Heartburn is not too much.
It is a not-enough.
Why the burning behind your sternum rarely comes from a stomach making too much acid. And what it is really telling you.
Heartburn is a pain that pushes upward. But what you feel up there is only the top floor of a story that begins on a completely different level. Sometimes in the nervous system. Sometimes in a weakened mucosa. Sometimes in a stomach that has been on acid blockers so long it has forgotten how acid is supposed to work.
Woman in her mid-40s, three weeks into the practice
She sits in front of me and says: "I have been on pantoprazole for eight years. When I try to stop, after three days it burns like fire. I cannot do this anymore." Her eyes are tired. Her hair is thin. She is in her job, she has two children, she does everything right. Her labs show: B12 low-normal, ferritin 18, vitamin D 22. She says: "I thought this was just getting older." She softens when I ask: "What if your stomach has been making too little acid the whole time, not too much?" We test parietal cell antibodies, run a hydrogen breath test, and an extended stool panel. Three weeks later we begin bitters before meals, diaphragmatic breathing after each meal, no bread, no sweets, plenty of meat, slow eating. Pantoprazole is reduced step by step with alginate as a bridge. After ten weeks she is without the pill. A single course is not a guarantee for the next. But it is a hint that another story is possible.
What heartburn really is.
Heartburn is not a diagnosis. It is a symptom. A burning pain that arises because stomach contents move upward into the oesophagus, where they do not belong. The mucosa of the oesophagus is not made for acid. The mucosa of the stomach is. That is the difference.
The old story says: your stomach makes too much acid, so we block the acid. This story is simple on one side and sometimes wrong on the other. It ignores that there are many ways for acid to end up where it should not be. And one of the most common is the opposite: you have too little acid, your meal ferments, pressure builds, and the pressure pushes everything upward.
When it burns, your stomach is not asking "why so much acid?", it is asking "why so little clarity about what is supposed to happen here?".
Several floors, one story.
In functional medicine and clinical psychoneuroimmunology, we look at heartburn through four lenses: the nervous system, the immune system, metabolism, and the hormonal system. They are not boxes. They are floors of a house in which your stomach lives.
The stomach is an electrochemical wonder. The parietal cells in your gastric mucosa produce hydrochloric acid at a pH of 0.8 to 1.5. That is the most acidic fluid your body makes. It is the first evolutionary firewall against microbes, it activates pepsin for protein digestion, it unlocks the iron in your food, it secures B12 binding, it keeps the microbiome where it belongs. When the acid quiets down, that firewall can break in several places at once.
The stomach is not a soloist, it is the conductor of an orchestra. When the acidic chyme reaches the duodenum, S-cells release secretin, which signals the pancreas to send bicarbonate. Almost at the same time, I-cells release cholecystokinin, which prompts the gallbladder to send bile and the pancreas to send digestive enzymes. Without an acidic signal the whole cascade starts only half-heartedly. Pancreatic enzymes underperform, bile stagnates, fats are not emulsified, fat-soluble vitamins A, D, E and K can be absorbed less well.
The vagus nerve is the main line. Before you swallow your first bite, your brain has already called your stomach through the vagus: "meal incoming, prepare acid." This is called the cephalic phase. Under stress that call does not come. The stomach is not prepared. The meal sits undigested. Pressure builds. You feel it as burning. There is also the migrating motor complex, a cleansing wave that travels through the small intestine every 90 to 120 minutes between meals. People who snack constantly switch off this wave and open the door to bacterial overgrowth.
Cortisol is the co-pilot who can take the steering wheel. Under chronic stress, cortisol can be persistently elevated or dysregulated. Cortisol relaxes the lower oesophageal sphincter and makes the oesophagus more sensitive to acid. That is not esoterics, that is pharmacology. Stress drives reflux, and reflux drives stress.
The hormone axis is in the mix, quieter than we often think. The thyroid regulates gastric motility and metabolic rate. An untreated or insufficiently treated hypothyroidism, especially the common Hashimoto variant, often comes with slowed gastric emptying and reduced acid production. Oestrogen and progesterone act on the oesophageal sphincter and on mucosal quality, which many women first start to feel during peri- and menopause.
And the mast cells sit at the gate. They line the entire gastrointestinal mucosa and react to bacterial products, to stress, to histamine in food. With hypochlorhydria the histamine load in food can rise because more bacteria survive and produce histamine. From there you can develop hot flushes, flushed cheeks, post-meal itching, runny nose, and migraine. In PNI we call this mast cell activation.
