Gut Guide · Irritable stomach and functional dyspepsia

Irritable stomach: when the upper abdomen will not settle and the examination finds nothing

Functional does not mean imagined. It means the disturbance sits in the control system and not in a wound. And the most interesting trail of recent years does not lead into the stomach, it leads into the duodenum.

SJ
Shukri Jarmoukli · Physician · Area of focus: integrative medicine · ViveCura Berlin
Rome IV and the two types The duodenum Numbers instead of promises 38 sources with DOI
ViveCura BlogGut Guide › Irritable stomach and functional dyspepsia

All articles from the Gut Guide

Why I am writing this

The most frequent sentence on this topic in my consultations is: they did not find anything. Yet something was found, namely the exclusion of the dangerous causes. And what remains after that is described far better today than most people suspect.

You are sitting at the table, third bite, and the plate is suddenly too full. Not in your head. In your belly.

There is pressure under the rib cage, as if someone had inflated a balloon from the inside. You put the fork down. Two hours later it is still there.

And then came the gastroscopy. On waking up, the sentence you had waited three weeks for: everything normal.

Many people know exactly this moment and the emptiness that follows. Relief and disappointment in the same breath. Nothing found means, for you: I still have the symptoms, and now I have no explanation either.

I would like to turn that sentence around. A normal result is a result: no ulcer, no tumour, no open inflammation. It simply does not answer the second question. And that question is: what is going on then? There is considerably more of an answer to that today than there was fifteen years ago.

What awaits you here

  • Why functional dyspepsia is a diagnosis with criteria and not a leftover finding
  • The two subgroups and the numbers on how common each one is
  • The fundus that makes too little room while you eat
  • The duodenum as the actual stage, with odds ratios
  • The distinction from reflux, ulcer, bile and gastroparesis
  • What a gastroscopy can do and from when it is recommended
  • The numbers behind eradication, acid blockers and neuromodulators
  • Fat, portion, pace, coffee, sleep, without a list of bans
RCT / Meta randomised or pooled Human cohort, cross section, registry Guideline consensus with systematic search Lab tissue or animal, not human

What functional dyspepsia is, and why the diagnosis feels like a non finding

Picture two slips of paper. On one there is a name for what you have. On the other there is what you do not have.

With functional dyspepsia you usually get the second slip. No ulcer, no inflammation, no tumour. That sounds like nothing, and that is exactly the thinking error that accompanies many people for years.

Because functional dyspepsia, in everyday German called irritable stomach, is a positively defined diagnosis. It has criteria, four cardinal symptoms, two subgroups. And since 2025 a German language guideline of its own.

Guideline · Rome IV Four symptoms, two faces

An international panel around Vincenzo Stanghellini and Jan Tack redefined the criteria for gastroduodenal functional disorders in 2016 within the Rome Foundation.

They name four cardinal symptoms: fullness after eating, early satiation, pain in the upper middle abdomen and burning in the upper middle abdomen. Plus two subgroups, postprandial distress syndrome and epigastric pain syndrome, which are allowed to overlap. Symptoms are required for at least three months, with onset at least six months before diagnosis.

For you this means: there is a definition that you either fit into or do not. That is something different from a collective term for the unexplained.

Stanghellini V, Chan FKL, Hasler WL, Malagelada JR, Suzuki H, Tack J, Talley NJ. Gastroenterology. 2016;150(6):1380-1392. PMID: 27147122 · DOI: 10.1053/j.gastro.2016.02.011 [Guideline]

The word functional carries a burden here that it does not deserve. In everyday speech it sounds like imagined. Something quite different is meant: the disturbance sits in the control system, not in the structure.

An image for it: a piano can be out of tune without a piece of wood being broken. From the outside you see nothing. You can hear it immediately.

Reframe

Functional does not mean that nothing is there. It means that the examination you had is not the tool with which this disturbance is seen.

A gastroscopy looks at the surface. Functional dyspepsia arises in places the camera cannot reach: the stretch response of the stomach, the sensitivity of the nerve pathways, the tightness of the lining in the duodenum. All three can be measured, just not in routine care.

How common this is

You are not rare with this, you are very ordinary.

Cross section, n=5,931 61 to 18 to 21

Imran Aziz and colleagues surveyed 6,300 adults in the USA, Canada and the United Kingdom with the Rome IV questionnaire, without revealing in the invitation that it was about the gut.

