We've got a special prompt today from a listener named Marcus Jakes. He's seven years out from gallbladder surgery and dealing with the aftermath — bloating, chronic gastritis, that whole constellation. He's tried the individual fixes, UDCA for bile reflux, ox bile supplements for bigger meals, but here's the knot he can't untie: the treatments contradict each other. More bile for digestion versus less bile damage in the stomach. Pick one problem and the other one flares. He's worked with a gastroenterologist and still feels stuck. So the real question is, how do you manage a condition where the solutions fight each other?
This is the post-cholecystectomy paradox in a nutshell. And Marcus is describing something that is genuinely underappreciated in gastroenterology — the fact that once the gallbladder is gone, you lose the organ that was supposed to time the release of bile. You have this continuous trickle instead of a coordinated squirt, and suddenly bile is in places it shouldn't be, at times it shouldn't be there, in concentrations that don't match what you're eating.
The gallbladder wasn't just a storage pouch. It was the conductor.
It concentrated bile, stored it, and released it in a pulsed fashion precisely when fat hit the duodenum. Remove that, and bile just drips continuously from the liver into the small intestine. Between meals, when there's no food to absorb it, that bile can pool in the duodenum and reflux backward into the stomach. That's the bile reflux gastritis piece. Then, during a meal, especially a fatty meal, there's not enough concentrated bile available all at once, so fat digestion suffers. You get bloating, steatorrhea, discomfort. Two problems with one root cause, but the treatments pull in opposite directions.
Like trying to fix a leaky faucet by turning up the water pressure.
That's actually not far off. The ox bile supplements make sense for the digestive side — you're supplementing the bile acid pool so there's enough to emulsify fats when you eat. But you're also increasing the total bile acid load circulating in your system, which means more substrate available to reflux into the stomach between meals. Meanwhile UDCA works by changing the composition of the bile acid pool. It's a more hydrophilic, less detergent bile acid, so it's less damaging to the gastric mucosa. But it doesn't necessarily stop the reflux itself. It just makes the bile that does reflux less corrosive.
You're not fixing the reflux. You're just making it...
And that's where Marcus's frustration is completely justified. He's being asked to manage a mechanical problem with chemical solutions, and the chemicals work at cross-purposes. A gastroenterologist can prescribe UDCA and suggest ox bile and maybe add a proton pump inhibitor, but none of those address the underlying motility issue — which is that bile is flowing the wrong direction because the normal timing mechanism is gone.
Let me pause on PPIs for a second. Because I've said before that prescribing PPIs for bile reflux is like prescribing sunglasses for a hearing problem. They reduce acid, but bile reflux is alkaline or at least not primarily acidic. So what's the actual rationale?
The rationale is usually thin. Some gastroenterologists argue that bile reflux and acid reflux often coexist, and reducing acid at least removes one component of the damage. There's also a theory that acid and bile together are synergistically more damaging to the mucosa than either alone, so eliminating the acid component reduces overall injury even if bile is still present. But you're right — it doesn't stop the bile. It's a partial band-aid. And long-term PPI use comes with its own set of problems: increased risk of small intestinal bacterial overgrowth, potential nutrient malabsorption, rebound hyperacidity if you try to stop.
Marcus has a menu of partial band-aids, and he's supposed to figure out which combination doesn't make things worse. That's not a treatment plan. That's alchemy.
This is where the literature on post-cholecystectomy syndrome gets really interesting, because the term itself is a bit of a confession. Post-cholecystectomy syndrome isn't a diagnosis — it's an admission that something went wrong and we're not entirely sure which mechanism is dominant in any given patient. It covers everything from biliary dyskinesia to sphincter of Oddi dysfunction to bile reflux to retained stones, and the symptoms can overlap so much that pinning down the primary driver is difficult.
The diagnosis is basically "you had your gallbladder out and now things are bad, good luck.
That's the cheeky version, but it's not far from the clinical reality. The more precise way to think about it is that cholecystectomy changes the entire biliary ecosystem. The bile acid pool circulates more frequently — studies show the enterohepatic cycling rate can increase two to threefold after gallbladder removal. The bile becomes less concentrated but more continuously present. The fasting gallbladder, which used to sequester about half the bile acid pool between meals, is gone. So you've got bile acids bathing the small intestine essentially around the clock.
That constant bathing — that's what drives the gastritis?
