--------------------------------------------------------------| | 00:28 | Katie's early experience with pain and illness | | 01:39 | Path to diagnosis and her decision to pursue research | | 02:45 | Limitations of hormonal treatments | | 03:04 | First discoveries: immune system's role | | 04:57 | Historical overview of endometriosis research | | 06:21 | Katie’s pivotal mouse experiment | | 09:13 | Evidence linking immune dysfunction to endometriosis | | 10:21 | Potential for immune-targeted therapies | | 11:54 | Search for non-invasive diagnosis via menstrual fluid | | 12:57 | Funding challenges and outlook | | 13:54 | Katie’s personal drive and worry about research continuity |

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Takeaways

• Cutting-edge studies show that abnormal immune cell activity is likely central to endometriosis origins—challenging decades of hormone-dominated thinking.
• Immune-targeted therapies and simple diagnostic tests using menstrual blood could revolutionize care for millions—pending greater research funding and awareness.
• Personal stories like Katie’s highlight both the real-world impact of the disease and the persistent gaps in understanding, treatment, and care.

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Transcript

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[Regina Barber]

You're listening to Short Wave from npr. When Katie Burns was a kid and she remembers being sicker than her brother.

[Katie Burns]

And sister, more colds, more sinus infections, more ear infections than my brother and sister.

[Regina Barber]

Then the abdominal pain started when she was around 10. It was so bad she went to the emergency room thinking it was appendicitis. But the doctors ruled that out and.

[Katie Burns]

They sent me home. And then I remember from there on having more and more pain. But it wasn't really till I started menstruating that that kind of my whole world was just completely shifted upside down.

[Regina Barber]

Katie has endometriosis, a disease where the tissue that lines the inside of the uterus grows outside of the uterus, often causing debilitating pain and fertility issues. Because of her pain, Katie avoided making friends for fear of having to cancel plans.

[Katie Burns]

I didn't live, I don't think as a normal teenager.

[Regina Barber]

Growing up, the adults around Katie told her the pain was normal, that they were growing pains and to ignore it.

[Katie Burns]

You would get your period and it would hurt and you move on with life. And that's what I did. I don't know if they understood the magnitude of the pain.

[Regina Barber]

Katie wouldn't get an endometriosis diagnosis until she was 20. A diagnosis was validating, but but it didn't provide relief. To manage the pain and exhaustion, she would take naps during the week and sleep through the weekend. She tried acupuncture, diet changes, even hypnosis. One outlet that helped distract Katie from the pain was studying, which led her to a research career. Eventually, she decided to study endometriosis. As she published her findings, Science reporter Meredith Wadman took notice.

[Meredith Wadman]

I found Katie because this force of nature named Linda Griffith, who's at MIT and develops endometriosis organoids, put me on to Katie's work that was quite new and exciting and said, this is worth looking at.

[Regina Barber]

That new and exciting work revolved around the origins of endometriosis. Previous thinking pointed to hormones as the root cause of the disease, but Katie's work was pointed in a different direction. The first clue was that hormone treatments in people with endometriosis didn't always work.

[Katie Burns]

You can quiet disease, but you don't cure it, you don't get rid of it.

[Regina Barber]

Then an experiment in mice showed a completely unexpected result.

[Katie Burns]

I tried to convince myself that I did something wrong. The data wasn't making sense.

[Regina Barber]

Katie did the experiment over and over again and kept getting the same results.

[Katie Burns]

It really showed that the immune system seems to be that important starting piece and not the hormone receptors.

[Regina Barber]

Today on the show, science journalist Meredith Wadman tells us how researchers are piecing together the surprising origins of a disease that affects millions of people worldwide and how it could lead to a simple non invasive test, better treatments, and perhaps one day a cure. I'm Regina Barber and you're listening to Shortwave, the science podcast from npr.

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[Regina Barber]

So Meredith, before Katie and other scientists like her began looking into the immune system as a potential like culprit for this disease, what was the main theory as to why researchers thought people were getting endometriosis?

[Meredith Wadman]

Well, there have been theories about the cause of the disease dating back literally hundreds of years. The most prominent and still the leading one is that something called retrograde menstruation is leading to endometriosis. In the people who get it, most menstrual blood goes out as it should, down through the cervix and out the vagina. But some of it refluxes. It goes back up the fallopian tubes which are open ended. They open into the pelvic cavity and believe it or not, 90% of women have some degree of menstrual blood going back out into the pelvic cavity. Why 90% of women don't get endometriosis? That's the question that people are pursuing, in essence, by trying to get to the root causes of the disease. And it it's really well established that estrogen secreted by the ovaries as a normal reproductive hormone kind of supercharges this tissue that's growing where it shouldn't be and resists the calming effects of another key reproductive hormone made by the ovaries, which is progesterone. So it's definitely driven or not calmed by these reproductive hormones, but we all have them, and everyone doesn't have endometriosis.

[Regina Barber]

This is really fascinating research. Now is turning to the immune system. Like in your article in Science magazine, you write about a study that Katie did that she had kind of this light bulb moment that she started connecting the immune system to endometriosis. Like, can you tell me about that study?

