The Endo Belly Signal No One Is Talking About: When Your Small Intestine Has a Seizure
There was study I couldn't stop thinking about for almost a year when I was writing my book Heal Endo.
It was published in 1998 in Fertility and Sterility, and not only did it uncover most endo sufferers have SIBO, but 100% of women with endometriosis — every single one — were having small intestinal seizures. [1]
Not cramping or spasms. Electrical misfiring at up to 44 cycles per minute, in a gut that's supposed to contract at 3. Seizure-like activity in the motility of the small intestine, present in every woman with endo they tested.
I mulled this study over for months and even tried to reach the researchers (they never responded). I'd never found another study that showed 100% of endo patients dealing with the same thing beyond their lesions — and in a disease this complex, with this much variability between women, a universal finding is almost unheard of. It's like finding a unicorn. I wondered if it was a root cause why so many of us have SIBO...
Finally, I put it away, because I couldn't find anything else on it. It was a small study to begin with, decades old... perhaps it was shelved because no one could replicate it.
Until now.
This is the sixth piece in my endo belly series, and if you've been following along, you already know that the constellation of GI symptoms we call "endo belly" isn't one thing. It's a stack of things: SIBO, hypertonic pelvic floor, core dysfunction, adhesions, inflammation, food reactivity, estrogen-microbiome crosstalk. Each of those deserves its own conversation.
But for today, we're going to talk about something striking that almost none of us are talking about, although nearly all of us may have it: gut seizures.
What a Normal Gut Actually Does (ps: It's Not Chronic Abdominal Bloating)
Before I get to what the newer studies found, it's worth knowing what a healthy intestine is even supposed to do.
You have a nervous system in your skull and spine — that much you knew. But you also have a nervous system dedicated entirely to your gut, called the enteric nervous system, or ENS, and it contains more neurons than your spinal cord! It's so complex and so autonomous that scientists sometimes call it "the second brain." It regulates your digestion, coordinates your immune cells, and talks to the rest of your body through the vagus nerve.
Among other things, the ENS keeps food moving through your intestines at a steady, coordinated rhythm — roughly three muscular contractions per minute in a healthy gut, moving in waves, the way ocean swells roll up a beach. That rhythm is called peristalsis, and when it works, you don't notice it. Food goes in. Nutrients get absorbed. Waste leaves. You feel, for lack of a better word, normal.
What the 1998 researchers measured in endo patients wasn't peristalsis. It was the opposite of peristalsis — electrical patterns firing at up to 44 cycles per minute instead of 3. Yes, seven to fifteen times faster than normal. Chaotic, spasmic, seizure-like activity in every woman with endo and gastrointestinal complaints they tested.
Beyond Endometriosis Belly: Are Small Intestinal Seizures As Common as Endo Lesions?
While the 1998 study was only looking at women with endo and pretty significant gastro issues, I was shocked to uncover more research demonstrates that not only women with "endo belly" symptoms have this gut siezure activity. In fact, it may be all of us with active endo.
In 2002, the same researchers from 1998 (Mathias) now looked at 300 women with confirmed endo, and not just gastro issues. They found this dysfunction in all 300 subjects, with a contraction rate between 22-44 cpm. Again, controls had 3 cpm.[2]
That was a long time ago, so you can imagine my excitement upon finding a 2024 study with a different cohort that included women with and without endo. They measured small intestinal activity through a different process — electrodes on the abdomen, kind of like an EKG for the gut. What did they find with the newer technology? All endo patients had a dysregulated small-intestinal pattern. None of the controls did. [3]
The pattern was present regardless of lesion location, stage, or age. Even women who had already had endometriosis surgery had it. A few limitations worth noting: the study didn't specify when patients had surgery or whether it was an excision, so we can't draw firm conclusions about whether surgery changes the signal.
