Daniel sent us this one — and it's a heavy one. He had his gallbladder removed after an ultrasound suggested stones. Pathology found no stones. He swapped an occasional mild pain for daily bloating, gastritis, terrible reflux, the whole digestive system going haywire. Low-fat diet for life, no one prepared him for it. And the truly unsettling part — it's irreversible. His question is whether there's any centralizing specialty, any centers of excellence, any researchers trying to find a joined-up approach to treating post-cholecystectomy syndrome. Because right now, patients seem to be left managing symptoms one at a time on an endless medication carousel. There's a lot to unpack here.
There really is. And the first thing I want to say is that this is not a rare outcome. Depending on which study you cite, somewhere between ten and forty percent of people who have their gallbladder removed go on to develop what's called post-cholecystectomy syndrome — PCS. That's not a rounding error. That's millions of people.
Ten to forty percent is a range so wide it's almost saying "we don't actually know.
It kind of is. The lower estimates tend to come from surgical follow-up studies where they ask "are you satisfied with the outcome" at six weeks. The higher estimates come from gastroenterology clinics where people show up years later with persistent symptoms. The definitional problem alone is a mess. PCS isn't one thing — it's a bucket term for "the patient had their gallbladder out and now has digestive symptoms that weren't there before, or got worse." That could be bile reflux gastritis, chronic diarrhea, sphincter of Oddi dysfunction, a retained stone they missed, or something entirely unrelated that was misattributed to the gallbladder in the first place.
Step one of the joined-up approach is just figuring out what you're actually treating.
And that's where it already breaks down, because the surgeon who did the operation isn't equipped to do that differential diagnosis, the primary care doctor often doesn't know the biliary system well enough to parse it, and the gastroenterologist may or may not have a specific interest in post-surgical biliary disorders. So the patient bounces between specialties like a pinball, collecting prescriptions at each bumper.
Daniel's point about treating symptoms one at a time being a bad idea — he's right, but that's exactly what happens. You get a PPI for the reflux, an anti-diarrheal for the diarrhea, an anti-spasmodic for the cramping, cholestyramine if someone thinks to check for bile acid malabsorption. None of it addresses the underlying mechanical and chemical derangement.
Let me pull on that mechanical thread, because I think most people don't understand what the gallbladder actually does. It's not a vestigial organ. It's not the appendix of the biliary system.
Walk me through what's actually lost.
The gallbladder is a storage and concentration reservoir. Your liver produces bile continuously — about six hundred to a thousand milliliters a day. The gallbladder stores roughly fifty milliliters and concentrates it five to tenfold. When you eat, particularly fat, the duodenum releases cholecystokinin, which signals the gallbladder to contract and squirt that concentrated bile into the small intestine in a timed bolus. That concentration matters. That timing matters.
Without the reservoir?
Without the reservoir, bile just trickles continuously into the duodenum. It's dilute, unregulated, and it drips whether you're eating or not. Between meals, that bile can pool and reflux backward into the stomach and even the esophagus. That's bile reflux — distinct from acid reflux, and proton pump inhibitors don't touch it, because the damaging agent isn't acid, it's bile salts. Meanwhile, when you do eat a fatty meal, there's no concentrated bolus ready to go. You're trying to emulsify fats with a trickle of dilute bile, so fat digestion is impaired. That leads to bloating, steatorrhea, discomfort. And later, unabsorbed fats and bile acids reach the colon, where they irritate the mucosa and cause diarrhea.
You've got bile where you don't want it when you're not eating, and not enough bile where you do want it when you are eating. It's the worst of both worlds.
That's the fundamental mismatch. Bile reflux gastritis is a chemical burn of the stomach lining. The stomach is built to handle acid, not bile. Bile is alkaline, disrupts the protective mucus layer, causes inflammation, and in some cases can lead to intestinal metaplasia — a precursor to more serious problems. Meanwhile, downstream, the colon is getting hammered by bile acids that should have been reabsorbed in the terminal ileum but weren't, because the whole system is out of sync.
This is a motility problem as much as a chemistry problem. The timing is broken.
And that's the piece that gets overlooked constantly. Most gastroenterology is organized around either structural problems you can see on a scope — ulcers, inflammation, polyps — or functional problems diagnosed by symptom criteria, like IBS. Post-cholecystectomy syndrome straddles both and fits neatly into neither. It's a structural alteration — the organ is gone — that produces a functional disorder — the timing and concentration of bile delivery is wrong — with downstream structural consequences. It falls through the cracks of how the specialty is organized.
