Episode 25: The Great GERD Mistake - How Medicine Made Heartburn Worse and How to Fix It

Episode 25: The Great GERD Mistake - How Medicine Made Heartburn Worse and How to Fix It

Heartburn is not too much acid. It is acid in the wrong place.
In this episode of The Dr. Kumar Discovery Podcast, Dr. Ravi Kumar explains what GERD really is, why medicine got it backward, and how to end reflux by fixing the barrier, the pressure, and the timing that keep acid where it belongs. You will learn when acid suppression is appropriate, how to taper safely if you are a candidate, and how to restore normal digestion without wrecking physiology.


Episode Highlights

  • GERD Reframed - why reflux is a mechanical problem, not an acid problem
  • Your Anti Reflux Barrier - how the lower esophageal sphincter and diaphragm work together
  • The Rebound Loop - hypergastrinemia and why PPIs create dependence when stopped abruptly
  • Real World Triggers - large meals, late eating, tight clothing, alcohol, nicotine, simple sugars, high fat meals, tea and theophylline
  • Hiatal Hernia and TLESR - how anatomy and reflexes increase reflux events
  • The GERD Reset - a two to four week plan to reduce abdominal pressure and improve clearance
  • Stepwise Taper - transitioning from PPIs to H2 blockers and off, with tools for breakthrough symptoms
  • When to Stay on Acid Suppression - Barrett’s esophagus, erosive esophagitis, ulcers, chronic NSAID use, large hernias

Show Notes

The Physiology of Reflux

GERD happens when stomach acid escapes into the esophagus, a tissue not built for acid. The stomach is designed for a pH near 1 to 2 and is protected by mucus and bicarbonate. The esophagus is not. The goal is not to shut off acid, it is to keep acid in the stomach.

Why Medicine Got GERD Backward

Acid in the esophagus led to the conclusion that there was too much acid. In reality the barrier failed. Long term acid suppression lowers symptoms but drives gastrin up, builds more proton pumps, and sets up rebound when the drug is stopped. This is why many people feel worse when they try to come off a PPI.

What Really Triggers Reflux

Three variables control reflux: barrier, pressure, and time. Large meals and late eating distend the stomach and relax the sphincter. Tight waistbands, central obesity, and heavy exertion after meals increase abdominal pressure. Alcohol, nicotine, chocolate, mint, onions, high fat meals, simple sugars, and tea can lower sphincter tone or slow emptying. Certain drugs such as calcium channel blockers, nitrates, benzodiazepines, opioids, and anticholinergics can worsen reflux.

The Two to Four Week GERD Reset

Finish dinner at least three hours before bed. Eat smaller evening meals. Reduce abdominal pressure with modest weight loss if needed. Avoid alcohol and nicotine during the reset. Loosen tight clothing, walk 10 to 30 minutes after meals, chew gum to boost saliva, elevate the head of your bed by six inches, and sleep on your left side.

Stepwise Taper Off Acid Suppressors

If you are a candidate to taper, first take your PPI 30 to 60 minutes before breakfast for two weeks to align timing. Then switch to an H2 blocker such as famotidine twice daily for one month, once daily for one month, then taper to half dose for one month, then quarter dose for one month. Expect temporary rebound. Use simple buffers such as half a teaspoon of baking soda in water as needed. Fennel seed after meals can aid motility. Work with your physician if you have complex disease.

When to Keep Acid Suppression

Continue or resume acid suppression and work with your doctor if you have Barrett’s esophagus, erosive esophagitis, active ulcer disease, chronic NSAID use, post surgical anatomy, or a large hiatal hernia.

Safety and When to Seek Care

Urgent care is appropriate for trouble swallowing, unintentional weight loss, vomiting blood, black stools, persistent vomiting, chest pain that could be cardiac, or symptoms that do not improve with a responsible trial.


Listen on your favorite platform:

Apple Podcasts → https://podcasts.apple.com/us/podcast/the-dr-kumar-discovery/id1808415094
Spotify → https://open.spotify.com/show/3UJhg3Y5jjLP8zO6hbpwfT

Explore more episodes and references:

https://drkumardiscovery.com/podcast/

Transcript

[00:00 –> 00:20] On this episode of Doctor. Kumar discovery. In The United States, about one in four adults experiences GERD at least once a week. It’s incredibly common, but also one of the most misunderstood and mistreated conditions in medicine. At the heart of the problem is a misunderstanding that spread through modern medicine.

[00:20 –> 00:48] The myth that GERD is caused by too much acid in the stomach. So even if you’re eating a perfect diet, you can still become malnourished if you don’t have enough acid in your stomach. Studies suggest that thirty to forty percent of people on PPIs today have no ongoing medical indication for them. Most stay on them because every time they try to stop, the reflux flares up worse than before. My message here isn’t anti medicine, it’s pro physiology.

[00:48 –> 00:59] It’s about understanding how your body is designed to work and helping it return to its natural rhythms. By the end, you’ll understand GERD better than most doctors do, What causes it, the key risk factors,

[00:59 –> 01:21] and how to fix it without wrecking your physiology. My name is Doctor. Ravi Kumar. I’m a neurosurgeon in search of the causes of human illness and the solutions that help us heal and thrive. I want you to join me on a journey of discovery as I turn over every stone in search of the roots of disease and the mysteries of our resilience.

[01:21 –> 01:36] The human body is a mysterious and miraculous machine with an amazing ability to self heal. Let us question everything and discover our true potentials. Welcome to the doctor Kumar discovery.

[01:37 –> 02:07] Welcome to the doctor Kumar discovery podcast. I’m doctor Ravi Kumar, a board certified neurosurgeon and assistant professor at UNC. Today, we’re talking about one of the most common problems in human health, gastroesophageal reflux disease or GERD, also sometimes called heartburn or indigestion. The symptoms of GERD happen when acid from the stomach rises into the very sensitive and unprotected esophagus, causing pain and discomfort. This is a disease that affects more than a billion people worldwide.