In a follow-up study from Brussels in 2025, they tested this new technology on endometriosis patients from a specialty clinic (so assuming they're all symptomatic as well), and we see that the technology accurately diagnosed endometriosis is 96% of cases--by measuring the seizure-like small intestinal pattern.[4]
Are there any other diseases that have the same issue? I wondered too, and I looked at everything I could think of: dysbiosis-driven conditions, inflammation-induced conditions, even blood sugar dysregulation (we know diabetes drives similar motility issues). But no. This pattern is not found in IBS, inflammatory bowel disease, PCOS, pelvic pain from other causes, or urinary infections. Studies of over 500 women with these other diagnoses failed to show the motility signature.[3]
It is endometriosis-specific. Full stop.
The pattern was so reliable that the 2024 paper proposed using it as a non-invasive diagnostic biomarker — so that women with endo wouldn't need surgery to get a diagnosis. They could simply look to see if the small intestine was spasming. And now that's exactly what's happening: a company in Canada is offering a test. Three electrode pads on the abdomen, a glass of water, thirty minutes. An EKG, essentially, but for the gut. The site claims to diagnose endometriosis with 98-99% accuracy. (https://endodiagnosis.com) That's far more accurate than a diagnostic laparoscopy.
Let that sit for a moment. A gut signal, of all things, that predicts one of the most confounding and under-diagnosed diseases in modern medicine. And not a single gastroenterologist I have ever spoken to — not mine, not my clients' — has mentioned it.**
**A reminder that these studies are still small in size, so we can’t say for certain that everyone with endo has it before we see larger studies. What we do see here is that all symptomatic women with endo have the seizure pattern in these cohorts.
So, why does it happen?
Is it Irritable Bowel Syndrome or Two Drunk Choreographers in Your Gut?
Meet prostaglandins PGE2 and PGF2α. Think of them as your body's smooth-muscle choreographers — chemical signals that help your uterus cramp during your period, help your gut coordinate peristalsis, and help your immune system mount an inflammatory response when something goes wrong. In a healthy body, they do their job, maybe with a little pinching, and then leave.
In the endo body we tend to have a lot of both, something not seen in any other disease. Why?
For one, our lesions make some of these buggers. Which is unpleasant, but probably not the root cause for all of us, since we see the same motility pattern in women with many lesions and in those with very few. So what else could it be?
The immune system, most likely, and a wonky immune response.
In our bodies, with endo, peritoneal macrophages — the immune cells patrolling the lining of your pelvic cavity — should be cleaning up endo lesions. But they're misbehaving (as I describe in my book), and the lesions persist. Moreover, they're producing PGE2 at roughly six times the normal rate and PGF2α at more than five times the normal rate.[5] Not twice. Five to six times as much! And this is happening continuously, regardless of what you eat, where you are in your cycle, or whether you've had surgery.
So while lesions themselves produce these prostaglandins too, the macrophage dysregulation is most likely the reason even women with minimal lesion burden carry this biochemical load of both. It's your immune system's response to the war in your pelvis — caused by many things, from too much retrograde flow, bacteria, LPS, hormones, endo lesions, and low oxygen, all of which we know drive macrophage dysregulation from the research. This overall inflammatory milieu leaves them stuck in a gear they cannot shift out of, so they pour out prostaglandins at a rate the body can't process.
Now these two choreographers are no longer keeping rhythm. They have grabbed the megaphone and started screaming contradictory instructions at the orchestra.
PGE2 keeps hitting the fire button on the gut's electrical system — triggering the constant high-frequency misfiring those electrodes picked up.
PGF2α slams all the muscle layers of the intestinal wall into simultaneous contraction, like every musician in the orchestra playing their loudest note at once instead of following the score.
The result is exactly what the researchers saw: seizure-like spasms replacing the normal forward-propelling waves. Food doesn't move through; it gets squeezed and shaken, held back and then shoved forward.
Why This Explains So Much About Endo Belly Symptoms
If you have active endo, there is high probability that the electrical system of your small intestine is firing in a pattern it shouldn't be, whether you're eating or not. Now, what does a small intestine that can't move food forward properly lead to?
Bacteria. Specifically, bacteria growing where it doesn't belong.
The small intestine is supposed to be a relatively low-bacteria environment. Bacteria live primarily in the large intestine, and your small intestine's forward propulsion is a major part of what keeps them there. When that propulsion breaks down, bacteria drift upstream and begin colonizing parts of the gut that were never designed to host them. This is small intestinal bacterial overgrowth — SIBO — and often its sibling, intestinal methanogen overgrowth, IMO.