RCTDiaphragmatic breathing halves reflux
In a randomized controlled trial with symptomatic GERD patients, post-meal diaphragmatic breathing reduced reflux episodes to 0.36 per phase, compared to 2.60 in the control group. The pressure difference between the lower oesophageal sphincter and the stomach increased, which functionally strengthens the sphincter.
Halland M et al., Am J Gastroenterol 2020. doi.org/10.14309/ajg.0000000000000656
RCTBreath training halves the PPI dose
An earlier randomized trial showed that active diaphragmatic training reduced oesophageal pH time below 4 from 9.1 to 4.7 percent. Quality of life improved by half. After nine months, the trained group needed only about a quarter of their original acid blocker dose.
Eherer AJ et al., Am J Gastroenterol 2012. doi.org/10.1038/ajg.2011.420
Two stomachs that look the same.
The most important thing you can learn about your stomach is how to tell its variants apart. Two people can both have heartburn and need exactly the opposite of each other. If you skip this distinction, you treat in the dark.
Variant A
Younger or middle-aged person, often stress, often poor sleep, often many meals eaten too fast. Acid normal to high, sphincter too loose, an acid pocket sits on top of the stomach contents and spills upward. Answer: fewer triggers, more breathing, address weight, raise the head of the bed, alginates as needed.
Variant B
Older person or long-term acid blocker patient, often atrophy, often B12 or iron quietly low. Acid too low, the meal ferments, pressure rises, the sphincter is mechanically overstretched. It does not burn because too much is coming up, it burns because the little that comes up does not belong there. Answer: support acid, bitters, breath, slow eating, diagnostic workup for cause.
MechanismStomach acid is the microbial firewall
A comprehensive review explains why gastric acid is phylogenetically conserved even though its production costs energy and occasionally causes disease. It is the first barrier against microorganisms. Hypochlorhydria opens the gate for SIBO and bacterial overgrowth in the upper digestive tract.
Martinsen TC et al., Int J Mol Sci 2019. doi.org/10.3390/ijms20236031
What mainstream gastro rarely looks at.
This is the part where functional medicine parts ways with classic mainstream care. Not because mainstream is wrong. But because it rarely looks exactly here, where the pain often has its real root.
1. Parasites and fungi that quietly turn your acid down
Parasitic stomach worms can damage parietal cells directly. In animal models this leads to hypergastrinaemia, acid suppression, and a loss of acid-producing cells. Fungi like Candida albicans can also colonize the stomach, especially when the pH has already been raised by long-term acid blockers. There are documented cases of gastric ulcers that did not heal for months despite pantoprazole and only resolved after antifungal therapy with fluconazole.
MechanismA parasite directly inhibits stomach acid
In an animal model, infection with the stomach worm Teladorsagia led to inhibition of gastric acid secretion, loss of parietal cells, and reactive hypergastrinaemia. Parasitic secretions diffused through the surface epithelium and attacked the acid-producing cells.
Scott I et al., PLoS ONE 2017. doi.org/10.1371/journal.pone.0186752
Clinical caseWhen PPIs fail, sometimes fungi are the cause
A 78-year-old patient had persistent gastric ulcers despite pantoprazole. A biopsy showed Candida involvement. Only antifungal therapy with fluconazole healed the mucosa fully. PPIs had not only failed to help, they had likely encouraged the fungal colonization.
Nguyen N et al., Am J Gastroenterol 2021. PMID 34555924
2. Mycotoxins from mould: the hidden irritant
Mould is not only a problem of damp walls. Aflatoxins in poorly stored grain, ochratoxins in coffee, patulin in apple juice, candidalysin from your own gut fungus, all of these can inflame the gastric mucosa and shift the microbiome. Mycotoxins can disrupt the mechanical and immunological barrier of the mucosa, inhibit protein synthesis, and drive pro-inflammatory cytokines such as interleukin 1-beta and interleukin 17.
ReviewMycotoxins disrupt the mucosal barrier
Mycotoxins such as aflatoxin, fumonisin, and deoxynivalenol disrupt the mechanical, chemical, immunological, and biological barrier of the intestinal mucosa. They alter mucin composition and drive systemic inflammation. The gastrointestinal mycobiome itself secretes further mycotoxins and candidalysin.