[02:07 –> 02:42] In The United States, about one in four adults experiences GERD at least once a week. It’s incredibly common, but also one of the most misunderstood and mistreated conditions in medicine. And it’s been exploited by the pharmaceutical industry, often misunderstood by doctors, and the very medications designed to treat it can also create dependency. In this episode, I’ll break it all down. By the end, you’ll understand GERD better than most doctors do, what causes it, the key risk factors, and how to fix it without wrecking your physiology.

[02:42 –> 03:02] If you’re already treating GERD with medication, I’ll explain to you who actually needs to do this. And if you’re one of the many people who don’t need acid suppression, I’ll explain how you can safely taper off. You’ll get a clear road map for restoring healthy stomach function and normal gastric rhythms. Okay. So before we dive in, I wanna give you a quick disclaimer.

[03:02 –> 03:26] I’m a medical doctor, but I’m not your doctor. This show is for informational purposes only. It’s not meant to diagnose or treat any condition. My goal is to give you the clearest, most unbiased, and most understandable information possible so you can use it to empower yourself and work more effectively with your own health care provider. And I also wanna mention that this show is completely separate from my role as assistant professor at UNC.

[03:26 –> 03:42] Now one more thing before we start. I need your help growing the show. This is episode 25, and it’s going great. We’ve got over 900 subscribers and tons of positive feedback. But all that has been organic with almost no help from the algorithms.

[03:42 –> 03:59] I’m talking about Apple Podcasts, Spotify, YouTube. To reach more people, I need the algorithms on our side. The best way you can help is by leaving a review, especially on Apple Podcasts. Just open the app, listen to an episode, and leave a star rating. And if you can, write a short review.

[03:59 –> 04:21] That’s all I’ll ever ask from you, and I’d be deeply grateful if you can do that for me. Honestly, the only thing separating the doctor Kumar discovery from the Huberman Lab Podcast right now is about 47,000 reviews. It’s you guys, the listeners, that truly tell the world and the algorithms which shows are worth listening to. If you like what I’m putting out here, please help me get it out to more people. Okay.

[04:21 –> 04:40] Let’s get back into the episode and start with some basics. GERD stands for gastroesophageal reflux disease. Gastro means stomach, and esophageal means your esophagus. So it literally describes acid from the stomach refluxing up into the esophagus where it doesn’t belong. You see, the stomach is built for acid.

[04:40 –> 05:09] It runs at a pH of one or two, which is roughly the same pH as battery acid. It’s protected by a thick mucus layer that doesn’t let the acid touch the living tissue underneath it. That acidity is essential for breaking down proteins in the food you eat, releasing vitamins, and starting the process of digestion. The esophagus, on the other hand, is not built for acid at all. Its only job is to transport food from your mouth to your stomach through a coordinated squeezing motion called peristalsis.

[05:09 –> 05:39] It has tons of sensory nerves but very little mucus protection. So when acid escapes up into the esophagus, it burns, and that searing burn is what people describe as heartburn or indigestion. Now indigestion can sometimes come from other conditions like gastritis or stomach ulcers, but by far the most common cause of heartburn and indigestion is GERD. And the key thing to understand is that acid isn’t the real problem here. The problem is one of abnormal movement.

[05:39 –> 06:02] Acid should never leave the stomach in the first place. It’s supposed to stay down in the acidic chamber where it can do its job safely. And the body has a simple mechanism to make sure of that. There’s a circular muscle at the bottom of your esophagus called the lower esophageal sphincter. And as the esophagus passes through the diaphragm, there’s another supportive ring of muscle called the diaphragmatic hiatus.

[06:02 –> 06:25] Together, they act like a valve that keeps acid in the stomach where it belongs. When that barrier weakens or slips, acid can move upward against gravity, and that’s when the damage starts. So GERD isn’t a problem of too much acid. It’s a problem of a faulty barrier between the esophagus and the stomach. And that’s a key point we’ll keep coming back to throughout this episode.

[06:25 –> 06:44] To really pull this all together, let me tell you a personal story. When I started medical school, life was pure stress. I was studying nonstop, living under constant pressure and trying to absorb a fire hose of information every single day. One afternoon, out of nowhere, I felt this crushing chest pain. It was miserable.

[06:44 –> 06:54] I honestly thought, that’s it. I’m having a heart attack. I’m not even gonna finish medical school. I told my wife, and she just looked at me and said, you’re not having a heart attack. Just go see your doctor.

[06:54 –> 07:04] So I did, and my doctor took one look at me and said, you’re having heartburn. It’s GERD. I said, really? Because it feels like a heart attack. He didn’t even wanna do an EKG.

[07:04 –> 07:24] He just handed me a note for omeprazole, a proton pump inhibitor that shuts down acid production in the stomach, and said, take this for two weeks. You’ll feel better. So I went to the store, bought a box right off the shelf, by then it was already sold over the counter, and started taking it. By the next day, I felt completely normal. No chest pain.

[07:24 –> 07:37] I thought, thank god. This drug is a miracle. But when I stopped taking it two weeks later, the pain came roaring back. I called my doctor, and he said, do another two week course. So I did.

[07:37 –> 07:55] Same thing. Relief, then rebound of my chest pain as soon as I stopped. Eventually, I just started taking it every day like a vitamin. If I skipped it, the chest pain came right back. Fast forward eight years, I was deep into my neurosurgery residency and completely dependent on that little purple pill.

[07:55 –> 08:17] At some point, I just thought, this can’t be normal. I can’t live the rest of my life with my stomach churned off. That’s when I decided to dig into the physiology, understand what was really happening, and figure out how to fix it. Over about four to six months, I built a plan, followed it, and finally got off the proton pump inhibitor. It wasn’t easy, but it was worth it.

[08:18 –> 08:38] I was free, and my stomach was working again. And later in this episode, I’m gonna share exactly how I did it. Because if you’re dependent on acid suppressing medication, this could be your way out too. So how did we end up here anyway? How did myself and millions of others end up stuck on a drug that churns off one of the body’s most vital functions?