Which brings us back to Daniel's core question. Is anyone trying to build a framework that doesn't have cracks for this to fall through?
There are a few places where this is being taken seriously as a unified problem. The first is the Mayo Clinic's motility and functional gastrointestinal disorders group. They have a specific clinical interest in post-surgical GI disorders, including PCS. The key word is "motility" — they're looking at the timing problem, not just the acid problem.
Motility as in how things move through the system.
The biliary system is fundamentally a motility system — the sphincter of Oddi opens and closes, the gallbladder contracts, bile moves through ducts, all coordinated by neural and hormonal signals. Remove the gallbladder and you've disrupted a key node in that network. The Mayo group does advanced motility testing — antroduodenal manometry, measuring pressure patterns in the stomach and small intestine. They can actually map the dysmotility that follows cholecystectomy. That's not something your average community GI practice can do.
If someone's thinking "I need to get to one of these centers," what's the landscape?
Beyond Mayo, the University of Michigan has a strong motility program and has published specifically on post-cholecystectomy bile reflux. Cleveland Clinic has a section of biliary endoscopy dealing with post-surgical complications, though they're more focused on structural problems like strictures and retained stones. Johns Hopkins has a pancreaticobiliary center that handles complex post-surgical cases. Stanford's neurogastroenterology and motility program is another. In Europe, the University of Bologna has done interesting work on bile acid malabsorption after cholecystectomy.
These are all still within general gastroenterology, right? There's no subspecialty board certification in "post-cholecystectomy medicine.
No formal subspecialty, no fellowship track, no board exam. What you have instead are individual clinicians and research groups who've developed a focused interest, often because they kept seeing these patients and realized the standard approach wasn't working. It's a self-selected group, and finding them requires knowing what to look for.
Which is itself a barrier. The patient has to self-advocate through a system that isn't designed to route them to the right person.
The Facebook groups Daniel mentioned — I share his mixed feelings — but one thing they do well is crowd-source that routing information. "Who did you see that actually helped?" That's valuable data the medical system doesn't surface on its own.
Though the problem with crowd-sourced medical advice is that it's a sample of people who are still suffering. The ones who got better stopped posting.
That's the selection bias. The Facebook groups become repositories of the worst outcomes, which makes them depressing and also makes it hard to gauge the real prognosis. But they're also where you learn practical things like "ask your doctor about cholestyramine" — things that, remarkably, many patients are never told about.
Let's talk about cholestyramine, because that came up as one of the few treatments that addresses a root mechanism rather than just suppressing a symptom.
Cholestyramine is a bile acid sequestrant. It's a powder you mix with water, and it binds to bile acids in the intestine, forming an insoluble complex that passes through without being reabsorbed or causing irritation. For the subset of PCS patients whose primary problem is bile acid diarrhea, it can be transformative. It's not a cure, but it directly addresses the mechanism by which the continuous bile drip causes diarrhea.
It's an old drug. This isn't some cutting-edge biologic.
From the nineteen seventies. Originally developed for cholesterol lowering, before statins. The bile acid diarrhea application is almost an off-label afterthought, but for the right patient it works remarkably well. The catch: it's gritty, can cause bloating and constipation, and dosing is tricky because you have to time it around meals and other medications — it binds to everything, not just bile acids.
It's a solution that creates its own management problems.
Which is the story of PCS treatment in a nutshell. Every intervention has trade-offs. PPIs reduce acid but don't touch bile reflux and may worsen bile-induced damage by reducing the stomach's acid barrier. Anti-diarrheals slow transit but don't address the chemical irritation. Low-fat diets reduce symptoms but are nutritionally restrictive and socially limiting. It's all partial fixes.
Are there any genuinely new approaches in development? Anything that tries to restore the missing function?
This is where I have to be careful about overpromising. One direction is neurostimulation — gastric electrical stimulation or vagal nerve stimulation to modulate GI motility. This is being studied for gastroparesis and functional dyspepsia, but there's theoretical application to post-cholecystectomy dysmotility. The idea is that if you can restore some of the neural coordination that was disrupted, you might improve the timing problem. The evidence is thin, but the logic is sound. A group at the University of Louisville has looked at this.
What about something more direct? An artificial gallbladder?