Kiran NS et al., Medical Oncology 2025; Ren Z et al., Int J Mol Sci 2019. doi.org/10.3390/ijms20112777
3. Autoimmune atrophic gastritis: the underdiagnosed silence
In autoimmune atrophic gastritis, your own immune system attacks the parietal cells that produce stomach acid. Acid production drops gradually, B12 drops with it, iron is no longer properly unlocked. These patients are often women, often over 50, often with other autoimmune conditions such as Hashimoto. They rarely come to me saying "heartburn", they come with fatigue, hair loss, burning tongue, tingling feet. Two blood tests can support the suspicion: parietal cell antibodies and intrinsic factor antibodies.
4. Stress and the cortisol carousel
The evidence here is stronger than I myself long thought. Chronic stress can drive cortisol up, cortisol relaxes the lower oesophageal sphincter, increases visceral sensitivity of the oesophagus, and weakens the mucosal barrier. A growing number of reviews describe the brain-gut axis as a central engine of refractory reflux symptoms. If your heartburn reliably gets worse in stressful weeks, that is not a psychosomatic fantasy. That is endocrinology.
Carnivore, vegan, or just clear?
I get this question often, and it is smarter than it sounds. There are patients who lose their years of heartburn on a carnivore diet. There are patients who lose their years of heartburn on a vegan diet. Both are right. Both remove the same thing.
The polarity works in both directions because it cuts out the same thing. The ultra-processed-sugar-FODMAP-fermenting snack-meal mix.
RCTSugar out, heartburn down
In a randomized trial with 98 veterans with symptomatic GERD, the group that reduced simple sugars by about 62 grams a day significantly reduced their oesophageal acid exposure. Heartburn frequency, heartburn intensity, sour taste in the mouth, throat lump, and sleep disturbances all improved measurably.
Gu C et al., Am J Gastroenterol 2022. doi.org/10.14309/ajg.0000000000001889
Low-carb cuts oesophageal acid time
A systematic review and meta-analysis of 21 dietary intervention studies showed that low-carb diets significantly reduce oesophageal acid exposure time, with a mean difference of minus 2.834 percentage points.
Lakananurak N et al., Nutrients 2023. doi.org/10.3390/nu15163615
MechanismAnimal protein wakes the acid response
In a human physiology study, a beef meal triggered 30 to 40 percent more gastric acid secretion than a soy protein meal, and the gastrin rise was 65 to 75 percent higher. Animal protein activates the natural acid response of the stomach particularly strongly.
McArthur K et al., Gastroenterology 1988. PMID 3402366
For the patient who comes in with hypochlorhydria and chronic gastric slowness, a protein-heavy or temporarily carnivore approach can be a real therapeutic lift. It activates the natural acid response, removes upper-abdominal fermentation, takes the constant sugar load off the microbiome, and gives the stomach a clear meal that can be answered with acid. Important: an adaptation phase of two to four weeks, good chewing, calm eating, and if necessary external acid support until the stomach pedals on its own again.
Carnivore is not a creed. It is a therapeutic option for a specific patient group and a specific phase. It is not indicated with biliary disorders, severe kidney disease, or without medical supervision. And: some patients reach the same improvement with the exact opposite, a plant-forward, fibre-rich, low-carb diet. What works for you gets clarified in the consultation, not in the forum.
Why PPIs often cost you more than they give.
PPIs, pantoprazole, omeprazole, and their relatives, are among the most prescribed drug classes in the Western world. In the right indications, like acute erosive reflux oesophagitis, the Helicobacter regimen, or ulcer prophylaxis under pain medication, they are a medical achievement. But they are also among the most prescribed long-term medications for a problem they do not solve on the long run, and often make worse.
What long-term PPIs can cost you
An umbrella review of 42 meta-analyses on long-term PPI safety summarized the major signals: increased risk for bone fractures, chronic kidney disease, magnesium deficiency, B12 deficiency, bacterial overgrowth, Clostridium difficile infections, pneumonia, and possibly cognitive change.
Salvo EM et al., Ther Adv Drug Saf 2021. doi.org/10.1177/20420986211038689
PPIs double the SIBO risk
A recent meta-analysis of 29 studies: PPI users have roughly twice the risk of small intestinal bacterial overgrowth, with an odds ratio of 2.14. An older observational study even found 50 percent SIBO prevalence in PPI users versus 6 percent in controls. The very symptoms SIBO produces are often the ones that drive people back to the next PPI dose. That is the loop.