The criteria for functional dyspepsia were met by 12 percent in the USA, 8 percent in Canada and 8 percent in the United Kingdom. The distribution across the subgroups was almost identical in all three countries: 61 percent meal related type, 18 percent pain type, 21 percent both. Those with both reported more physical symptoms overall and a poorer quality of life.

For you this means: the most common form is the one tied to eating. And if you have both, your everyday life is on average harder, and that is statistically demonstrable.

Aziz I, Palsson OS, Törnblom H, Sperber AD, Whitehead WE, Simrén M. Lancet Gastroenterol Hepatol. 2018;3(4):252-262. PMID: 29396034 · DOI: 10.1016/S2468-1253(18)30003-7 [Cohort, n=5,931]
10 %of adults meet the Rome IV criteria, and the German guideline of 2025 works with the same order of magnitude
20.8 %worldwide have uninvestigated dyspepsia, pooled across 312,415 people
80 %of all people with dyspepsia have no structural explanation for it, according to the 2020 Lancet review, see source 5

The 20.8 percent come from a meta-analysis of 100 study populations with 312,415 people. More often affected: women, smokers, people with Helicobacter pylori and people who regularly take painkillers of the NSAID type, with an odds ratio of 1.59. That last number is the only one that can be changed. And even so: long term medication is never stopped single handedly.

Please read this first

These red flags need medical assessment and are not to be self treated

  • Blood in the bowel movement or black tarry stool
  • Vomiting blood
  • Unintentional weight loss
  • Fever without an obvious reason
  • Night time symptoms that wake you up
  • Repeated vomiting
  • Difficulty swallowing or the feeling that food gets stuck
  • A new persistent change in bowel habit from around 45 to 50 years of age
  • Anaemia, that is a low haemoglobin value
  • A family history of bowel cancer, stomach cancer or inflammatory bowel disease

Two sentences that stand above everything else. If a gastroscopy, a colonoscopy or laboratory testing has been recommended, it is not postponed and not replaced by anything in this text.

And: acid blockers, laxatives, antibiotics or antidepressants are never started, changed or stopped on your own. Every change belongs under medical guidance.

One more frame that holds for the whole text: for pregnant women, breastfeeding women, children and adolescents, separate rules apply to almost every remedy discussed here, and solid data are often missing. Interactions are possible too. Acid blockers can change the absorption of other medicines, for example, and tricyclics do not go with every other substance. Both belong in a medical check before anything is started.

Since April 2025 there has been a German language guideline on functional dyspepsia for the first time. The S1 guideline of the German Society for Neurogastroenterology and Motility classifies it as a disorder of gut brain interaction and works with a prevalence in the order of 10 percent. It places psychoeducation, dietary counselling, mind body approaches, psychotherapy and medication next to each other, not against each other.

I give the guideline here in its broad outline. Some details I have from secondary accounts, which is why I put them cautiously.

Anyone still hearing today that there is nothing binding on functional dyspepsia is simply not up to date.

The core sentence of this section

The examination was not without result. It ruled something out. And now you know why that still feels like a rejection: the exclusion is written on the slip, the explanation is not.

The two faces: fullness after eating, or burning independent of it

Ask yourself once: is your symptom coupled to the meal or not?

This single question separates the two subgroups more cleanly than any device. It is also the question that is skipped too quickly in many consultations, because both pictures end up under the same word.

Rome IV

Two patterns, one name

Postprandial distress syndrome · PDS · 61 percent
Everything hangs on the meal
  • Fullness that stays after eating and bothers you
  • Early satiation, the plate does not get emptied
  • By the Rome IV definition on at least three days per week
  • Often accompanied by upper abdominal bloating, nausea, belching
  • Closely linked to disturbed gastric accommodation
Epigastric pain syndrome · EPS · 18 percent
The pain comes without eating too
  • Pain in the upper middle abdomen, pressing or gnawing
  • Burning in the upper middle abdomen, without it having to be heartburn
  • By the Rome IV definition on at least one day per week
  • Not exclusively after eating, sometimes even eased by it
  • Closely linked to increased pain sensitivity

21 percent have both. In the Rome IV survey this group carried the heaviest burden. The exact frequency thresholds are in the Rome IV criteria tables and serve research, not self classification.

Why is this distinction worth making if the diagnosis is the same in the end? Because it describes two very different worlds of experience. In the meal related type everything revolves around portions, pace and the question of whether you still enjoy eating at all. In the pain type everything revolves around burning, pressure and the fear that something is there after all.