No artificial gallbladder exists. There have been conceptual designs — implantable reservoirs with controlled-release mechanisms — but nothing past the prototype stage. The engineering challenges are significant. You need something that can store bile, concentrate it, and release it in response to meals, all without clotting, leaking, or causing infection. It's a harder problem than an artificial heart valve.
The market incentive isn't there because cholecystectomy is framed as a definitive cure. If the surgery is a success by definition, there's no problem to solve.
That's the cultural problem within surgery. Cholecystectomy is one of the most common operations in the world — about seven hundred thousand a year in the United States alone. The surgical literature overwhelmingly reports it as safe and effective, with high patient satisfaction. And for many patients, it is. If you had recurrent biliary colic from stones and the surgery eliminated that pain, you're probably satisfied. But the satisfaction surveys are typically done at surgical follow-up, not two or five years later when the chronic symptoms have set in.
If the pathology comes back negative — no stones, no inflammation — the surgeon's response is often "well, your gallbladder is out, so the pain should be gone." Which is a non-answer when the pain has been replaced by different, more diffuse misery.
Daniel mentioned that exact experience. Negative pathology after an ultrasound said stones. It happens more often than surgeons like to admit. Ultrasound can produce false positives — sludge can look like small stones, polyps can be misread, and sometimes the gallbladder just looks abnormal on imaging without actually being the source of the pain. When the pathology comes back clean, it raises the uncomfortable possibility that the gallbladder wasn't the problem in the first place.
Which makes the irreversibility hit even harder.
That's what I don't think is communicated well enough pre-operatively. It's pitched as a routine surgery with a quick recovery, which it is from a surgical standpoint — laparoscopic cholecystectomy is technically straightforward, small incisions, home the same day. But "routine" doesn't mean "consequence-free." The gallbladder is not a spare part. It has a function. Removing it changes your digestive physiology permanently.
The consent form lists the surgical risks — bleeding, infection, bile duct injury — but it doesn't list "your digestive system may never work the same way again.
Because that's not considered a surgical complication. It's considered a separate condition — PCS — which falls under gastroenterology, not surgery. The surgeon's responsibility ends when the incisions heal. What happens after that is someone else's problem.
The patient is handed off from a discipline that considers the problem solved to a discipline that didn't create the problem and isn't organized to address it holistically.
That's the structural gap. Filling it would require something that doesn't currently exist — a clinical pathway specifically for post-cholecystectomy patients that integrates motility testing, bile acid assessment, endoscopic evaluation for bile reflux, and a coordinated treatment plan. Right now, none of those pieces talk to each other routinely.
Let's talk about what that assessment actually looks like, because I think many people in Daniel's position have never had a proper workup. They were told "you had your gallbladder out, some people just have trouble with fatty foods now, avoid fat" and sent on their way.
A proper workup for suspected PCS should include several things. First, an upper endoscopy to look for bile reflux gastritis — you can actually see bile pooling in the stomach, and biopsies can show the characteristic chemical gastropathy pattern distinct from H. pylori or NSAID damage. Second, bile acid malabsorption assessment — the gold standard is the SeHCAT scan, which measures how well you're retaining bile acids, but it's not widely available in the United States. There are blood tests like 7-alpha-hydroxy-four-cholesten-three-one — C4 for short — that can serve as a proxy. Third, if there's pain, an MRCP or ERCP to look for retained stones, strictures, or sphincter of Oddi dysfunction.
How many people get all three of those?
Very few, unless they're at a center with a specific interest in this. The SeHCAT scan isn't even approved in the US — it's used in Europe and Canada. The C4 blood test is available but not widely ordered. Most community gastroenterologists aren't thinking about bile acid malabsorption in the post-cholecystectomy context. They're thinking about acid reflux and IBS.
The diagnostic tools exist but they're fragmented across different systems and levels of awareness.
The UK actually does better on this than the US, because the NHS has a more centralized approach to post-surgical follow-up and some centers have established pathways for bile acid malabsorption testing. But even there, it's patchy.
What about the dietary side? Daniel mentioned adhering to a low-fat diet. Is that actually the right approach, or just the default advice because nobody knows what else to say?
It's both. A very low-fat diet does reduce symptoms for many people, because you're reducing the demand on a bile delivery system that can't meet peak demand. But it's not a physiologically sound long-term solution. Dietary fat is essential for absorbing fat-soluble vitamins — A, D, E, and K. Long-term very low-fat diets can lead to deficiencies. And the diet is hard to sustain — socially isolating, makes eating at restaurants difficult.