[08:38 –> 09:07] Well, at the heart of the problem is a misunderstanding that’s spread through modern medicine, the myth that GERD is caused by too much acid in the stomach. That idea is completely backwards. It’s one of those convenient oversimplifications that medicine loves to embrace because it’s easy to explain, easy to medicate, and completely misses the root cause. Medicine often uses reductionist logic. We see one piece of the puzzle and build a whole treatment philosophy around it.

[09:07 –> 09:25] Take cholesterol for example. LDL cholesterol is essential for life. Your hormones, your vitamin d, your cell membranes, even your brain function all depend on it. Without LDL, you die. Yet when scientists first saw cholesterol in arterial plaques, they assumed it must be the villain causing heart disease.

[09:25 –> 09:48] So the response was to drive LDL as low as possible with statins and PSK nine inhibitors. The problem is we were targeting an innocent bystander instead of fixing the real root cause of vascular injury. That same flawed logic applies to GERD. Acid refluxes up into the esophagus, so the conclusion becomes you make too much acid. But acid is not the enemy.

[09:48 –> 10:11] It’s the foundation of digestion, actually. You need acid to digest proteins, free up micronutrients, and kill pathogens before they can infect you. Without it, you can’t absorb magnesium, calcium, iron, or vitamin b twelve properly. You’re left nutrient deficient and more susceptible to infection without acid in your stomach. Think of your stomach as a power tool, and stomach acid is the battery.

[10:11 –> 10:37] Without the battery, it can’t do its job. The stomach tries to maintain your vitality with one hand tied behind its back when it can’t make acid. Instead of asking, how do we stop the acid? We should be asking, how do we fix the barrier that keeps acid where it belongs? If the valve between the stomach and the esophagus works properly, you can have all the acid you need in your stomach for digestion without burning your esophagus.

[10:37 –> 11:02] Now let’s talk about how the system actually works. The stomach lining is made up of specialized cells, each with a role in this chemical symphony. Parietal cells are the acid producers. They contain hydrogen potassium ATPase pumps, often called proton pumps, that move hydrogen into the stomach in exchange for potassium. When hydrogen combines with chloride, you get hydrochloric acid, the main acid in your stomach.

[11:02 –> 11:29] Those same parietal cells also make intrinsic factor, a protein that binds to vitamin b twelve and allows it to be absorbed further down in the intestines. Without intrinsic factor, you can’t absorb b twelve at all. That’s why older adults often need b twelve injections because the stomach simply stops making enough intrinsic factor. Next, there are chief cells. They release pepsinogen, an inactive enzyme that turns into pepsin when it encounters acid.

[11:29 –> 11:54] Pepsin then breaks down proteins, opening them up so acid can denature them further and release nutrients like B vitamins and minerals. Without acid, pepsinogen never activates, so protein digestion slows significantly. Then there are g cells, which secrete gastrin. Gastrin tells the parietal cells to ramp up acid production, especially when you eat. It also signals the stomach tissue to grow and maintain itself.

[11:55 –> 12:23] When acid levels drop, gastrin rises, a feedback loop designed to keep things completely balanced. There’s another group called enterochromaffin like cells that release histamine, which also stimulates parietal cells to make acid. That’s why over the counter h two blockers like famotidine or cimetidine work. They block histamine’s ability to trigger acid production. And finally, mucus and bicarbonate secreting cells form protective coatings that keep the stomach from digesting itself.

[12:23 –> 12:57] Bicarbonate acts like built in baking soda, neutralizing acid right at the cell surface so the tissue underneath stays unharmed, and mucus forms a physical barrier between the acid and the stomach wall. Now when you take a proton pump inhibitor, like omeprazole or panprotozole, it blocks the proton pumps in your stomach. Acid production drops and gastrin levels surge to compensate. And it’s important to realize here that when you block your acid production, digestion weakens across the board. Proteins stay partially broken down, minerals remain bound, and pathogens survive.

[12:57 –> 13:24] Iron can’t convert from ferric to ferrous form for absorption, and calcium, magnesium, and zinc don’t dissolve properly. So even if you’re eating a perfect diet, you can still become malnourished if you don’t have enough acid in your stomach. So that’s why the stomach’s acidity is so essential to optimal human biology. Okay. Now that we understand why stomach acid is essential, let’s talk about why it sometimes escapes into the esophagus in the first place.

[13:24 –> 13:43] To get this, we need to understand a little anatomy. The junction between the esophagus and the stomach is called the gastroesophageal junction. Around the esophagus at that junction is a ring of smooth muscle called the lower esophageal sphincter. Think of it as a valve. It opens to let food drop into the stomach and then closes tightly to keep acid from coming back up.

[13:44 –> 14:20] As the diaphragm travels from the throat down into the chest and through the diaphragm, it passes through a small opening in the diaphragm called the hiatus. The diaphragm itself has a loop of muscle called the cruel diaphragm, and this structure wraps around the esophagus at the level of the lower esophageal sphincter. These two structures, the lower esophageal sphincter and the cruel diaphragm, work together. When they’re properly aligned and coordinated, they seal the stomach off from the esophagus. When you swallow, the valve briefly relaxes to let food pass, then snaps shut again.

[14:20 –> 14:50] But if either of those closing mechanisms weakens or falls out of alignment, acid can escape upwards. So here’s where the physics come in. Your abdomen is a high pressure zone, while your chest is a low pressure zone. That pressure difference is what allows your lungs to expand and draw air in. But it also means that anything increasing abdominal pressure, like eating a large meal, bending forward, lying down after dinner, gaining weight around your midsection, or doing heavy lifting, can push the stomach contents upward.

[14:50 –> 15:23] Normally, the lower esophageal sphincter in the diaphragm can resist that pressure. But if you build up too much pressure, or if the alignment between the diaphragm and the lower esophageal sphincter slips, the seal weakens. Acid then washes up into the esophagus, which has very little protection, and you feel that sharp burning pain. In many people, this alignment problem between the lower esophageal sphincter and the diaphragm leads to something called a hiatal hernia. That’s when part of the stomach actually slides up through the diaphragm into the chest cavity.