Khurmatullina A et al., 2025; Lombardo L et al., Clin Gastroenterol Hepatol 2010. doi.org/10.1016/j.cgh.2009.12.022
The official AGA Clinical Practice Update from 2022 was the first to explicitly use the term "deprescribing" for PPIs. It is no longer awkward to take a patient off the pill. It is medical work.
What you can start today.
You do not need to wait for the big diagnostic marathon. There are levers you can pull today, and most of them cost nothing.
Low-threshold levers
- Apple cider vinegar before meals. A tablespoon in a glass of warm water, ten minutes before the main meal. If it clearly helps after the first try, you most likely have low acid. If it burns, leave it.
- Bitters before meals. A bitter plant extract on the tongue, a minute before the first bite, activates the cephalic phase through bitter receptors and vagus. Classics: gentian, wormwood, yarrow, dandelion.
- Diaphragmatic breathing after each meal. Twenty calm belly breaths after the meal, seated, not lying down.
- No food three hours before sleep. Night reflux is the worst, because lying down tips the acid pocket against the sphincter.
- Left-side sleeping. Anatomically reduces night-time acid exposure.
- Raise the head of the bed. Ten to fifteen centimetres, not just a higher pillow.
The food line
- Simple sugar out. Sweet breakfast, sweet drinks, sweet after meals. The RCT data is strongest here.
- Reduce fermentable FODMAPs. Especially in the acute phase. Onion, garlic, legumes, wheat, milk can all ferment and build pressure.
- More animal protein, cleanly sourced. Activates the natural acid response. Carnivore or protein-heavy, depending on constitution.
- Eat slowly. Twenty minutes per main meal. Chew well.
- Less water with meals. Dilutes the acid. Drink between meals.
Gastric acid support
- Betaine HCl. Off-label but clinical tradition. When testing confirms genuine hypochlorhydria, betaine HCl with pepsin at meals can be a therapeutic bridge. Only start under medical guidance.
- Zinc carnosine. Mucosal regeneration of the stomach, well documented for mucosal wound healing.
- L-glutamine. Amino acid for gastrointestinal mucosal repair.
- Mastic (Pistacia lentiscus). From Mediterranean tradition, with studies in functional dyspepsia.
Stress regulation
- Breathwork daily. Not only when it burns. Ten minutes in the morning, ten in the evening.
- Sleep above all. Sleep loss raises cortisol, cortisol drives reflux.
- Aerobic movement. Lowers stress markers long-term without acutely provoking reflux.
- Contact, meaning, pause. These are among the most reliable long-term cortisol levellers we know.
Do not stop your PPI suddenly. A rebound hyperacidity can dramatically worsen heartburn for weeks and push you back into the pill. Step down gradually, bridge with alginate, with bitters and breath.
Six steps you can take now
Each a puzzle piece. Together they paint the picture.
- Differentiate. Do the apple cider vinegar test for three days before meals. Note whether it improves or worsens.
- Lower the triggers. One week with no simple sugar, no bread in the evening, no snacks between meals, no food three hours before bed.
- Wake the vagus. Bitters before each meal, diaphragmatic breathing after, slow chewing.
- Go into the diagnostics. B12, ferritin, vitamin D, parietal cell antibodies, intrinsic factor antibodies, Helicobacter test, stool panel for parasites and fungi, hydrogen breath test for SIBO if suspected.
- Talk to your doctor about deprescribing. If you have been on a PPI for months or years without erosive reflux disease, a stepwise reduction plan belongs on the table.
- Get accompaniment. A well-made individual plan in the consultation takes you out of the symptom escalation and into healing.
What your stomach really needs.
Your stomach has never betrayed you. It has been sending you a message the whole time, in a language you were never taught. Burning does not mean "too much". Burning means: "something is not where it should be." Sometimes it is the acid. Sometimes it is the calm before the meal. Sometimes it is an undetected parasite, a quietly working fungus, a flat in which mould lives in the wall, an autoimmune reaction, a ten-year stress phase, or a meal that needs twenty minutes but only got two.
You are not too complicated. You are not too sensitive. Your stomach is an electrochemical wonder, and it deserves the right to work the way it was evolutionarily meant to.
True freedom is not taking a pill every day so you can eat what you want. True freedom is feeling again that your stomach is on the same side as you.
Common questions from my consultation
Can too little stomach acid also cause heartburn?