It doesn't address the between-meal bile drip. You can eat zero fat and still have bile pooling in your stomach overnight.
That's why some patients do better with smaller, more frequent meals — it gives the continuous bile trickle something to do, so it's less likely to pool and reflux. But that's a management strategy, not a fix.
Are there dietary approaches beyond "eat less fat" with some evidence?
Soluble fiber can help by binding bile acids in the intestine, similar to cholestyramine but milder — psyllium husk, oat bran. Some people find taking a fiber supplement before meals reduces post-meal diarrhea. There's also interest in spreading fat across the day rather than having it all in one meal, so the continuous trickle can handle small amounts better than a large bolus. And a subset of patients benefit from digestive enzyme supplements, particularly lipase, though the evidence is mixed.
None of this sounds like it was communicated to Daniel pre-operatively.
Almost certainly not. And that's the informed consent problem. The risks discussed are surgical risks. The long-term functional risks are either not mentioned or minimized. "Most people do fine" is true but not helpful to the minority who don't.
Let's go back to the treatment pipeline. Beyond cholestyramine and dietary modification, what else is in the toolkit? I'm particularly interested in whether there's anything that addresses bile reflux directly, since that seems to be one of the most damaging components.
Bile reflux is difficult to treat. PPIs don't help because the problem isn't acid — in fact, by reducing acid, you may be making the stomach more vulnerable to bile-induced damage. There are mucosal protective agents — sucralfate is the main one. It coats the stomach lining and can provide some barrier against bile. Ursodeoxycholic acid — UDCA — is a bile acid that's less toxic to the mucosa, and there's some evidence that supplementing with UDCA can shift the bile acid pool toward a less damaging composition. But the evidence for both in post-cholecystectomy bile reflux is limited.
We're in "might help, won't hurt, evidence is thin" territory.
That's most of the pharmacopeia for PCS, unfortunately. There are also prokinetics — metoclopramide, domperidone — that speed up gastric emptying and might reduce the time bile spends pooling in the stomach. But they have their own side effect profiles and aren't great long-term solutions.
What about surgical interventions? If the problem is bile reflux, can you surgically reroute things?
Roux-en-Y gastric bypass essentially diverts bile away from the stomach, which is why it eliminates bile reflux. But that's a major bariatric surgery with its own consequences — not something you'd do solely for post-cholecystectomy bile reflux. There's also a Roux-en-Y hepaticojejunostomy, a biliary diversion procedure, but again, it's a major operation with significant morbidity. These are last-resort options for the most severe cases.
The surgical solution to the surgical problem is more surgery, each with its own cascade of potential complications.
Which is why the joined-up approach Daniel is asking about is so important. You want to avoid the situation where each intervention creates new problems requiring new interventions. The goal should be to understand the specific pathophysiology in each patient and target the mechanism, not just suppress symptoms.
Let's talk about the research landscape. Are there any clinical trials or studies that give reason for optimism?
Post-cholecystectomy syndrome is under-researched relative to its prevalence, but there are some interesting directions. One is the microbiome angle — there's emerging evidence that cholecystectomy alters the gut microbiome, possibly because the continuous bile flow changes the intestinal environment in ways that shift bacterial populations. A group in China published a study in twenty twenty-three looking at specific probiotic strains for post-cholecystectomy diarrhea, with modestly positive results.
Modestly positive is the phrase of the episode, it seems.
Another direction is better diagnostics for bile acid malabsorption. There's work on developing simpler breath tests or blood markers that could replace the SeHCAT scan, which would make it much easier to identify patients who would benefit from bile acid sequestrants. Right now, a lot of PCS patients are treated empirically — try the cholestyramine and see if it helps — which means some who might benefit never try it, and some who try it and don't need it get side effects for no reason.
The empiric approach is basically "throw things at the wall and see what sticks," which is exhausting for the patient.
Expensive, time-consuming, and it erodes trust. When you've tried four different medications and none of them helped, you start to feel like nobody knows what they're doing.
I want to circle back to something Daniel mentioned — the Facebook groups being both useful and depressing. There's a broader question here about how patients with chronic post-surgical conditions find community and information when the medical system doesn't have a clear home for them.