And because the guidelines assign the treatment options differently. Whether that holds up against the data is a story of its own, and it comes further down.

The accompanying symptoms that are allowed to belong

The European consensus of 41 experts from 22 countries stated explicitly in 2021 which complaints are allowed to belong without breaking the diagnosis: a bloated feeling in the upper abdomen, nausea and belching.

That is more important than it sounds. Many people think that constant fullness and belching are a different problem. They often belong to the same picture.

What does not belong is everything that takes place below the navel. Abdominal pain that changes with the bowel movement belongs in another category. That is irritable bowel syndrome, and having both together is still common.

Air in the belly also has an article of its own, because it often has quite different roots than upper abdominal pressure. If a bloated belly is what mainly troubles you, this may take you further: where the air comes from.

Reframe

Many people try to press themselves into a single label. Functional dyspepsia or irritable bowel syndrome. Reflux or functional dyspepsia. Either or.

The body does not work with drawers. In disorders of gut brain interaction, overlap is the rule, not the exception. And now you know why your symptoms do not keep to the chapter boundaries of the guidebooks.

What happens in the body: the fundus, the volume and the duodenum

If you want to know why three bites are enough, you need to know a reflex that hardly anyone has ever heard of.

The stomach is not a rigid sack. Its upper part, the fundus, relaxes while you eat and makes room before anything arrives. This is called accommodation. A good host clears the hallway before the guests come.

When this reflex turns out too weak, the food arrives in a space that has not grown yet. Pressure rises immediately, and satiation reports in far too early.

Barostat, n=75 40 percent make too little room

Jan Tack and colleagues measured in Leuven with a gastric barostat how strongly the stomach adapts to a meal in 35 healthy people and 40 people with functional dyspepsia.

In 40 percent of the patients, accommodation was impaired. In the analysis a single symptom remained linked to this finding: early satiation. Not gastric emptying, not Helicobacter, not pain sensitivity.

For you this means: if you are full after three bites, that is often not a problem in your head. It is a reflex that comes out too quietly.

Tack J, Piessevaux H, Coulie B, Caenepeel P, Janssens J. Gastroenterology. 1998;115(6):1346-1352. PMID: 9834261 · DOI: 10.1016/s0016-5085(98)70012-5 [Cohort, n=75]

The second mechanism concerns not the space but the volume. Every stomach reports distension to the brain. In some people the dial for that report is turned up. The same portion, a different experience.

Barostat, n=240 34 percent hear the report too loudly

The same research group examined 80 healthy people and 160 people with functional dyspepsia in the barostat for their sensitivity to gastric distension.

34 percent reacted hypersensitively. They did not differ from the others in age, sex or the remaining measurements. The hypersensitivity was linked to pain after eating, to belching and to weight loss.

For you this means: the stomach is not damaged. The message it sends arrives louder than in other people. That is physiology, not a question of character.

Tack J, Caenepeel P, Fischler B, Piessevaux H, Janssens J. Gastroenterology. 2001;121(3):526-535. PMID: 11522735 · DOI: 10.1053/gast.2001.27180 [Cohort, n=240]

And gastric emptying? It stands at the very front of almost every guidebook and deserves a place, but not the first one. A meta-analysis of 25 evaluable studies with more than 6,000 participants found only loose associations where measurement technique was clean: nausea with an odds ratio of 1.6, vomiting 2.0, abdominal pain 1.5, early satiation and fullness 1.8.

Translated: slow gastric emptying can contribute to your symptoms. It does not explain them on its own.

And now the part that turns the matter around

The most interesting trail of the last decade and a half does not lead into the stomach. It leads one step further, into the duodenum.

That is the roughly 25 centimetre passage behind the stomach outlet. This is where the food pulp lands first, this is where it is measured how acidic and how fatty it is. From there the signals go back that determine how quickly the stomach passes things on and when satiation is reported.

So the duodenum is the control room, the stomach is the waiting room. And in this control room, in a subset of those affected, something turns up that you would not expect there.

Case control, n=1,001 Odds ratio 11.7

Nicholas Talley and Marjorie Walker examined a random sample of the Swedish adult population. 1,001 people underwent endoscopy, 51 with non ulcer dyspepsia were compared with 48 randomly chosen controls. Two blinded observers counted eosinophils at five sites.