Yes, that can happen. When stomach acid is too low, undigested food can sit too long in the stomach, ferment, build pressure, and the pressure can push stomach contents upward. The burning feels similar to high-acid heartburn, but the cause may be the opposite.
What is the difference between reflux and hypochlorhydria?
Reflux is stomach contents flowing back into the oesophagus. Hypochlorhydria is too little acid being produced in the stomach. Both can overlap.
Should I stop my acid blocker?
Please not suddenly, and never alone. Stopping a PPI causes a rebound hyperacidity that can dramatically worsen heartburn for weeks. Step down gradually, bridge with alginates, bitters, diaphragmatic breathing, and nutrition.
What about a carnivore diet for heartburn?
A carnivore or heavily protein-based diet can clearly improve heartburn in some people, because it removes simple sugars, ultra-processed foods, and FODMAPs entirely. The literature shows that low-carb significantly reduces oesophageal acid exposure, and that animal protein activates the natural acid response strongly.
Can parasites or mould cause my heartburn?
Yes, this is possible and often overlooked. Stomach parasites and fungi like Candida can damage parietal cells and inhibit acid production directly. Mould exposure can inflame the gastric mucosa and shift the microbiome.
Does apple cider vinegar help with heartburn?
For many patients yes, especially those with too little instead of too much acid. A tablespoon of apple cider vinegar in a glass of warm water ten minutes before a meal can support gastric function. If it burns after the first attempt, leave it.
How long does it take for my stomach to recover?
Six to twelve weeks is a realistic horizon when several levers are combined.
Sources
- Halland M et al. Diaphragmatic breathing exercise as adjunctive treatment for GERD. Am J Gastroenterol 2020. doi.org/10.14309/ajg.0000000000000656
- Eherer AJ et al. Positive effect of abdominal breathing exercise on GERD. Am J Gastroenterol 2012. doi.org/10.1038/ajg.2011.420
- Gu C et al. Effects of modifying carbohydrate on esophageal acid exposure in GERD: an RCT. Am J Gastroenterol 2022. doi.org/10.14309/ajg.0000000000001889
- Lakananurak N et al. Efficacy of dietary interventions in GERD. Nutrients 2023. doi.org/10.3390/nu15163615
- McArthur K et al. Soy protein meals stimulate less gastric acid secretion than beef meals. Gastroenterology 1988. PMID 3402366
- Martinsen TC et al. The phylogeny and biological function of gastric juice. Int J Mol Sci 2019. doi.org/10.3390/ijms20236031
- Engevik AC et al. The physiology of the gastric parietal cell. Physiol Rev 2019. doi.org/10.1152/physrev.00016.2019
- Scott I et al. Abomasal dysfunction during parasitic infection. PLoS ONE 2017. doi.org/10.1371/journal.pone.0186752
- Nguyen N et al. PPI-refractory Candida-associated peptic ulcer disease. Am J Gastroenterol 2021. PMID 34555924
- Kiran NS et al. The gastrointestinal mycobiome in inflammation and cancer. Medical Oncology 2025.
- Ren Z et al. Progress in mycotoxins affecting intestinal mucosal barrier function. Int J Mol Sci 2019. doi.org/10.3390/ijms20112777
- Neumann WL et al. Autoimmune atrophic gastritis. Nat Rev Gastroenterol Hepatol 2013. doi.org/10.1038/nrgastro.2013.101
- Salvo EM et al. PPI long-term safety: umbrella review. Ther Adv Drug Saf 2021. doi.org/10.1177/20420986211038689
- Khurmatullina A et al. PPI use and SIBO risk: updated meta-analysis. 2025.
- Lombardo L et al. Increased incidence of SIBO during PPI therapy. Clin Gastroenterol Hepatol 2010. doi.org/10.1016/j.cgh.2009.12.022
- Macke L et al. Effects of PPI on the microbiome. Aliment Pharmacol Ther 2020. doi.org/10.1111/apt.15604
- Imhann F et al. Proton pump inhibitors affect the gut microbiome. Gut 2015. doi.org/10.1136/gutjnl-2015-310376
- Targownik LE et al. AGA Clinical Practice Update on De-Prescribing of PPI. Gastroenterology 2022. doi.org/10.1053/j.gastro.2021.12.247
- Taylor M. Re-evaluating betaine HCl: a clinical review. 2024.
- Rizzo G et al. The role of a plant-only diet in GERD. Nutrients 2023. doi.org/10.3390/nu15224725