This is a phenomenon not unique to PCS. It happens with post-vasectomy pain syndrome, post-hernia repair chronic pain, post-spinal fusion syndrome. Any time a surgery is considered routine and definitive by the surgical community but leaves a minority with chronic problems, those patients end up forming their own information networks because the official channels don't serve them.
Those networks can be both a lifeline and an echo chamber of misery.
But they also serve a function the medical system should be serving — they aggregate patient experiences, identify patterns, circulate practical tips. The fact that patients have to do this themselves is an indictment of how we handle post-surgical follow-up.
If you were designing an ideal system, what would it look like?
Every patient undergoing cholecystectomy would have a pre-operative consultation that honestly discusses the risk of PCS — including the specific mechanisms, not just "some people have ongoing symptoms." They'd have a baseline symptom assessment and, ideally, some baseline motility or bile acid testing, so there's something to compare to if problems develop. Post-operatively, there'd be a structured follow-up at three months, six months, and one year that screens for PCS symptoms and triggers a referral to a dedicated post-cholecystectomy clinic if symptoms are present. That clinic would have access to motility testing, bile acid assessment, endoscopy with bile reflux evaluation, and a coordinated team including a gastroenterologist, a dietitian, and potentially a pain psychologist.
This doesn't exist anywhere.
Not in that integrated form, to my knowledge. Pieces of it exist. The Mayo motility group does something close. Some European centers have more structured pathways. But the fully integrated, multi-disciplinary post-cholecystectomy clinic is something I haven't found evidence of.
Which means the burden remains on the patient to assemble their own team and coordinate their own care.
And that's especially difficult when you're already dealing with chronic symptoms that are exhausting and demoralizing. The people best positioned to navigate a complex medical system are the people who feel the least well.
What's the practical advice for someone in Daniel's position? If you've had your gallbladder out and your digestive system has never been the same, what do you actually do?
First, get a proper workup if you haven't had one. That means an upper endoscopy with biopsies looking specifically for bile reflux gastritis — tell the gastroenterologist before the procedure that this is what you're concerned about, because they may not look for it otherwise. Ask about bile acid malabsorption testing — the C4 blood test if SeHCAT isn't available. If there's pain, push for an MRCP to rule out retained stones or strictures.
If your local gastroenterologist looks at you blankly when you mention bile acid malabsorption?
Find a motility specialist. That's the keyword. "Neurogastroenterology and motility" is the subspecialty within GI most likely to understand these problems. Most academic medical centers have at least one person in this area. It may require traveling. It's not ideal, but that's the current reality.
In terms of treatment, what's the ladder?
Start with the lowest-hanging fruit. If diarrhea is dominant, a trial of cholestyramine or colesevelam — another bile acid sequestrant — is reasonable and relatively low-risk. If reflux is dominant, sucralfate is worth trying, and don't assume PPIs will help because the problem may not be acid. If bloating and dyspepsia are dominant, smaller, more frequent meals with moderate fat distributed across the day, plus soluble fiber. Ursodeoxycholic acid is worth discussing with a knowledgeable gastroenterologist. And if none of the medical management works and symptoms are severe, that's when you consider referral to one of the major centers for advanced motility testing and potentially more aggressive interventions.
None of this is a cure. It's all management.
That's the honest truth. Once the gallbladder is out, there's no putting it back. The goal is to understand the specific mechanism of your symptoms and target that mechanism as precisely as possible, so you're not on five different medications with overlapping side effects and unclear benefit.
Which brings us back to Daniel's central question about whether there's any centralizing specialty or center of excellence. The answer seems to be: not formally, but there are people and places that come close, and you have to know how to find them.
The keyword is motility. If you're looking for a clinician who might actually understand what's happening, look for someone whose practice focuses on GI motility and functional disorders. They're the ones who think about timing and coordination, not just acid and inflammation.
It strikes me that this is a problem that's going to grow, not shrink. Cholecystectomy rates aren't declining. The population is aging. And as more people live for decades after the surgery, the cumulative burden of PCS is going to increase.
Yet the research funding is minimal. It's not a glamorous area. It's not cancer. It's not a novel drug target that pharma companies are excited about. It's a chronic, quality-of-life condition affecting millions but without a strong advocacy voice.
The Facebook groups are the advocacy voice, and they're not being heard.