The direct mechanism is duodenogastric reflux — bile flowing backward from the duodenum into the stomach. The stomach lining is not built to handle bile acids. They disrupt the mucous layer, increase permeability, cause chemical gastritis. But there's also a secondary effect. Continuous bile in the small intestine alters the gut microbiome. Bile acids are antimicrobial. When they're present at the wrong times and in the wrong concentrations, they can selectively suppress certain bacterial populations and favor others. That dysbiosis can contribute to bloating, gas, and altered motility.
The bloating isn't just "I ate something fatty and couldn't digest it." It's also a microbiome problem.
Almost certainly multifactorial. You've got impaired fat digestion from the loss of the concentrated bile bolus. You've got altered small intestinal transit because bile acids themselves affect motility — they stimulate the release of hormones like FGF19 that regulate gut speed. And you've got a microbial community that's been reshaped by the new bile acid environment. All three of those can produce bloating, and they can interact in ways that are hard to disentangle.
Okay, so let's get practical. Marcus is taking ox bile with meals for fat digestion. That helps the bloating from undigested fat. But it adds to the total bile load, and some of that presumably ends up in his stomach later. He's taking UDCA to make that refluxed bile less damaging. Those two are the core tension. What does the evidence actually say about how to sequence or balance these?
The evidence is frustratingly sparse. There are no large randomized controlled trials looking at combined UDCA and ox bile supplementation in post-cholecystectomy patients. What we have are small studies, clinical experience, and mechanistic reasoning. UDCA has decent evidence for bile reflux gastritis — studies show it reduces symptoms and endoscopic signs of gastritis in a subset of patients, probably by displacing more toxic bile acids from the pool. Ox bile has almost no formal evidence base. It's a supplement, not a pharmaceutical, so nobody's funding big trials. The rationale is physiologically plausible, but we're operating on plausibility, not proof.
Marcus's gastroenterologist probably couldn't point to a protocol either. That explains the lack of clarity.
And this is a broader problem in gastroenterology. Once you're past the first-line interventions, you enter this territory where the evidence thins out dramatically and clinical practice becomes highly variable. One gastroenterologist might swear by sucralfate as a coating agent for bile gastritis. Another might favor a prokinetic to speed gastric emptying and reduce the contact time of refluxed bile. Another might push for a Roux-en-Y reconstruction to divert bile away from the stomach entirely, which is a major surgery. None of these approaches has been compared head-to-head in a rigorous way.
The Roux-en-Y option — that's essentially surgically rerouting the plumbing so bile can't back up into the stomach. That's a big swing for a problem that started with a supposedly routine gallbladder surgery.
And it's typically reserved for severe, refractory cases. But the fact that it's even on the menu tells you something about how poorly the medical management options work for some patients. You don't propose surgically reconfiguring someone's upper GI tract unless the non-surgical options have been inadequate.
Let's talk about timing. One thing I've wondered — and Marcus didn't mention this directly — is whether the timing of these supplements relative to meals matters more than people think. If ox bile taken with a meal helps digestion, but then you've got hours between meals where bile is just pooling, is there a window where you could take something to bind or neutralize bile during the fasting periods?
That's a really smart question, and it gets at something that is almost entirely neglected in standard post-cholecystectomy management. The gallbladder's job was temporal. It separated the fed state from the fasted state in terms of bile delivery. Without it, you need to artificially recreate that separation. Taking ox bile with meals makes sense for the fed state. For the fasted state, there are a few strategies that have some rationale. One is bile acid sequestrants — cholestyramine or colesevelam. These are resins that bind bile acids in the intestine and prevent their reabsorption. If you take a small dose of a sequestrant between meals or at bedtime, you could theoretically mop up some of the excess bile before it has a chance to reflux.
Then you're adding a third pill with a different timing schedule. The litany of supplements problem that Marcus mentioned just gets worse.
And each addition has its own side effect profile. Cholestyramine can cause constipation, bloating, and can interfere with the absorption of other medications and fat-soluble vitamins. So you solve one problem and potentially create two more. This is the whack-a-mole nature of managing post-cholecystectomy syndrome. Every intervention has a cost, and the costs compound.
There's something almost tragic about this from a medical design perspective. The gallbladder evolved for a reason. It's not a vestigial organ. We treat cholecystectomy as this routine procedure — over seven hundred thousand a year in the US alone — but for a significant minority of patients, the aftermath is a lifelong management puzzle that medicine hasn't really figured out how to solve.
The numbers are sobering. Depending on which study you look at, somewhere between five and forty percent of post-cholecystectomy patients report persistent symptoms. The wide range reflects differences in how you define symptoms and how long you follow patients, but even at the low end, we're talking about tens of thousands of people every year who don't just bounce back.