Where the eosinophil count in the duodenal bulb was high, that is in the first section directly behind the stomach, the odds ratio for dyspepsia was 11.7 (95 percent confidence interval 3.9 to 34.9), adjusted for age, sex and Helicobacter. In the descending section it was 7.3 (2.9 to 18.1). In the stomach itself the eosinophils were not raised. And early satiation in particular was linked to this finding.

For you this means: there was something to find. Just not where the camera was looking, and not with the naked eye.

Talley NJ, Walker MM, Aro P, Ronkainen J, Storskrubb T, Hindley LA, Harmsen WS, Zinsmeister AR, Agréus L. Clin Gastroenterol Hepatol. 2007;5(10):1175-1183. PMID: 17686660 · DOI: 10.1016/j.cgh.2007.05.015 [Cohort, n=1,001]

Eosinophils are white blood cells from the parasite defence and allergy department. They do not indicate a wound, they indicate an immune system that is busy at this spot. Quietly, but persistently.

In the same Swedish sample a clean difference showed up: in functional dyspepsia the eosinophils were raised, in irritable bowel syndrome the mast cells were. Two related pictures, two different cell types. More on mast cells is in the article on mast cell activation.

Ex vivo, n=30 The barrier is more permeable, measured

Hanne Vanheel and a Belgian, Swedish and Spanish team took duodenal biopsies from 15 people with functional dyspepsia and 15 healthy comparison persons and mounted them in Ussing chambers.

In the patients, the electrical resistance of the tissue was lower and the passage between the cells was increased. The connecting proteins between the cells were altered. In addition, more mast cells and eosinophils were found as a sign of low grade inflammation. The authors write explicitly that this calls into question the old paradigm that functional dyspepsia goes without structural changes.

For you this means: a more permeable barrier plus quiet immune activity, measured rather than assumed. What the concept of a permeable gut barrier means overall is described in detail under leaky gut and zonulin.

Vanheel H, Vicario M, Vanuytsel T, Van Oudenhove L, Martinez C, Keita ÅV, Pardon N, Santos J, Söderholm JD, Tack J, Farré R. Gut. 2014;63(2):262-271. PMID: 23474421 · DOI: 10.1136/gutjnl-2012-303857 [Cohort, n=30]
The counter finding that belongs here

A Mayo Clinic cohort did not find the cells

A team at the Mayo Clinic examined 40 people with functional dyspepsia against 24 controls. Gene expression of the barrier proteins was moderately reduced, by a factor of 0.8 to 0.85, and the lactulose mannitol ratio was increased. So the barrier findings were confirmed.

But: eosinophils, mast cells and intraepithelial lymphocytes did not differ significantly between the groups. Neither did tissue resistance and the spacing between cells.

The 2025 review names an impaired duodenal barrier and duodenal immune activation as the most consistent findings, yet states the contradictions between studies openly. What stays honest: a robust trend, not a finished picture.

Puthanmadhom Narayanan S, O'Brien DR, Sharma M, Smyrk TC, Graham RP, Grover M, Bharucha AE. Clin Gastroenterol Hepatol. 2022;20(5):1019-1028. PMID: 34607017 · DOI: 10.1016/j.cgh.2021.09.029 [Cohort, n=64]
Important against misunderstandings

Duodenal eosinophilia is not a test you can order. There is no accepted counting threshold for everyday clinical work, the counts come from study protocols, and as you saw above, they do not replicate in every cohort.

It is a research finding that explains why the old formula of a purely functional complaint was too narrow. It is not more than that today.

Mechanism, as I put it together

From the stimulus in the duodenum to the pressure in the upper abdomen

  1. Trigger in the gut lumen. Acid, bile salts, food components or the remnants of an infection meet the lining of the duodenum. These candidates are documented as candidates, not as a cause.
  2. The barrier gives way. Connecting proteins between the cells change, the passage between the cells increases. Measured in tissue chambers and with sugar tests.
  3. The immune system moves in. Eosinophils and mast cells gather and release messengers. This is not an inflammation you can see, it is one you have to count.
  4. The nerves report more loudly. Messengers from these cells sit close to the nerve endings. The threshold above which distension counts as unpleasant drops.
  5. The stomach reacts. Via reflex arcs back from the duodenum, accommodation and emptying change. The fundus makes less room, satiation comes earlier.

Placing this: steps 2 and 3 are measured in humans, with the contradictions named above. Steps 1, 4 and 5 are mechanistically plausible, but the continuous causal chain has not been proven in humans. The 2020 review states exactly that.

