Heartburn is not too much.
It is a not-enough.

What can sit behind heartburn.

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 familiar explanation says: your stomach makes too much acid, so we block the acid. For many people that explanation is right and important. It is simply not the only one. It leaves aside that there are several ways acid can end up where it does not belong. One route that gets checked less often could be this: with too little acid the meal can sit longer, ferment and build pressure. How often that actually happens has not been studied in humans.

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.

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.

What routine workup less often has in view.

This is the part where functional medicine adds further lenses. Not because established gastroenterology is wrong, it achieves a great deal in heartburn and regularly protects mucosa and lives with endoscopy and acid blockers. But because some of the following factors come up less often in a routine workup. The evidence here is consistently thinner. So for each point I write what it rests on.

1. Parasites and fungi that quietly turn your acid down

In sheep, an abomasal worm can damage the acid-producing cells, with hypergastrinaemia, acid suppression, and a loss of parietal cells. These are data from veterinary research, measured in the abomasum of a ruminant. I am not claiming a transfer to the human stomach, that transfer is not established. Fungi like Candida albicans can also colonize the stomach, especially when the pH has already been raised by long-term acid blockers. Whether such colonization then causes symptoms or is merely an incidental finding is judged differently across the literature. In people with chronic courses I still look at this lens.

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 irritate 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. These findings come mostly from cell and animal experiments. In humans, a link between mycotoxin exposure and heartburn is not established. In people with mould exposure at home or at work this lens can still be a piece of the puzzle worth looking at.

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 can drop gradually, B12 can drop with it, and iron can be unlocked less well. 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. The diagnosis itself is secured by endoscopy with biopsy.

4. Stress and the cortisol carousel

Chronic stress can drive cortisol up. Cortisol can relax the lower oesophageal sphincter, increase visceral sensitivity of the oesophagus, and weaken the mucosal barrier. A growing number of reviews describe the brain-gut axis as one engine of stubborn reflux symptoms. Solid intervention trials are largely missing here, the link is mechanistically plausible and visible in observational data. So if your heartburn reliably gets worse in stressful weeks, that is not a fantasy. It has a physical side.

Carnivore, vegan, or just clear?

I get this question often, and it is smarter than it sounds. Some people tell me their heartburn changed on a carnivore diet. Others tell me the same about a vegan diet. These are individual reports from conversations, not a success rate and not proof. Studies testing either route do not exist. What I find interesting is that both routes remove something similar.

For the patient who comes in with hypochlorhydria and chronic gastric slowness, a protein-heavy or temporarily carnivore approach can be an attempt worth discussing together. It is conceivable that it prompts the natural acid response more strongly, reduces upper-abdominal fermentation, takes the constant sugar load off the microbiome, and gives the stomach a clear meal that can be answered with acid. There are no studies on a carnivore diet in reflux specifically, so this is a physiological line of reasoning without study evidence and not a proven claim of effect. 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.

What acid blockers can cost you long-term.

PPIs, that is proton pump inhibitors such as pantoprazole or omeprazole, 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, and that is exactly where they belong. But they are also frequently continued as long-term medication in situations where the underlying cause is not being addressed. And for long-term use there are observational data worth knowing.

The AGA Clinical Practice Update from 2022 explicitly took up the term "deprescribing" for PPIs. Stepping down is thereby named as regular medical work, where no long-term indication exists. The other side matters just as much: where a long-term indication does exist, for example after an upper gastrointestinal bleed, with Barrett oesophagus, with severe erosive oesophagitis, or as gastric protection under aspirin, antiplatelet drugs, oral anticoagulants and NSAID-type pain medication, the acid blocker stays important and should not be stopped. That check is made in the practice, not by this text.

What you can start today.

You do not need to wait for the big diagnostic marathon. There are levers you can discuss and try today, and most of them cost nothing. That does not make them harmless: home remedies and food supplements have contraindications too, so each point below says what to watch for.

What your stomach may be missing.

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 automatically mean "too much". Burning can also mean: "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.