If any other elective procedure had a forty percent persistent symptom rate, we'd call that a crisis.
And part of the problem is that the symptoms are nonspecific — bloating, dyspepsia, altered bowel habits — so they're easy to dismiss or attribute to functional disorders. A patient comes in six months after surgery saying they feel bloated all the time, and the surgeon says the surgery went fine, the gastroenterologist does an endoscopy and maybe sees some mild gastritis, and everyone shrugs. Meanwhile the patient is trying to figure out on their own which combination of supplements might let them get through a meal without feeling miserable.
Which is exactly where Marcus is. Seven years of self-experimentation and he's still not sure he's got it right. So let's try to build a framework. If we accept that the core problem is loss of temporal control over bile delivery, and that the available tools all have trade-offs, what principles should guide how someone thinks about managing this?
I think there are a few principles that make sense, even if the evidence isn't perfect. First, dietary modification is underrated. Smaller, more frequent meals reduce the fat load per meal, which means you need less bile per digestive event, and you reduce the volume of bile that pools between meals because the fasting windows are shorter. Lower fat intake overall reduces the total bile acid flux. These are not exciting interventions, but they address the physiology directly.
Grazing rather than feasting.
Second, if you're going to use ox bile, timing it precisely matters. Taking it mid-meal or toward the end of a meal, rather than before, might better mimic the natural timing of gallbladder emptying, which occurs after food is already in the duodenum. Some people find that splitting the dose during a larger meal helps. Third, UDCA is probably the best-supported pharmaceutical option for the gastritis component, but it works slowly and it's more about reducing damage than preventing reflux.
What about the prokinetic angle? You mentioned some gastroenterologists favor speeding up gastric emptying.
Prokinetics like metoclopramide or domperidone can reduce the contact time of refluxed bile with the gastric mucosa by moving contents out of the stomach faster. The logic is sound. The problem is that the available prokinetics have significant limitations. Metoclopramide crosses the blood-brain barrier and can cause neurological side effects, including tardive dyskinesia with long-term use. Domperidone doesn't cross as readily but has cardiac concerns, particularly QT prolongation. Neither is ideal for chronic use.
We're back to dietary timing, carefully dosed supplements, and UDCA as the least-bad pharmaceutical anchor. That's not nothing, but it's also not a solution.
It's a management strategy, not a cure. And I think one of the hardest things for patients in Marcus's position is accepting that distinction. The expectation after surgery is often that the problem is solved. When it's not, there's a grieving process — grieving the loss of normal digestive function, grieving the simplicity of just eating without thinking about it. And the medical system is not great at supporting that psychological piece.
That's a real thing. The loss of uncomplicated eating. You don't realize how much social life and daily pleasure is built around food until eating becomes a calculation every time.
Every meal becomes a negotiation. Should I take the ox bile? How much fat is in this? Will I pay for this later? Is this restaurant meal worth the evening of bloating? It's exhausting, and it's invisible to everyone around you.
Let me ask about one thing Marcus didn't mention but that I've seen in some of the literature — the role of soluble fiber. I've read that certain fibers can bind bile acids and might help with the between-meal bile pooling without the side effects of pharmaceutical sequestrants.
That's an under-explored area, but there's some interesting evidence. Soluble fiber — things like psyllium, oat beta-glucan, pectin — can bind bile acids in the intestinal lumen and increase their fecal excretion. It's a much gentler effect than cholestyramine, but it's also something you can incorporate into the diet regularly without adding another pill. A tablespoon of psyllium husk in water between meals could theoretically help mop up excess bile. The effect is modest, but it has almost no downside.
It's cheap.
It's cheap. The challenge is compliance and timing. You don't want to take it with meals because it can interfere with nutrient absorption, and you don't want to take it too close to medications. But as a between-meal or bedtime intervention, it's a low-risk addition to the toolkit.
If we're sketching a day for Marcus — and I want to be clear we're not giving medical advice, we're mapping out what a coherent strategy might look like based on the physiology — it's something like: smaller meals spread through the day, ox bile mid-meal or split across the meal for anything with significant fat, UDCA on whatever schedule his doctor prescribed, and maybe a fiber supplement between meals to bind excess bile during fasting windows.
I'd add one more element that's often overlooked: sleeping position. If you have bile reflux, elevating the head of the bed can make a meaningful difference. It's a mechanical intervention for a mechanical problem. Gravity is free and has no side effects.