The core sentence of this section

Three things are measurably different in functional dyspepsia: how much room the stomach makes, how loudly it reports, and how tight the duodenum is. And now you know why a camera that only looks at the surface cannot see any of that.

When it started after an infection, and what stress has to do with it

There is a sentence I often hear in my consultations, usually half apologetically: ever since that stomach bug two years ago it has never fully gone away. People say it quietly, because they suspect it sounds like an excuse. It is not an excuse, it is a described pattern with a number attached.

Meta-analysis, k=19 9.55 percent after the infection

Seiji Futagami and colleagues pooled 19 studies in which people were followed up after an acute gastrointestinal infection.

In 9.55 percent functional dyspepsia was present afterwards, that is 909 cases among 9,517 infections. The pooled odds ratio compared with controls from the same population was 2.54 (95 percent confidence interval 1.76 to 3.65), measured more than six months after the infection. The studies differed markedly from one another, with heterogeneity of just under 73 percent. So the direction is clear, the exact size of the number less so. Pathogens named: salmonella, E. coli O157, Campylobacter jejuni, Giardia lamblia, norovirus.

For you this means: if your gut was never the same after an infection, you are not alone with that and you did not invent it.

Futagami S, Itoh T, Sakamoto C. Aliment Pharmacol Ther. 2015;41(2):177-188. PMID: 25348873 · DOI: 10.1111/apt.13006 [Meta-analysis, k=19]

For comparison: for post infectious irritable bowel syndrome the same odds ratio was 3.51. The details are in the article on irritable bowel syndrome.

And then there is the question almost everyone gets asked at some point, usually in a friendly tone that still stings: could this not be psychological? I answer it with two studies that point in different directions. Both are well done, both are true.

Cohort, 10 years, n=703 First the anxiety, then the stomach

Peter Aro and colleagues invited participants of the Swedish Kalixanda study back ten years after their endoscopy. 703 of 887 responded.

Marked anxiety at baseline was linked to new onset functional dyspepsia ten years later, with an odds ratio of 7.61. The confidence interval is very wide, 1.21 to 47.73 as a 99 percent interval, but the direction is clear.

In a separate analysis of the same work, the link with anxiety showed up only for the meal related type, with odds ratios of 4.83 at baseline and 8.12 at follow up, and not for epigastric pain syndrome. Depression was not predictive in either analysis.

For you this means: tension can precede this pattern. In a subgroup, not in everyone.

Aro P, Talley NJ, Johansson SE, Agréus L, Ronkainen J. Gastroenterology. 2015;148(5):928-937. PMID: 25644097 · DOI: 10.1053/j.gastro.2015.01.039 [Cohort, n=703]
Cohort, 12 years, n=1,775 And in others exactly the other way round

Natasha Koloski and Nicholas Talley followed an Australian random sample over twelve years.

Those who had no functional gastrointestinal disorder at baseline but higher anxiety scores developed one more often. Conversely the same held: those who had normal anxiety and depression scores at baseline but already had a functional disorder had significantly higher anxiety and depression scores twelve years later.

For you this means: the path runs in both directions. In some it starts in the head, in some in the gut. Both are documented, and neither is your fault.

Koloski NA, Jones M, Kalantar J, Weltman M, Zaguirre J, Talley NJ. Gut. 2012;61(9):1284-1290. PMID: 22234979 · DOI: 10.1136/gutjnl-2011-300474 [Cohort, n=1,775]
Reframe

Psychosomatic is often used as a polite paraphrase for invented. That is wrong, and wrong in both directions.

The connection between gut and brain is an anatomical line, not a metaphor. It transmits in both directions. If your gut reacts to tension, that is no proof that nothing is there. It is proof that the line works. How this axis operates is described in detail under gut brain axis and vagus nerve.

And now you know why the question about the psyche is neither an insult nor an explanation. It is one of several trails, and it does not rule out the others.

What else it can be: the honest differential

Before functional dyspepsia goes on the label, other things have to be ruled out. Not all of them are rare, and some are regularly confused. I go through the list briefly, each topic with two sentences and a link.

This stands above the whole list

If it is acute, it is not functional dyspepsia

If the pain comes on suddenly and severely. If it pulls into the arm, jaw or back. If breathlessness, cold sweat, nausea or a sense of dread come with it. Or if the abdomen becomes board hard.

A heart attack, unstable angina, a perforated ulcer, acute pancreatitis and vascular emergencies such as an abdominal aortic aneurysm can feel exactly like pressure or burning in the upper abdomen. In women, in people with diabetes and in older age this atypical form is not rare.