Or they're being heard but dismissed as the vocal minority. "Most people do fine, these are just the ones who don't." Which is true, but ten to forty percent of seven hundred thousand cholecystectomies a year in the US alone is somewhere between seventy thousand and two hundred eighty thousand new PCS cases annually. That's not a rounding error. That's a public health problem.
That's just the US. Scale it globally.
The global numbers are in the millions annually. And we have no systematic approach to preventing, diagnosing, or treating this condition.
If there's a call to action embedded in this episode, it's probably directed at the gastroenterology community: this deserves a formal subspecialty focus. It deserves dedicated clinics. It deserves research funding. And in the meantime, it deserves honest pre-operative counseling that doesn't minimize the functional consequences of removing an organ.
I'd add that it also deserves better diagnostic tools. A simple, widely available test for bile acid malabsorption would change the landscape overnight, because it would identify the subset of patients who can be helped by existing medications. That's low-hanging fruit that nobody seems to be picking.
For the patient listening to this who's in the thick of it — there are things to try, there are people who understand this, and you're not crazy. The symptoms are real, they have a physiological basis, and they're not just something you have to accept.
The physiology is clear. The gallbladder does something important. Removing it has consequences. Acknowledging that doesn't mean the surgery was a mistake — for many people with genuine gallbladder disease, it's necessary and beneficial. But it does mean the medical system needs to take the consequences seriously and build the infrastructure to address them.
Now: Hilbert's daily fun fact.
Now: Hilbert's daily fun fact.
Hilbert: In the late sixteen hundreds, a single bloom of mauve stinger jellyfish in Australia's Simpson Desert — a region that was briefly an inland sea during a flood year — produced an estimated four hundred million individuals in under six weeks before the waters receded and the entire population died.
The Simpson Desert was briefly an inland sea full of jellyfish.
Then it wasn't. And they all died.
One thing I keep thinking about is the informed consent process. We've talked about it a few times, but it's worth naming directly: if you're told gallbladder removal is routine and recovery is simple, you're not being given the full picture. I don't think it's necessarily malice — I think it's a system where surgeons are trained to think about surgical outcomes, not long-term functional outcomes. But the result is the same. People walk into an irreversible procedure without understanding what they're risking.
There's a paper I came across that looked at what patients are told pre-operatively about post-cholecystectomy diarrhea specifically. Fewer than twenty percent of patients recalled being informed about the risk of chronic diarrhea. And that's just one symptom. The rates for bile reflux, dyspepsia, the need for long-term dietary modification — they're even lower.
The consent is legally valid but functionally meaningless.
Informed consent requires understanding. If the information isn't communicated in a way the patient can absorb and weigh, it's not truly informed. And the framing of cholecystectomy as "routine" actively undermines understanding, because "routine" implies low-consequence.
"Routine" is doing a lot of work to make people not ask questions they should be asking.
The alternative to surgery is often presented as "you could get gallstone complications" — pancreatitis, cholecystitis, cholangitis — which are real and serious. But the framing is binary: surgery versus dangerous complications. There's rarely a discussion of watchful waiting for asymptomatic or minimally symptomatic stones, or of the fact that many people with gallstones never develop symptoms at all.
Especially when the symptoms are vague. An on-off mild pain that feels like a muscle pull — that's what Daniel described. That's not biliary colic classically described. That's not a clear indication for surgery.
When the pathology comes back negative, you have to wonder whether that pain was ever coming from the gallbladder. It could have been musculoskeletal, functional dyspepsia, any number of things. But once the gallbladder is out, you can't go back and run the control experiment.
The control experiment being "keep the gallbladder and see if the pain goes away on its own.
Which, for many people with mild symptoms, it does. Gallstones are common. Most people with gallstones never need surgery. But the default in many healthcare systems is that if there are stones on imaging and any symptoms at all, the gallbladder comes out.
Once it's out, you're in a different physiological state permanently. There's no undo button.
That's the thing I wish more people understood before surgery. It's not that cholecystectomy is a bad operation — it's a good operation for the right indication. But it's not a neutral operation. It changes how your body handles every meal for the rest of your life. For most people, that change is manageable or even unnoticeable. For a significant minority, it's disabling.
This has been My Weird Prompts. Thanks to our producer Hilbert Flumingtop. If you want more episodes, you can find us at myweirdprompts.com or wherever you get your podcasts. Leave us a review if you're enjoying the show — it helps other people find us.
Until next time.