The most underutilized therapeutic in medicine.
There's decent evidence for head-of-bed elevation in acid reflux, and the same physics applies to bile. If you're horizontal, there's no gravitational barrier to duodenal contents flowing back into the stomach and even the esophagus. Raise the head of the bed six to eight inches, and you create a slope that works in your favor all night.
I want to come back to something you mentioned earlier about the microbiome. If continuous bile exposure reshapes the gut bacterial community, is there any role for probiotics or dietary interventions that might push the microbiome back in a healthier direction?
The microbiome angle is fascinating but the evidence for specific interventions is still immature. We know that bile acids shape the gut microbiome and that the microbiome in turn modifies bile acids through deconjugation and dehydroxylation. It's a two-way street. In theory, certain probiotics might help by competing with bile-tolerant pathogens or by modifying bile acid metabolism. Some lactobacillus and bifidobacterium strains can deconjugate bile acids, potentially reducing their toxicity. But we're a long way from having a specific probiotic protocol for post-cholecystectomy patients.
It's plausible, but we're in "might help, probably won't hurt" territory.
And that's a frustrating phrase to hear when you're the patient, but it's honest. The microbiome field has generated enormous excitement and relatively few actionable clinical protocols. Post-cholecystectomy dysbiosis is a real phenomenon, but we don't yet know how to fix it reliably.
Let's talk about the gastroenterology visit itself. Marcus said he worked with a gastroenterologist but still feels no clearer on how to manage this. What should a productive GI consultation look like for this kind of problem?
A good gastroenterologist for post-cholecystectomy syndrome should be doing a few things. First, they should rule out structural problems that might be fixable — retained stones, sphincter of Oddi dysfunction, strictures. An MRCP or ERCP can visualize the biliary tree. Second, they should do an upper endoscopy to assess the severity and pattern of gastritis and to rule out other causes. Third, and this is where many fall short, they should have a systematic approach to medical management that goes beyond "try a PPI and see me in six months.
What does that systematic approach look like?
It should include a trial of UDCA if bile reflux gastritis is confirmed or strongly suspected. It should include dietary counseling — not just "avoid fatty foods" but specific guidance on meal timing, meal size, and fat distribution. It should address the possibility of bile acid diarrhea, which is a distinct post-cholecystectomy syndrome that responds to sequestrants. And it should include follow-up that assesses response to each intervention rather than just throwing everything at the wall at once.
One intervention at a time, so you know what's doing what.
If you start UDCA, ox bile, a PPI, and a probiotic all in the same month, and you feel better, you have no idea which one helped. If you feel worse, you don't know which one caused it. A methodical, sequential approach is tedious but essential.
That's probably the single most practical thing we've said so far. Don't change everything at once. You can't debug a system by flipping all the switches simultaneously.
That's a general principle that applies far beyond gastroenterology, but it's especially important here because the symptoms can fluctuate on their own. You might have a good week and attribute it to the new supplement you started, when actually it was just a random fluctuation. Without a systematic approach, you end up with a supplement graveyard full of things you're not sure ever worked.
The supplement graveyard. I feel like every chronic condition has one of those. A drawer full of bottles you bought in moments of desperate hope.
Post-cholecystectomy syndrome is particularly prone to it because the mainstream medical options are limited. Patients go looking for alternatives — digestive enzymes, herbal bitters, apple cider vinegar, activated charcoal, you name it. Some of these have mechanistic plausibility, some are harmless, some can actually make things worse. Apple cider vinegar, for example, adds acid to a stomach that's already being damaged by bile. That's not a great combination.
Activated charcoal I've seen touted for bloating. What's the actual story there?
Activated charcoal can bind gases and some toxins in the gut, which is why it's used in acute poisoning. For bloating, the theory is that it adsorbs gas-producing compounds. The problem is it's nonspecific — it'll bind your medications, your nutrients, anything else in the gut. Using it occasionally for acute bloating might make sense for some people, but daily use is a bad idea. You'd be slowly malnourishing yourself while also making your medications ineffective.
The supplement graveyard has landmines in it.
And this is why I get nervous when the conversation shifts entirely away from evidence-based medicine into the world of supplements. The regulatory framework isn't there. Quality control is inconsistent. Drug-supplement interactions are poorly studied. You can end up doing real harm while trying to help yourself.