[15:23 –> 15:53] When that happens, the cruel diaphragm and the lower esophageal sphincter are no longer working together. They’re out of sync. The diaphragm can’t reinforce the sphincter the way it should, and the result is a weak, leaky barrier. When acid sits higher in the chest, it can irritate nerves that cause symptoms that mimic other conditions, chest pain, cough, even asthma like wheezing. I felt that same crushing chest pain back in medical school and thought it was a heart attack, but it was really acid in my esophagus in my chest.

[15:53 –> 16:27] Even if you don’t have a hiatal hernia, there’s another mechanism at play called transient lower esophageal sphincter relaxation or TLESR. This is when the sphincter relaxes briefly to let gas escape after eating or to allow vomiting when needed. It’s a normal reflex, but in some people, it happens too often or too easily, especially after large or fatty meals that distend the stomach. Each time that valve relaxes, acid can surge upwards. So when you think about reflux mechanically, it comes down to three variables, barrier, pressure, and time.

[16:28 –> 17:01] The barrier is the strength and alignment of that sphincter diaphragm pair. The pressure is how much force the abdomen is pushing upwards with, and the time is how long acid stays in the esophagus before it clears. If the barrier weakens, the pressure rises, and the acid lingers longer, you’ve got a perfect storm for GERD. Over time, chronic acid exposure inflames the esophagus leading to erosive esophagitis. If it continues, the esophagus can even start changing its own cell lining to intestinal type tissue, a process called Barrett’s esophagus.

[17:01 –> 17:26] That’s the body’s desperate attempt to adapt to the constant acid exposure. And Barrett’s esophagus is a precancerous condition that can progress to esophageal adenocarcinoma, which is one of the most aggressive cancers we know. So fixing reflux isn’t just about comfort or getting rid of heartburn. It’s about preventing long term structural and even cellular damage. Now let’s talk about the biggest lifestyle factors that drive gastroesophageal reflux disease.

[17:26 –> 17:53] Remember, GERD, as we just talked about, is a problem of three things. The barrier between the esophagus and the stomach, the pressure pushing upward from the abdomen, and the time that acid sits in the esophagus. The more those three are disrupted, the worse the reflux. The first and most powerful trigger is eating large meals. When you overload the stomach, it stretches the upper part called the fundus, and that distension triggers relaxation of the lower esophageal sphincter.

[17:53 –> 18:18] In lab experiments, simply inflating a balloon inside the stomach is enough to trigger reflux events. The stomach just gets overwhelmed and vents pressure upward. Another major trigger is late night eating. If you lie down soon after dinner, gravity stops helping you keep acid down. Studies using wireless pH capsules show that eating within three hours of bedtime dramatically increases nighttime acid exposure.

[18:18 –> 18:41] So one of the simplest fixes for reflux is to stop eating late. Abdominal pressure is another major contributor. Tight waistbands, belts, tight clothes, or central obesity all squeeze the stomach just like that balloon experiment we talked about. Even in healthy volunteers, researchers have shown that wearing a tight belt after eating can provoke reflux. Exercise right after a meal does the same thing.

[18:42 –> 19:01] Lifting weights or straining increases abdominal pressure through what’s called the Valsalva maneuver. Waiting a bit between eating and training can make a big difference. Now let’s talk about chemical triggers. Foods and drinks that relax the lower esophageal sphincter or irritate the esophagus. Two of the biggest culprits are chocolate and mint.

[19:01 –> 19:29] Both contain natural compounds that relax smooth muscle, including the sphincter at the bottom of your esophagus. Manometry studies, which measure pressure along the esophagus, show that chocolate and peppermint oil significantly reduce lower esophageal sphincter pressure. High fat meals are another common culprit. Fat slows gastric emptying and triggers transient sphincter relaxations. Clinical studies show more reflux episodes after high fat meals compared to low fat ones.

[19:29 –> 19:46] Tea and coffee are often blamed because of caffeine, but caffeine isn’t the only factor. I actually discovered that tea triggered my reflux way more than coffee. Tea contains theophylline, a compound that relaxes smooth muscle and lowers sphincter pressure. Coffee doesn’t. So if you’re cutting back, think beyond caffeine.

[19:47 –> 20:06] Theophylline and tea may be the hidden issue. Alcohol is a double hit. It relaxes the lower esophageal sphincter and slows stomach emptying. Beer and white wine have both been shown to trigger reflux even in healthy volunteers. On top of that, alcohol directly irritates the esophagus, making even mild reflux feel worse.

[20:07 –> 20:33] Other frequent offenders include onions, garlic, spicy foods. In one study, raw onions significantly increased acid exposure and symptom scores in people with reflux. For me personally, garlic is a guaranteed trigger. I still eat garlic, but I’m judicious, and I try to eat it earlier in the day. Carbonated beverages are another common trigger because the dissolved gas expands in your stomach and distends it, again triggering relaxation of the sphincter.

[20:33 –> 20:59] Cutting soda, sparkling water, or beer often helps people more than they expect. And a lesser known but very real trigger is simple carbohydrates and sugars. A 2022 randomized controlled trial showed that reducing processed carbs and sugars decreased acid exposure in obese adults with GERD. The likely reason, less fermentation and gas buildup in the gut, which means less pressure pushing up. If you smoke or use nicotine, that’s another big one.

[20:59 –> 21:23] Nicotine directly relaxes the sphincter and slows acid clearance from the esophagus. In controlled studies, even nicotine patches reduce sphincter pressure by up to 40%. Combine alcohol and nicotine, and you have a perfect storm. Your stomach doesn’t empty, your sphincter relaxes, and acid lingers longer in the esophagus. There’s also a group of prescription medications that can worsen reflux by lowering sphincter tone.