In that case please call the emergency number immediately, 112 in Germany, and do not wait to see whether it gets better. Not even if you already have the diagnosis of functional dyspepsia. A known functional dyspepsia does not protect you from something acute on top of it.

Differential diagnosis

What else presses and burns in the upper abdomen

Reflux disease
When acid rises into the oesophagus, it burns behind the breastbone, often when lying down. Functional dyspepsia and reflux overlap frequently. More under heartburn and acid blockers.
Gastric ulcer and duodenal ulcer
An ulcer is visible at endoscopy and rules out the diagnosis of functional dyspepsia. That is exactly why the examination was so important.
Helicobacter pylori
The bacterium belongs in the workup of dyspepsia, because eradication can reduce symptoms in a subset of those affected. The numbers are further down, everything else under Helicobacter pylori.
Biliary tract
Gallstones typically cause colic, that is attacks of pain in the upper right, often after fatty food. An ultrasound scan clarifies this quickly, more on the topic under bile and bile acids.
Pancreas
Chronic inflammation causes belt like pain, fatty stools and weight loss. A different picture that needs to be examined specifically.
Painkillers of the NSAID type
In the large meta-analysis, regular use was linked to dyspepsia with an odds ratio of 1.59. Whether long term medication still fits is discussed medically and never changed on your own.
Coeliac disease
Coeliac disease can present with upper abdominal symptoms and is then easily overlooked. More under recognising coeliac disease.

This list does not replace an examination. It is meant to help you ask more precise questions at your next appointment.

The most important precaution in this field

If you are considering testing for coeliac disease, do not eat gluten free beforehand. Both the antibodies in the blood and the tissue sample need an ongoing gluten intake to be usable.

Anyone who eats gluten free for weeks and then gets tested may receive a normal result and know less afterwards than before. This is the most common practical mistake with this topic. What gluten can trigger without coeliac disease being present is described under gluten without coeliac disease.

Functional dyspepsia and gastroparesis: the border is more permeable than assumed

Gastroparesis is delayed gastric emptying as a condition in its own right. It has an article of its own: gastroparesis, when the stomach is too slow. Only one number belongs here, and it leaves many people speechless.

Registry, 48 weeks, n=944 42 percent switch diagnosis

Pankaj Pasricha and an American multicentre consortium followed 944 people with chronic upper abdominal symptoms over 48 weeks. Classification was based on a gastric emptying test.

After 48 weeks, 42 percent of those initially classified as gastroparesis were reclassified as functional dyspepsia, and 37 percent the other way round. Symptoms did not change accordingly. In full thickness biopsies both groups showed the same loss of interstitial cells of Cajal, that is the pacemaker cells of the stomach muscle.

For you this means: a single gastric emptying test is a snapshot, not a label for life. And in specialist centres the two diagnoses are closer to each other than their names suggest.

Pasricha PJ, Grover M, Yates KP et al. Gastroenterology. 2021;160(6):2006-2017. PMID: 33548234 · DOI: 10.1053/j.gastro.2021.01.230 [Cohort, n=944]
Reframe

A list of differentials sounds like bureaucracy. It is however the part that protects you.

Every diagnosis that is cleanly ruled out is a treatment you are spared. And now you know why a careful differential is more work than a quick diagnosis: it is the precondition for the words functional dyspepsia to mean anything at all.

What the diagnostics can do and where they stop

Does everyone with upper abdominal pain really need a gastroscopy? This is one of the most frequently asked questions, and the answer is uncomfortable because it comes in two parts.

No, not everyone. And yes, some absolutely and quickly.

The guidelines tie this distinction to two things: to the red flags and to age. Both together, not one alone. And there is a very good reason for that.

Meta-analysis, k=15 Why red flags alone are not enough

Nimish Vakil and colleagues evaluated 15 cohort studies with a total of 57,363 people in whom red flags were compared with the actual endoscopy result.

458 people, that is 0.8 percent, had a tumour. The sensitivity of the red flags varied between 0 and 83 percent depending on the study, the specificity between 40 and 98 percent. Clinical judgement by the doctor was highly specific but not very sensitive.

For you this means: red flags are a coarse sieve, not a test. Their presence is a clear reason for assessment. Their absence is not an all clear for every individual case, and that is exactly why the guidelines combine them with age thresholds.