Let's circle back to something fundamental. The gallbladder was removed for a reason. Presumably gallstones or biliary dyskinesia. Once it's out, you can't put it back. But are there any emerging approaches that try to restore the timing function? Not a new gallbladder, but something that mimics what the gallbladder did?
There's nothing in clinical practice yet, but there are some interesting research directions. One is neuromodulation — using electrical stimulation to influence the sphincter of Oddi or gastric motility. The idea would be to coordinate bile release with meals by artificially stimulating the right nerves. It's very early stage. Another is the development of bile acid formulations with modified release profiles — essentially a pill that releases bile acids gradually during digestion rather than dumping them all at once. That's closer to feasible, but nobody's brought it to market.
The gallbladder replacement — a bioengineered organ or a mechanical device — that's still science fiction?
It's been attempted in animal models. There are tissue engineering approaches that try to grow a new gallbladder-like structure from the patient's own cells. But the gallbladder turns out to be surprisingly complex. It's not just a bag. It concentrates bile by actively transporting water and electrolytes out. It has a muscular wall that contracts in a coordinated way. It receives neural and hormonal signals that time its emptying precisely. Replicating all of that is a much harder problem than building a passive reservoir.
For the foreseeable future, it's management, not restoration.
And that's the honest answer that Marcus probably didn't get from his gastroenterologist. The tools we have are imperfect and they require ongoing tinkering. Some people do find a regimen that works well enough that they can mostly stop thinking about it. Others never quite get there and have to continually adjust.
Which brings us back to the contradiction Marcus identified. The treatments fight each other. More bile for digestion, less bile damage in the stomach. Is there a way to have both? Or is it always going to be a trade-off?
I think the most honest answer is that it's a trade-off, but it's a manageable one if you think temporally. Ox bile during meals, when you need it. UDCA and possibly fiber between meals, to protect the stomach and mop up excess bile. The interventions don't have to conflict if they're separated by time. The gallbladder's job was temporal. The management strategy has to be temporal too.
Time-separated pharmacology. It's so obvious when you say it, but it's not how most people think about supplements. We think about what to take, not when to take it relative to meals and to each other.
To be fair, most medication instructions are written around convenience and compliance, not around mimicking lost physiological timing. The idea that you might need different things at different points in the digestive cycle isn't built into how we prescribe.
Part of what Marcus might need is a more sophisticated timing protocol. Not just what to take, but a schedule that respects the fed-fast cycle.
And I'd add that keeping a symptom and meal diary for a few weeks can be revelatory. You might discover that your bloating is worst at a particular time of day, or that certain foods are reliably problematic in ways you hadn't noticed. That data lets you tailor the timing. Maybe you need more ox bile at dinner but not at breakfast. Maybe you need a fiber supplement before bed but not during the day. The pattern is individual, and finding it requires systematic observation.
The quantified self meets gastroenterology.
And there are now apps that make this easier — track meals, symptoms, bowel habits, supplement timing. Some people find patterns they'd never have noticed otherwise. A patient once told me she discovered through tracking that her bloating was always worst about three hours after her largest meal, which happened to be lunch. She shifted her largest meal to an early dinner instead, and the bloating moved to a time when she was at home rather than at work. Same physiology, completely different quality of life impact.
That's a brilliant reframe. You can't always eliminate the symptom, but you might be able to shift it to a less disruptive time window.
And that's another thing gastroenterologists rarely discuss. The goal doesn't have to be zero symptoms. The goal can be symptoms that don't interfere with your life. That's a more achievable target for a lot of people.
Which is a healthier psychological frame anyway. Chasing perfection with a chronic condition is a recipe for frustration.
And I think Marcus's frustration comes through clearly in his prompt. He's been at this for seven years. He's tried things. He's worked with a specialist. And he still feels like he's choosing which problem to have on any given day. That's exhausting.
Let's give him something concrete. If you were sitting down with a patient in Marcus's position — seven years post-cholecystectomy, tried the basics, still struggling — what's your stepwise plan?
Step one, stop everything except what's clearly essential. Do a washout for two weeks if possible, with a symptom diary. You need a clean baseline. Step two, reintroduce one intervention at a time, starting with the one most likely to address the dominant symptom. If gastritis is the worst problem, start with UDCA. If fat digestion is the worst, start with ox bile. Give each intervention two to three weeks before adding the next. Step three, once you know what each thing does individually, experiment with timing — ox bile mid-meal versus before, UDCA at bedtime versus morning, fiber between meals versus at bedtime. Step four, only after you've optimized the timing of the core interventions, consider adding secondary things like a prokinetic or a sequestrant if there's still a gap.