[21:23 –> 21:57] Calcium channel blockers such as nifedipine, diltiazem, and verapamil reduce sphincter pressure by about 25 to 30%. Nitrates, often used for angina, can drop it by a third within minutes. Benzodiazepines like Valium, Ativan, and Xanax relax smooth muscle and slow acid clearance. Opioids slow the entire digestive tract so the stomach doesn’t empty, and beta two agonists like albuterol and theophylline do the same thing. And then there’s also direct irritants, medications that can physically damage the esophagus if they get stuck on the way down.

[21:57 –> 22:19] These include NSAIDs, iron tablets, tetracycline, and bisphosphonates. Always take these with a full glass of water so they reach the stomach quickly. Now before you start eliminating everything I just mentioned, remember, everyone’s chemistry is different. Some people can eat chocolate or drink tea without a problem. Others might react strongly to one specific food that isn’t even on this list.

[22:19 –> 22:49] These are starting points, not commandments. The goal is to find your triggers through awareness and experimentation, not all out restriction. So now that we’ve talked about the risk factors that lead to GERD, it’s a good time to talk about how modern medicine actually treats it and how the treatment often becomes the problem itself. The go to solution for GERD has always been acid suppression, and the darling of the medical community is proton pump inhibitors or PPIs. These drugs block your stomach’s ability to produce acid.

[22:49 –> 23:17] They were originally prescription only, but in the early two thousands, they went over the counter. Suddenly, anyone could walk into a pharmacy and buy a fourteen day course and keep buying it again and again, just like I did. Once that happened, PPI use exploded. At certain points, over fifteen million Americans were taking prescription PPIs every month, not counting over the counter versions. They became some of the most prescribed and most profitable drugs on earth.

[23:17 –> 23:39] And that’s worth pausing on. One of the most prescribed drugs in human history is a medication that shuts off acid production, acid that’s essential for digestion, nutrient absorption, and immune defense. Now in fairness, PPIs were revolutionary when they came out. For ulcers or bleeding in the stomach, they were lifesaving. But once they hit the pharmacy shelves, their use got out of control.

[23:39 –> 24:04] Studies suggest that thirty to forty percent of people on PPIs today have no ongoing medical indication for them. Most stay on them because every time they try to stop, the reflux flares up worse than before. That rebound makes it feel like you have a permanent disease, but it’s really a biological backlash to being on the medication for so long. Here’s what happens. When you block acid production, your stomach doesn’t just give up.

[24:04 –> 24:28] It tries harder. The hormone gastrin, the one that tells your stomach to make acid, rises dramatically, screaming at your parietal cells to produce more acid. But those cells can’t win because the pumps are chemically blocked by the PPI. So the stomach starts building more acid producing machinery, waiting for the block to lift. When you finally stop the medication, all that machinery switches on at once.

[24:28 –> 24:51] The result is a flood of acid and a surge in heartburn that’s worse than when you started. That’s why coming off a PPI after years of use feels like releasing a coiled spring that’s been held down too long. Your stomach rebounds with full force. That’s how these drugs become physiologically addictive. One story that really stuck with me was during my third year of medical school during my gastroenterology rotation.

[24:51 –> 25:12] I’d already been on a PPI for two years at this point. I was in the Endoscopy Suite watching an upper endoscopy. That’s where the gastroenterologist puts a scope through the mouth down into the stomach to get a good view of what’s going on there. And on the monitor, I saw a stomach that looked like a field of waving seagrass. Long, smooth polyps covering the entire lining of the stomach.

[25:12 –> 25:27] I froze thinking, oh no, This patient has stomach cancer. The gastroenterologist saw the look on my face and smiled. He said, nope. This is a PPI stomach. He explained that these were fundic gland polyps, totally benign, caused by long term PPI use.

[25:27 –> 25:40] This patient had been on omeprazole for years. I remember thinking, wait a second. I’m on omeprazole too. Here’s what was happening inside the patient’s stomach and probably mine. The PPIs had shut off the proton pumps, which dropped acid levels.

[25:41 –> 25:58] In response, gastrin went up, telling the stomach to make more acid. Since it couldn’t, it built more and more acid making tissue. The result was hypertrophy, a thickened, overgrown stomach lining full of benign polyps. Those polyps usually shrink once you stop the medication. But here’s the paradox.

[25:58 –> 26:25] The same rebound surge that helps them regress is the same surge that sends patients running right back to their PPIs. And the long term consequences of being on a proton pump inhibitor are real. Chronic acid suppression can cause protein malnutrition, b twelve deficiency, iron and magnesium deficiencies, low calcium and zinc levels. It increases the risk for bone fractures and kidney inflammation called acute interstitial nephritis. It raises susceptibility to infections like C.

[26:25 –> 26:38] Diff and campylobacter because the acid that normally kills those pathogens is gone. So the stomach, this powerful chemical gatekeeper, is left handicapped. It can’t digest. It can’t protect. It can’t do its job.

[26:38 –> 26:57] And that’s why in so many people, GERD and its pharmaceutical treatment become a problem that hurts the body systemically. So are you one of these people? Do you find yourself constantly dealing with reflux, or are you now dependent on acid suppressing medication? I was, and guess what? I got off it completely.

[26:57 –> 27:27] This is the part of the episode where I’m gonna show you how. I’ll tell you exactly what I did, what the research supports, and how you can restore normal acid production, normal gastric rhythms, and a healthy digestive flow. The first phase is what I call a two to four week reset. Anyone can start with this, whether you get mild heartburn or you’ve been diagnosed with erosive esophagitis or even Barrett’s esophagus. These steps are low risk, evidence based, and they target the root mechanics of reflux, pressure, barrier, and time.

[27:28 –> 27:48] Start by working on reducing abdominal pressure. Even a small amount of weight loss, around five to 10%, can dramatically reduce reflux episodes. Less fat around the midsection means less pressure pushing upward on that valve that separates the stomach from the esophagus. It doesn’t take much to make a big, big difference. Then look at when you’re eating.