Vakil N, Moayyedi P, Fennerty MB, Talley NJ. Gastroenterology. 2006;131(2):390-401. PMID: 16890592 · DOI: 10.1053/j.gastro.2006.04.029 [Meta-analysis, k=15]

The American and Canadian guideline recommends endoscopy from the age of 60, earlier where the risk of stomach cancer is raised. The 2020 Lancet seminar names 55 years or concerning features. The European consensus considers endoscopy obligatory for a secure diagnosis, but regards a treatment trial without endoscopy as defensible in primary care when there are no red flags. The German guideline of 2025 makes it dependent on severity, duration and red flags.

What a sensible workup typically contains

  • A careful history. Coupled to the meal? When did it start? Was there an infection before? Which medications are running?
  • The red flag question. Asked systematically, not in passing.
  • A Helicobacter test. The European consensus recommends determining the status in every affected person.
  • Basic laboratory tests. Blood count, inflammatory markers, liver and pancreatic values, coeliac serology, depending on the picture. Important with coeliac serology: it needs an ongoing gluten intake. Eating gluten free beforehand can make the test unusable.
  • An abdominal ultrasound. It clarifies biliary tract, liver and pancreas within minutes.
  • An endoscopy according to age, severity and red flags. The decision for or against it belongs in medical hands, not in a blog article.
Mandatory sentence

Nothing in this section implies that a recommended examination should be skipped. A recommended gastroscopy is not postponed and not replaced, neither by supplements nor by dietary change nor by waiting.

This section describes why not every person with upper abdominal pressure needs a camera straight away. It does not describe how to sidestep a recommendation.

What I observe clinically

Two questions before I give anything

The first question is always whether the red flags have been asked about cleanly and the necessary workup has taken place. Without that foundation, everything else has no ground under it.

The second question sounds surprising to some: is there actually enough stomach acid up there? Before I think about enzymes, plants or dietary changes, this order interests me, because in my experience it can change the steps that follow. What lies behind it, and why low acid causes different symptoms than many expect, is described under low stomach acid and betaine HCl.

Honesty requires this: that is my clinical order, not a guideline recommendation. It is not proven. I did not find solid randomised evidence on digestive enzymes in functional dyspepsia in this search. For placing enzymes: when they make sense.

And a warning that belongs with it: acid containing preparations such as betaine HCl do not belong in a self experiment as long as an ulcer or an irritated lining has not been ruled out. They can make symptoms worse in that situation. The same applies while painkillers of the NSAID type are being taken. This belongs in a medical conversation beforehand, not afterwards.

Reframe

Many people measure the value of a workup by how much it finds. I measure it by how much it puts in order.

And now you know why the diagnostics in functional dyspepsia have two jobs: they rule out what is dangerous, and then they deliberately stop. The next examination is not automatically the better answer.

What has been tested in studies, with the numbers behind it

Now comes the part where many guidebooks turn vague. They write that something is effective and leave open how effective. I consider these numbers important, because they protect you from two disappointments: from the fact that a medication does not do everything, and from throwing away something usable too early.

The number that carries the most weight here is called number needed to treat, NNT for short. It says: this many people have to be treated for one additional person to benefit. The smaller the number, the larger the effect.

Numbers from randomised trials and meta-analyses in functional dyspepsia. None of these figures is a recommendation for you personally.
ApproachData baseEffectPlacing it
Helicobacter eradication29 RCTs, 6,781 peopleNNT 9 for improvement, 14 for symptom freedom, 4.5 where the bacterium was actually clearedhigh evidence quality, modest benefit, no repetition needed
Proton pump inhibitors25 RCTs with 8,453 people, of which 18 RCTs with 6,172 people against placeboNNT 11 in the placebo comparisonmoderate quality, low and standard doses were analysed combined
Prokinetics29 RCTs against placeboNNT 7GRADE very low, heterogeneity 91 percent, quality of life unchanged
Neuromodulators13 RCTs, 1,241 peopleNNT 6benefit only with tricyclics and antipsychotics, side effects more frequent
Herbal combinationseveral RCTs, 120 to 315 peoplesignificant, but small differences from placebomostly manufacturer linked trials, inconsistent composition
Psychological approaches9 small RCTsstandardised mean difference minus 1.33high risk of bias, only 3 trials with a sham arm

Helicobacter pylori: a small effect that can last

Meta-analysis, k=29 One in nine

Alexander Ford and colleagues pooled 29 randomised trials with 6,781 Helicobacter positive people with functional dyspepsia.