It's tedious, but it's a few weeks of tedium for potentially years of benefit. The alternative is another seven years of guessing.
That's the thing about chronic condition management that nobody tells you. The work is front-loaded. You do the annoying systematic stuff up front, and then you can mostly coast. But if you skip that step, you're tinkering forever.
The medical system doesn't incentivize that front-loaded work. A gastroenterologist gets paid for a fifteen-minute follow-up visit, not for helping you design and interpret a four-week n-of-one trial. The economics push toward quick prescriptions and vague advice, not toward the kind of systematic approach that actually solves the problem.
Patients have to become their own project managers. Which is a lot to ask of someone who's already dealing with daily symptoms.
And that's why peer support communities can be so valuable. There are forums and patient groups where people share what worked for them, what didn't, what questions to ask your doctor. The collective wisdom of thousands of patients who've been through the same thing can sometimes be more practically useful than a single specialist who spends ten minutes with you.
The wisdom of the post-cholecystectomy hive mind.
Not a phrase I expected to say on this show, but yes.
One last thing I want to touch on — and this might seem obvious, but I think it's worth saying explicitly. Marcus mentioned he's seven years out. Is it possible that some of what he's experiencing isn't directly from the surgery anymore, but is a new normal that his body has settled into? And if so, does that change the approach?
That's a really important question. Seven years is a long time. The body does adapt — the bile duct dilates somewhat to partially compensate for the lost storage capacity, the enterohepatic circulation establishes a new rhythm, the microbiome reaches a new equilibrium. But adaptation isn't the same as normalization. Some people adapt well and are largely asymptomatic. Others adapt poorly and have persistent symptoms indefinitely. The fact that Marcus is still struggling suggests his adaptation was in the second category.
It's not that his body hasn't had time. It's that the adaptation it found isn't working well for him.
And that means the goal isn't to wait for more adaptation. It's to actively reshape the system with the tools we've discussed. The body found a maladaptive equilibrium. The job of management is to push it toward a better one.
Which circles back to the systematic approach. You're not just managing symptoms. You're trying to nudge the whole system into a different steady state.
And that's why the shotgun approach of starting everything at once doesn't work. You can't nudge a complex system effectively if you're pushing on all the levers simultaneously and you don't know which lever does what.
Alright, let's land this plane. If Marcus takes one thing away from this conversation, what should it be?
I'd say it's this: the contradiction he's identified between his treatments is real, but it's resolvable through timing. The gallbladder's job was to separate bile delivery into fed and fasted states. His management strategy can do the same thing. Support digestion during meals with ox bile. Protect the stomach between meals with UDCA, fiber, and mechanical interventions like head-of-bed elevation. And figure out his individual pattern through systematic observation rather than guesswork.
The gastroenterologist who left him feeling unclear — maybe it's worth a second opinion from someone who specializes in motility disorders or post-surgical syndromes. Not all GIs are equally equipped for this.
If your gastroenterologist's entire toolkit for post-cholecystectomy syndrome is PPIs and a shrug, find someone who thinks about biliary motility. They're just not the majority.
Time-separated pharmacology, systematic reintroduction, and finding a GI who actually thinks about the biliary system as a dynamic thing rather than a static plumbing problem. That's a better framework than "pick which problem to have today.
I think that's what Marcus was really asking for. Not a magic bullet, because there isn't one. But a coherent framework that acknowledges the contradiction and offers a way to navigate it rather than just living with it.
Now: Hilbert's daily fun fact.
Hilbert: In the 1840s, the British explorer Robert Schomburgk observed that the rainbows visible at Kaieteur Falls in Guyana often appear as complete circles rather than arcs. This occurs because the immense spray plume from the seven-hundred-forty-one-foot drop creates a water droplet field large enough for the full circular optical phenomenon to form, with the observer's shadow sometimes visible at the circle's center.
A full circle rainbow. That's actually kind of beautiful.
This has been My Weird Prompts. Thanks to Marcus Jakes for sending in such a thoughtful, honest prompt. These are the kinds of questions that don't get enough attention in medicine — the chronic, messy, trade-off-laden problems that don't have a clean solution.
If you want to send us your own weird prompt, you can find us at myweirdprompts.And if you enjoyed this episode, leave us a review wherever you listen. It helps other people find the show.
We're produced by the indefatigable Hilbert Flumingtop. I'm Herman Poppleberry.
I'm Corn. We'll be back soon.