[27:48 –> 28:04] Try to finish dinner at least three hours before bed and avoid those late night snacks. Gravity is your friend here. You want that time upright so food can move through and the stomach can empty. Also, make your evening meal lighter. Large dinners stretch the stomach and directly trigger reflux.

[28:04 –> 28:22] So eat early and eat light. Also, take a break from alcohol and nicotine during this reset. Alcohol is a double hit. It relaxes the valve and slows stomach emptying, especially beer and wine. If you drink daily or heavily, taper safely or talk with your doctor first since stopping suddenly can sometimes be dangerous.

[28:22 –> 28:39] But for most people, simply cutting alcohol for a few weeks makes a big difference. And nicotine is another major trigger. It relaxes the same lower esophageal sphincter by up to 40%. Quitting even temporarily helps your stomach reset its normal tone. Next, loosen your belt.

[28:39 –> 29:02] Avoid tight waistbands, skin tight clothes, shapewear, or anything that squeezes your midsection, especially after meals. When it comes to sleep, elevate the head of your bed by about six inches using wooden blocks under the head of your bed frame. Pillows alone don’t work. You have to elevate the head of the bed. That small inclination uses gravity to keep acid in the stomach and moving downward where it belongs.

[29:02 –> 29:27] And if you can, sleep on your left side too. The entrance to the esophagus sits on the upper right side of the stomach, so lying on your left side keeps the acid pool below the valve. Research shows that left sided sleeping can reduce nighttime reflux by as much as 70%. Another thing you can do is after meals, chew gum for about a half an hour. Chewing increases saliva, and every time you swallow, that saliva flushes acid out of the esophagus.

[29:27 –> 29:46] It also tells your stomach to empty downward and naturally buffers the leftover acid. And then take a gentle walk. Ten to thirty minutes is enough. That light movement activates digestion, improves stomach emptying, and drastically reduces reflux compared to lying down or sitting still. So let’s bring it all together.

[29:46 –> 30:00] Reduce abdominal pressure by losing a little weight. Finish dinner early and keep it light. Take a break from alcohol and nicotine. Loosen anything tight around your abdomen. Raise the head of your bed, sleep on your left side, and chew gum and walk after meals.

[30:00 –> 30:21] These are simple steps, but don’t underestimate them. They’re powerful, evidence based, and they give your body a chance to reestablish a natural rhythm. The weight loss might take some effort, and if alcohol or nicotine are daily habits, that might need support. But the rest of these changes are easy wins. And for most people, they make a massive difference in just a few weeks.

[30:21 –> 30:49] The next thing I’d recommend, and this is something anyone can do no matter how far along you are in your reflux journey, is to start identifying your own personal triggers. For me, the big culprits were tea and garlic. Those two surprised me, and you might have totally different ones. We already talked about some of the common offenders, chocolate, mint, onions, high fat meals, carbonated drinks, simple sugars, but everyone’s chemistry is different. What bothers one person might have no effect on the other.

[30:49 –> 31:08] The best way to figure it out is through a simple elimination approach. Don’t try to cut everything out at once. That just creates a ton of confusion, and you won’t understand your results. Instead, remove one food or drink per week and track your symptoms with a simple one to five scale. A five means your reflux is at its worst, and a one means it’s minimal.

[31:08 –> 31:22] For example, in week one, maybe take out chocolate. In week two, drop onions. In week three, skip tea or fatty meals. Each week, pay attention to how you feel. If removing that food noticeably improves your symptoms, keep it out.

[31:22 –> 31:41] If it doesn’t make a difference, you can bring it back in. The key here is consistency. Write it down, track your progress, and let your own body teach you what works. When I finally cut out tea, it was shocking how much better my reflux became. I would have never guessed that that one small change could make such a huge difference.

[31:41 –> 32:02] So use that same method. One change at a time, track it, evaluate it, and only discard what you find helpful. It’s simple, it’s low effort, and it gives you your own personalized data on what your stomach loves and what it hates. Okay. Now let’s talk about how to actually get off acid suppressing medications because I know many of you are on them.

[32:02 –> 32:21] And like I said earlier, these drugs can cause true physiological dependence. That’s what makes coming off them feel almost impossible, but it’s not impossible. It just has to be done right. So before I give you a specific road map, let me say this clearly. There are some people who should not try to come off these medications on their own.

[32:21 –> 32:46] If you have Barrett’s esophagus, erosive esophagitis, bleeding ulcers, chronic NSAID use, a gastric bypass, or large hiatal hernia, talk to your doctor first. In those cases, the benefits of acid suppression can outweigh the risks. And if your doctor was the one who prescribed you your medication, tell them what you’re doing and bring them this plan. A good physician will help you step down safely. Okay.

[32:46 –> 33:17] Here’s how to get off your acid suppressing medication in a safe step by step way. If you’re taking a PPI, proton pump inhibitor, that’s omeprazole, pantoprazole, or anything ending in prazole, first make sure you’re taking it at the right time. Take it only thirty to sixty minutes before breakfast, not at bedtime, and not randomly during the day. That timing matters because that’s when your stomach naturally gears up to produce acid, and you want the drug active when those pumps switch on. Do this for two weeks to get your rhythm set.

[33:17 –> 33:49] After those two weeks, the next step is to switch from a PPI, proton pump inhibitor, to a gentler medication called an h two blocker, something like famotidine, which you might know as Pepcid. These medications also reduce acid, but in a milder way by blocking histamine receptors on the acid producing cells. Now here’s the logic. While you’re on a PPI, your stomach builds up tons of acid making proton pumps, but those pumps are locked down by the PPI. When you switch to an h two blocker, you still suppress acid, but not as much.

[33:49 –> 34:09] That gives your body a chance to start adjusting the proton pump numbers downward. So for one month, take the h two blocker twice a day before breakfast and before dinner. After that month, reduce it to once a day before dinner. Do that for another month. Then in the third month, cut the dose in half.