If you talk to any IMO or SIBO specialist in the world, they will tell you that small intestinal peristalsis is a major factor in developing SIBO or having recurring SIBO. And they're talking about the general population! Not those are are dealing with small intestinal seizures as a part of their disease.
This may be why so many of us with endo deal with SIBO or IMO. A 2025 case-control study of 148 women with confirmed endometriosis found that 91.9% of them tested positive for SIBO or IMO. [6] That is probably not a coincidence. I would bet our motility disorder produces a predictable downstream microbial consequence in many, if not most of us.
If you want to learn more about SIBO and IMO and endo, I have this article here.
It may also be why we suffer from so many digestive irregularities in general. In the 1998 study, when researchers addressed the seizures, gastrointestinal symptoms diminished.
And it explains something that has frustrated endo women for decades, me included: why so many of us have gut problems even when our diets are clean, our nervous systems are calmer, and our lesions (perhaps) have been removed.
What Can We Actually Do? Managing Endo belly and Seizures
What we don't yet see in any of the studies is whether the seizure activity itself can be stopped. No one, not a single researcher, has tried! #annoying. But we do see that symptoms associated with it can be minimized in one study.
The 1998 study proposed that addressing the prostaglandins could potentially stop the trigger. However, they also proposed that the seizures could be exacerbated by an insulin sensitivity issue and an overstimulated nervous system issue.
To treat, they threw all the mud at the proverbial wall they could think of: They prescribed low-dose clonazepam (which can be addictive) to calm the nervous system, a low-glycemic diet for insulin, omega-3, 6, and 9 oils for prostaglandins, and a low nervous-system stimulation diet (no caffeine or tyramine-rich foods). Lots of interventions at once, which makes it tricky to understand what actually helped and what was fluff.
Nonetheless, all participants started the study with unexplained chronic abdominal pain (epigastric to right upper quadrant), nausea, vomiting, early satiety, abdominal distention, altered bowel habits, or some combination of these. By 8 weeks of treatment, they rated their symptoms at an average of 2.8 out of 10. That's a substantial gain.
However, what they didn't check was whether the seizure activity itself had eased, or just the symptoms! And what we know from all the interventions is that it could have been a sort of "raising of tides" for all boats to float. These interventions together can lower inflammation, reverse dysbiosis (starving it of sugar and increasing omega 3's), and calm a stressed system (eliminating caffeine and putting patients on pharmaceutical-grade anti-anxiety medicine, clonazepam!).
So we really don’t know if we can, indeed, stop the seizures with specific interventions based on these endo studies alone.
So what does one do?
We can extrapolate from research on other diseases to see what we can find. If the driver is too much PGE2 and PGF2α, produced by dysregulated immune cells, then the intervention worth considering is two-part:
How can we stop those pesky prostaglandins?
Can we turn down production at the source?
1) Stop the Pesky Prostaglandins
Can we dial down inflammatory prostaglandins? Yes, with the most well-studied answer: long-chain omega-3 fatty acids — specifically EPA and DHA, the kind found in fish oil.
Here's why, in plain terms: your body makes PGE2 from a fat called arachidonic acid. EPA competes with arachidonic acid for the same enzymes, and when EPA wins the competition, your body produces a different, far less inflammatory prostaglandin (PGE3) instead. More EPA in your tissues means less raw material for PGE2 production. It's a supply-chain problem, and EPA is the intervention that cuts the supply.
If you want to read about the science of EPA/DHA in the endo-affected body, read this article here.
How much do we need? A lot, potentially, considering we have SO MUCH PGA2 and PGA2a that our intestines are doing the Macarena. I want you to hear the numbers clearly, because most omega-3 dosing advice you've read online is far. too. low. to do this job.