[Meredith Wadman]

Well, let me preface this by saying at the time, estrogen, estrogen was the name of the game for many decades as the driver of endometriosis as the cause. But at this point in time, which was kind of in the aughts, Katie did this experiment where the mice he developed were deprived of estrogen, their ovaries were removed, and they were engineered not to have key estrogen receptors. And at the same time, the mouse donors whose uteruses were sliced up and injected also lacked estrogen receptors. What she found was that even in the absence of this estrogen influence, the absence of the receptors, the absence of almost any internally generated estrogen, these mice developed rudimentary endometriosis lesions. They weren't very healthy, they didn't thrive, they didn't grow, but they were there and they were getting established. And that was the light bulb moment for Katie where she said, something is helping these get established that does not have to do with estrogen.

[Regina Barber]

Yeah. And how did she get to the point where that something was related to the immune system?

[Meredith Wadman]

Well, she went on to do further experiments in which she actually watched what happened in these recipient mice in the, like, earliest hours, 24 to 48 hours after the minced uterine tissue was injected. And she found that the peritoneal cavity, the pelvic cavity, essentially was flooded with these innate immune cells called neutrophils and macrophages that were on the scene. And she proposed out of this, a model that said it's these cells that are needed to get these errant deposits of endometrium, like tissue growing where it shouldn't be. And then only after about 72 hours is estrogen absolutely required and becoming the primary actor.

[Regina Barber]

So since then, have other scientists kind of connected the dots between endometriosis and the immune system?

[Meredith Wadman]

Oh, yes. There have been ranks and ranks of scientists, often unsung, probing the role of the immune system in endometriosis.

[Regina Barber]

Yeah, what are some of the things they found?

[Meredith Wadman]

Yeah, they have found a lot and even more since that 2012 paper by Katie Burns. They have found that natural killer cells that should be targeting and removing and zapping this misplaced tissue are few in number. And they're not putting out the cell killing substances they should be. They found that neutrophils are hanging around the scene and getting, being inflammatory instead of quick zooming in and doing their hoovering up function and disappearing. And they found that macrophages, which are another early player at the scene of tissue turning up where it shouldn't be, are really helping the tissue launch and nurturing it as it gets embedded in places it shouldn't be instead of vacuuming it up and removing it. And genetics is clearly a piece of all of this. Probably about 50% of endometriosis is down to genetics. But it's not simple and straightforward like there being an endometriosis gene.

[Regina Barber]

So what does this mean for, like, treatment if the immune system is the culprit? Like, given that a lot of endometriosis, like you said, focuses on estrogen therapies, what could be a different treatment?

[Meredith Wadman]

Right. So this is, you know, what's really promising and yet virtually almost entirely unrealized is that the immune system could present targets for drugs that would be more effective. And endometriosis in one woman or person is not the same as in another. Like, it's more complicated. And so what, a drug that works for one person might not work for another. But basically the immune system could allow, for instance, antibodies manufactured to attack a particular inflammatory product of the immune system, a so called cytokine. These antibodies could target these cytokines and basically calm everything down, stop the inflammation that is driving the pain in these people. And there are other approaches, like a team at the University of Edinburgh that is just about to launch a human study of a drug called nibrozetone. And it goes after macrophages, I shouldn't say goes after. It improves their ability to clean up cells that are growing where they shouldn't be.

[Regina Barber]

So Meredith researchers have also started collecting menstrual fluid to try and understand endometriosis. What have they learned so far from that?

[Meredith Wadman]

Oh, they're learning a lot. And really hats off to this group at the Feinstein Institutes for Medical Research on Long island who pioneered this more than 10 years ago and were getting laughed at. And it was messy. It was Icky. Why would you study menstrual blood? And they persisted and they are well on their way to developing what's hoped will be a diagnostic test. Why is that important? Because right now, the only way you can get an ironclad diagnosis of endometriosis is by having surgery and having it visualized. And that really needs to change.

[Regina Barber]

Yeah, that would be amazing. So after reporting on this topic and, like, taking stock of what's been going on for 10, 15 years of research, what is your outlook for the future of this field?

[Meredith Wadman]

I wish I could say that it was, like, fantastically exciting. And it is by virtue of the researchers doing great things with not nearly enough money. I want to note for the nth time that the National Institutes of Health, the world's largest funder of medical research, spent something like 0.03% of its budget on this disease in 2024, which affects probably around 1 in 10 women of reproductive age.

[Regina Barber]

Meredith, thank you so much for talking with us today. I learned a lot.

[Meredith Wadman]

I'm glad you did. I really enjoyed speaking with you, Gina.

[Regina Barber]

For her part, Katie is hopeful about her future research while worrying about the future of research funding.

[Katie Burns]

We have some really exciting discoveries that I want to take forward, but the uncertainty with NIH is palpable. I have never felt such stress from everybody around me. If I don't get grants approved, then the lab shuts down for the sake of endometriosis, for the sake of the young girls that are trying to avoid living the life that I did. That's what drives me.

[Regina Barber]

This episode was Produced by Burleigh McCoy, edited by Amina Khan, and fact checked by Tyler Jones. The audio engineer was Robert Rodriguez. I'm Regina Barber. Thank you for listening to Short Wave from npr.

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