[34:09 –> 34:33] If your tablets are twenty milligrams, such as with famotidine, use a pill cutter and take ten milligrams in the evening before dinner, and do that for another month. Finally, in the fourth month, cut that in half again down to a quarter dose. So that’d be around 5 milligrams if you’re taking famotidine. Hold that for another month and then stop. Now during any point in this taper, you might feel heartburn flare up.

[34:33 –> 34:45] Actually, just expect it. That’s your stomach trying to recalibrate. Remember that coiled spring analogy? Years of suppression means the stomach’s been building pressure behind the scenes. When you release that, it can rebound for a while.

[34:46 –> 35:00] So what do you do when that happens? Well, first go back to the basics. Stay upright after meals, elevate the head of your bed, and sleep on your left side. Avoid tight clothing, skip alcohol and nicotine, and chew gum or take a short walk after meals. All those things will help.

[35:00 –> 35:31] But here’s my favorite trick, and it’s one that’s helped me the most out of anything, And that’s using plain baking soda, also called sodium bicarbonate. I just mix a half a teaspoon in four to six ounces of water and drink it. It instantly neutralizes acid. And if you have high blood pressure and need to limit your sodium, you can find mixed formulations that combine sodium, potassium, and magnesium bicarbonate. And if a half a teaspoon of sodium bicarbonate feels too much, start with a quarter teaspoon or even an eighth teaspoon mixed in water.

[35:31 –> 35:47] Adjust it to your comfort. Baking soda provides pure bicarbonate, the same compound your body already makes to buffer acid naturally. When you drink it, it coats the esophagus and instantly reduces the burn. And it’s safe, simple, and dirt cheap. Forget the Tums and the Rolaids.

[35:47 –> 36:06] Plain baking soda works far better. There’s also a natural remedy that I love that comes straight out of Ayurvedic medicine, and that’s fennel seeds. If you’ve ever been to an Indian restaurant, you’ve probably seen a little bowl of candy colored seeds at the counter. Those are fennel seeds. They’ve been used for centuries to aid digestion and calm the stomach after meals.

[36:06 –> 36:32] Fennel contains a compound called anethyl that relaxes the gastrointestinal tract and improves gastric emptying. Studies have even shown that it helps with bloating and functional dyspepsia. You don’t need anything fancy. Just grab a jar of organic fennel seeds at the grocery store, and after a meal, take a half a teaspoon to a full teaspoon in your palm, pop them in your mouth, chew them thoroughly, and swallow. Within minutes, your stomach feels lighter and calmer.

[36:32 –> 36:41] It’s totally amazing. If you’re pregnant or allergic to fennel, skip it. But for most people, it’s completely safe. After all, it is just food. So that’s your road map.

[36:41 –> 37:13] If you follow it, tapering slowly on the medication, using baking soda for rebound relief, and chewing fennel seeds after meals, and sticking with the lifestyle principles we already covered, you can absolutely retrain your stomach to work normally again. And when you do, you’ll feel it. Meals will digest better, your energy will rise, and most importantly, you’ll know you freed yourself from a pill you thought you’d need forever. Okay. Before we wrap up, I wanna mention a few other conditions that can drive reflux despite optimizing diet and lifestyle.

[37:13 –> 37:40] SIBO or small intestinal bacterial overgrowth happens when bacteria from the large intestine start multiplying in the small intestine. They ferment food, create gas, and raise abdominal pressure, which can push acid up and trigger reflux. There are also medical conditions that can make reflux worse by altering digestion or weakening the bowel between the stomach and the esophagus. Hypothyroidism slows metabolism and gastric emptying. Diabetes can cause gastroparesis.

[37:40 –> 38:04] Connective tissue disorders like scleroderma can weaken the lower esophageal sphincter, and pregnancy hormones can do the same. That’s why a lot of pregnant women get reflux. So if your GERD is stubborn or not improving, it’s worth checking for these root causes. Treating them with your doctor or functional medicine provider often reduces reflux dramatically and helps restore your body’s natural rhythm. Okay.

[38:04 –> 38:37] Let’s sum it up. We talked about the mechanics of GERD, how the lower esophageal sphincter and the diaphragm work together to keep acid where it belongs, and how increased abdominal pressure can push that acid up. We covered the real world triggers, obesity, large meals, tight clothing, alcohol, nicotine, late night eating, and even certain foods and medications, all of which can weaken that barrier and lead to reflux. And we went through what happens when you’re on acid suppressing medications. We talked about who actually needs them, who can safely taper off of them, and how you do it step by step.

[38:37 –> 38:59] Because, yes, these drugs create physiological dependence, but with the right plan, freedom is absolutely possible. My message here isn’t anti medicine. It’s pro physiology. It’s about understanding how your body is designed to work and helping it return to its natural rhythms, not fighting against it. If you’ve been living with reflux, this is your moment to reset.

[38:59 –> 39:16] Then if you’re a good candidate, begin tapering off acid suppressing medications methodically. Use simple tools like baking soda and fennel seed for breakthrough symptoms. They really work. That’s how you’ll reclaim your digestive health and your freedom from acid suppressing medications. Okay.

[39:16 –> 39:50] So I hope you enjoyed that episode. On next week’s show, we’re going back to tribulations, and this one’s a little different. We’re not talking directly about medicine, but about a scientific breakthrough that has saved more lives than almost any other discovery in human history. This is the story of Norman Borlaug, a man whose relentless work with a plant changed the course of global health, reduced famine, and literally saved over a billion people. It’s a story of science, persistence, and one man’s obsession that reshaped not just food, but the survival of nations.

[39:50 –> 40:01] It’s one of the greatest stories of how science saved humanity, and I can’t wait to share it with you. So until then, stay curious, stay skeptical, and stay healthy. Cheers.

References & Resources

Global Prevalence and Risk Factors of Gastro-oesophageal Reflux Disease (GORD): Systematic Review with Meta-analysis

The target of therapies: pathophysiology of gastroesophageal reflux disease

Esophageal Motility Disorders and Gastroesophageal Reflux Disease

Testing for refractory gastroesophageal reflux disease

The Changing Epidemiology of Gastroesophageal Reflux Disease: Are Patients Getting Younger?