In rheumatoid arthritis — a disease driven by the same PGE2 pathway we're talking about here — the research suggests an anti-inflammatory dose of approximately 2.7 to 3 grams of combined EPA + DHA per day.[7] Not total fish oil. This is EPA + DHA specifically. (Check the back of the bottle. A "1000 mg fish oil" softgel typically contains only 300 mg of actual EPA + DHA, which means hitting 2.7 grams usually takes 8 softgels a day, or more)
A 2022 randomized trial in Frontiers in Nutrition tested this directly. Participants taking 3.6 grams of EPA+DHA daily for six months showed significant reductions in plasma PGE2 along with reduced C-reactive protein, a broader marker of systemic inflammation. Notably, the more DHA people had in their red blood cell membranes, the lower their PGE2 levels — a direct demonstration that shifting membrane fatty acid composition changes how much inflammatory signal the body produces.[8]
How quickly does this shift start? Maybe faster than we think, with participants in one study having noticable shifts within one week of fish oil intervention. Thirty-eight cancer patients were given either a fish-oil-enriched medical food or a placebo drink for one week. After only seven days, EPA levels in the active group's white blood cells more than doubled — from 1.0% to 2.6% of total fatty acids — and serum PGE2 levels significantly decreased, while the control group's PGE2 actually rose. Same week, same cells, and the EPA/DHA group had measurably less inflammatory signal. The body responds to the change faster than you'd expect. [9]
A few things to know before you run to the supplement aisle:
1) There are no studies on how this would affect the seizure; I’m just extrapolating here because this makes physiologic sense.
2) Quality matters more than almost any other category of supplement. Fish oil oxidizes easily, and oxidized fish oil is pro-inflammatory — which is the opposite of what we're trying to accomplish here. Look for third-party-tested brands, check the manufacturing date, and store the bottle in the fridge once opened.
3) My recommendation is the Nordic Naturals brand (third-party tested for purity), ProOmega 2000, which has 2150 mg EPA + DHA in 2 capsules, so you could take 3 per day. If you want 15% off you can order through my Fullscript here.
4) If you're on blood thinners, have a bleeding disorder, or are approaching surgery, talk to your doctor about dosing. EPA has mild antiplatelet effects, and at 3 grams a day, this is worth a conversation!
Balance Blood Sugar
Blood sugar is the avenue through which I found these extra articles on small intestinal seizures in the first place. (I'm writing a book about endometriosis and blood sugar, more on that below, and both the 1998 and 2002 papers implicate too much insulin as part of the seizure picture.)
Why does insulin matter here? Because insulin hypersecretion — something those of us with endo appear to have, producing about twice the amount of a healthy adult — is upstream of the PGE2/PGF2α overproduction.[10] Thus, lowering insulin can help reduce prostaglandins.[11]
This is why the metabolic piece of the terrain matters so much: it sits upstream of the inflammatory cascade. So stabilizing blood sugar isn't just "also helpful." Even in the 1998 gut-seizure research model, it's one of the primary levers researchers used for reducing prostaglandin overproduction.
2) Stopping the Macrophages From Where They Come From
Why do our peritoneal macrophages produce so much PGE2 and PGF2α? And where do they come from?
Newer research suggests that a significant portion of the macrophages found in the peritoneal cavity of endometriosis patients originate from the uterus itself, migrating with refluxed menstrual tissue into the peritoneum. [12]
But why would uterine-origin macrophages be so inflammatory? Here, the research is newer, and we have to lean into synthesis.
And what's emerging in the research — pulling from studies on chronic endometritis, reproductive tract dysbiosis, and a concept called 'trained immunity' — is that these macrophages may have been learning their pro-inflammatory (oozing Prostaglandins) behavior inside a reproductive tract that was chronically inflamed. One reason why? They could have been exposed to the wrong bacteria. We know women with endo have elevated E. coli in menstrual blood, lactobacillus depletion, and reproductive tract bacterial dysbiosis in up to 81.5% of us. If the inflammation never stops, the immune cells will retain a memory on how to behave (here, very viciously with lots of pro-inflammatory mediators), and then carry what they learned into the peritoneum with each cycle — a pattern consistent with the trained immunity framework demonstrated in mouse models of endometriosis.[13]
What this means, in practical terms, is that the PGE2 problem may not originate in the peritoneum. It may start in the uterus, with a bacterial imbalance or other inflammatory issues, training immune cells to behave in an inflammatory way before they're ever delivered to the site where they do the damage. Which changes where the real therapeutic lever sits — and it's not in another supplement that blocks PGE2 after it's already been made. It's upstream, in the reproductive tract microbiome itself.
Can the cells themselves be retrained once they've been imprinted? The research suggests yes — but slowly, and primarily by changing the environment that's been training them in the first place. Which is why the entire reproductive tract terrain is the real long-game lever. I write about this in my best-selling book, Heal Endo.
Where This Is Going: The Endo Metabolism
I've been writing about endo belly for years — the gut dysbiosis, the reproductive tract dysbiosis, the core dysfunction, the whole exhausting stack of it. But for the past year, I've been deep in a different book, on blood sugar and metabolism and endometriosis. And the odd thing about writing this book is that it keeps pulling threads I didn't mean to pull. This motility piece is one of them.
Because when your gut is electrically misfiring, bacteria aren't the only thing that goes wrong upstream. Your blood sugar does too.
Research on upper GI motility has shown that how fast food moves through your digestive tract — from stomach emptying to small intestinal transit — accounts for approximately 30 to 40 percent of the variance in how your blood sugar responds to a given meal. [14] When the gut is firing chaotically, glucose delivery to the bloodstream becomes erratic — sometimes late, sometimes as a flood — and the pancreas, trying to match insulin to food, ends up overshooting.
This is probably a piece of why so many of us with endo feel so hair-trigger sensitive to blood sugar highs and lows, even when we're eating in ways that ought to keep us steady. In fact, when a glucose strses test was given to the 300 endo patients with intestinal seizures, all 300 had reactive hypoglycemia. One hundred percent![2] The rate in the general population is a small fraction of that.
I'll be writing much more about the blood sugar piece in the months ahead. It's the spine of the book. But I wanted you to have this motility piece on its own, first, because I think it reframes something important about what "endo belly" even is. It's a huge and overlooked piece of the puzzle, and probably part of why so many of the interventions you've done carefully and in good faith have only gotten you partway there.
It's also another way to look at how the terrain of the endo body is interconnected, something I talk about at length in my book when discussing "body ecology." It's why we can't just look at our endo as a sum of specific parts, but rather as an entire terrain that needs to be balanced and healed as a whole.
References
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Mathias, J. R., & Franklin, R. R. (2002). Neural dysfunction of the gastrointestinal tract associated with endometriosis: A disease of insulin sensitivity [Conference abstract]. Fertility and Sterility, 77(Suppl. 1).
Noar, M., Mathias, J., & Kolatkar, A. (2024). Gastrointestinal myoelectrical activity (GIMA) biomarker for noninvasive diagnosis of endometriosis. Journal of Clinical Medicine, 13(10), 2866.
Tanos P, Donders F, Massaro A, Philippe S, Karampelas S. "Defining the role of the gastrointestinal myoelectrical activity (GIMA) biomarker in the diagnosis of endometriosis." Journal of Minimally Invasive Gynecology, 2025;32(11)(suppl):S23.
Karck U, et al. "PGE2 and PGF2α release by human peritoneal macrophages in endometriosis." Prostaglandins, 1996;51(1):49-60.
Halfon, M., Estrade, J. P., Pénaranda, G., et al. (2025). High prevalence of small intestinal bacterial overgrowth and intestinal methanogen overgrowth in endometriosis patients: A case-control study. International Journal of Gynecology & Obstetrics, 170(1), 284–291.
Cleland LG, et al. "Fish oil: what the prescriber needs to know." Arthritis Research & Therapy, 2006;8(1):202
Frisardi V, et al. "Omega 3 supplementation reduces C-reactive protein, prostaglandin E2 and the granulocyte/lymphocyte ratio in heavy smokers." Frontiers in Nutrition, 2022.
Faber J, et al. "Rapid EPA and DHA incorporation and reduced PGE2 levels after one week intervention with a medical food in cancer patients receiving radiotherapy." Clinical Nutrition. 2013.
Florova MS, Yarmolinskaya MI, et al., "Role of insulin and insulin-like growth factor I receptor expression in the pathogenesis of genital endometriosis" (Journal of Obstetrics and Women's Diseases, 2021, Vol 70, Issue 3)
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