Improving treatment of people with gastro-esophageal reflux disease refractory to proton pump inhibitors

Regurgitation is less responsive to acid suppression than heartburn in patients with gastroesophageal reflux disease

Regurgitation is less responsive to acid suppression than heartburn in patients with gastroesophageal reflux disease

Meta-analysis: obesity and the risk for gastroesophageal reflux disease and its complications

The Association Between Obesity and GERD: A Review of the Epidemiological Evidence

Clinical Significance of Hiatal Hernia

Hiatal hernia, lower esophageal sphincter and their combined effect on the natural history of gastroesophageal reflux disease: implications for surgical therap

Specific Movement of Esophagus During Transient Lower Esophageal Sphincter Relaxation in Gastroesophageal Reflux Disease

Current Advancement on the Dynamic Mechanism of Gastroesophageal Reflux Disease

Gastroesophageal reflux and gastric emptying, revisited

Severe Delayed Gastric Emptying Induces Non-acid Reflux up to Proximal Esophagus in Neurologically Impaired Patients

Obesity: a challenge to esophagogastric junction integrity

Obesity increases oesophageal acid exposure

Are Lifestyle Measures Effective in Patients With Gastroesophageal Reflux Disease? An Evidence-Based Approach

Distension of the esophagogastric junction augments triggering of transient lower esophageal sphincter relaxation

Simultaneous intraesophageal impedance and pH measurement of acid and nonacid gastroesophageal reflux: Effect of omeprazole

The Effects of Modifying Amount and Type of Dietary Carbohydrate on Esophageal Acid Exposure Time and Esophageal Reflux Symptoms: A Randomized Controlled Trial

A very low-carbohydrate diet improves gastroesophageal reflux and its symptoms

The Effects of Dietary Fat and Calorie Density on Esophageal Acid Exposure and Reflux Symptoms

Effect of low and high fat meals on lower esophageal sphincter motility and gastroesophageal reflux in healthy subjects

Waist belt and central obesity cause partial hiatus hernia and short-segment acid reflux in asymptomatic volunteers

Gastroesophageal reflux induced by exercise in healthy volunteers

Body position affects recumbent postprandial reflux

ACG Clinical Guideline: Guidelines for the Diagnosis and Management of Gastroesophageal Reflux Disease

The effect of chewing sugar-free gum on gastro-esophageal reflux

Walking and chewing reduce postprandial acid reflux

Effects of transdermal nicotine on lower esophageal sphincter and esophageal motility

Mechanisms of acid reflux associated with cigarette smoking

Pharmacologic Specificity of Nicotinic Receptor-Mediated Relaxation of Muscarinic Receptor Precontracted Human Gastric Clasp and Sling Muscle Fibers within the Gastroesophageal Junction

Effects of transdermal nicotine on lower esophageal sphincter and esophageal motility

Effect of Sublingual Nitroglycerin and Long-Acting Nitrate Preparations on Esophageal Motility

Use of anti-inflammatory drugs and lower esophageal sphincter relaxing drugs and risk of esophageal and gastric cancers

Which drugs are risk factors for the development of gastroesophageal reflux disease?

Physiology, Pepsin

Influence of Gastric Acidity on Bacterial and Parasitic Enteric Infections: A Perspective

The role of gastric acid in preventing foodborne disease and how bacteria overcome acid conditions

Proton pump inhibitors therapy and risk of Clostridium difficile infection: Systematic review and meta-analysis

Meta-analysis: proton pump inhibitors moderately increase the risk of small intestinal bacterial overgrowth

Proton Pump Inhibitor Use and the Risk of Small Intestinal Bacterial Overgrowth: A Meta-analysis

Physiology, Gastric Intrinsic Factor

Vitamin B12 Intake From Animal Foods, Biomarkers, and Health Aspects

Proton Pump Inhibitor and Histamine 2 Receptor Antagonist Use and Vitamin B12 Deficiency

Role of gastric acid in food iron absorption

Use of proton pump inhibitors and risk of iron deficiency: a population-based case-control study

Calcium Absorption and Achlorhydria

Proton pump inhibitors and hypomagnesemia

Proton Pump Inhibitors Interfere With Zinc Absorption and Zinc Body Stores

Physiology, Stomach

Acid secretion and the H,K ATPase of stomach

Pharmacology of Proton Pump Inhibitors

Fundic gland polyps: Should my patient stop taking PPIs?

Proton pump inhibitor‐induced large gastric polyps can regress within 2 months after discontinuation: Experience from two cases

AGA Clinical Practice Update on De-Prescribing of Proton Pump Inhibitors: Expert Review

Acute interstitial nephritis due to proton pump inhibitors

The Effects of Pantoprazole on Kidney Outcomes

Proton pump inhibitors and risk of fractures: a meta-analysis of 11 international studies

Osseous implications of proton pump inhibitor therapy: An umbrella review

Proton Pump Inhibitors and Osteoporosis: Is Collagen a Direct Target?

Proton Pump Inhibitors and Bone Health: An Update Narrative Review

Gastroesophageal Reflux Disease and Helicobacter pylori: What May Be the Relationship?

Helicobacter pylori infection reduces the risk of Barrett’s esophagus: A meta‐analysis and systematic review

Helicobacter pylori eradication does not exacerbate reflux symptoms in gastroesophageal reflux disease

Pimpinella anisum in modifying the quality of life in patients with functional dyspepsia: A double-blind randomized clinical trial

Left lateral decubitus sleeping position is associated with improved gastroesophageal reflux disease symptoms: A systematic review and meta-analysis

The Effects of Modifying Amount and Type of Dietary Carbohydrate on Esophageal Acid Exposure Time and Esophageal Reflux Symptoms: A Randomized Controlled Trial

Cheers,
Ravi Kumar MD