Eradication was superior to the control arm: NNT 9 for an improvement, NNT 14 for symptom freedom. Where eradication had actually succeeded, the NNT was 4.5. Side effects were more than twice as frequent, as were dropouts because of them. The authors rate the evidence quality as high and the benefit as modest.

For you this means: out of nine people with functional dyspepsia and a positive test, one additional person benefits on paper. That is small, it is real, and unlike long term medication a successful eradication does not have to be repeated. How long the benefit lasts beyond the follow up periods of these trials is not documented.

Whether eradication makes sense in your case is decided by a medical judgement, not by this text. Declining a recommended eradication or stopping a course of antibiotics early would not be a good idea: with Helicobacter more is at stake than upper abdominal pressure, among other things gastric ulcers and the risk of stomach cancer. What is known about this is described in detail under Helicobacter pylori.

Ford AC, Tsipotis E, Yuan Y, Leontiadis GI, Moayyedi P. Gut. 2022;71(10):1967-1975. PMID: 35022266 · DOI: 10.1136/gutjnl-2021-326583 [Meta-analysis, k=29]

Acid blockers: a small effect, surprising details

Cochrane, k=25 NNT 11, and the dose was not the lever

Maria Ines Pinto-Sanchez and colleagues evaluated 25 randomised trials with 8,453 participants for Cochrane. For the direct comparison with placebo, 18 of those trials with 6,172 people were available.

There, proton pump inhibitors were superior to placebo, with an NNT of 11 at moderate evidence quality. Low and standard doses worked so similarly that the authors combined them for the analysis. The review therefore did not answer a dedicated dose response question. Compared with H2 blockers there was hardly any difference. And no difference by Rome III subgroup was found, nor by Helicobacter status, country of origin or accompanying reflux symptoms.

For you this means: acid blockers can do something for a subset of those affected, and more dose does not automatically bring more effect. What that means for your ongoing therapy belongs in the next consultation and not in a self experiment.

Pinto-Sanchez MI, Yuan Y, Hassan A, Bercik P, Moayyedi P. Cochrane Database Syst Rev. 2017;11(11):CD011194. PMID: 29161458 · DOI: 10.1002/14651858.CD011194.pub3 [Meta-analysis, k=25]
The contradiction I do not dissolve

Guideline logic against Cochrane data

In almost every text it says: acid blockers for the pain type, prokinetics for the fullness type. That is clinically plausible, it appears in that or a similar form in guidelines, and many experienced colleagues work with it.

Only, the Cochrane review found no difference by subgroup. Both statements stand next to each other in the room, and I do not think much of brushing one of them away.

I read it like this: the assignment is a useful ordering aid, but not a secure prediction of who responds to what. Knowing this makes the disappointment smaller when the theoretically fitting medication does nothing.

And then there is a finding on acid blockers that makes the matter more complicated.

Intervention, n=75 Down in patients, up in healthy people

Lucas Wauters and a team in Leuven gave 30 healthy people and 27 untreated people with functional dyspepsia a proton pump inhibitor for four weeks and examined the duodenum before and after.

In the patients, symptoms, duodenal eosinophils, mast cells and permeability went down. In the healthy people, immune cells and permeability went up under the same medication, together with changes in bile salts. Symptoms correlated with the eosinophil count.

For you this means: acid blockers might do more in functional dyspepsia than just dampen acid. And at the same time this is an argument for not regarding long term use in people without a finding as harmless.

Important so this paragraph does not land wrongly: it is not a reason to stop or reduce an acid blocker you are taking. For many people there are good reasons for this medication, for instance reflux disease, an ulcer that has since closed up or gastric protection alongside painkillers. Whether long term therapy still fits is a question for the next consultation, and abrupt discontinuation can be followed by increased acid production for a few days. This question belongs under medical guidance.

Wauters L, Ceulemans M, Frings D et al. Gastroenterology. 2021;160(5):1521-1531. PMID: 33346007 · DOI: 10.1053/j.gastro.2020.12.016 [Cohort, n=75]

Prokinetics: the best number on the weakest foundation

Prokinetics are meant to stimulate gastric movement. The meta-analysis of 29 placebo controlled trials names an NNT of 7, independent of subgroup and origin. Sounds good. Then come the limitations: heterogeneity of 91 percent, a GRADE rating of very low, and quality of life did not improve alongside. A number you cannot feel in everyday life is a difficult number.

On top of that comes a second point that does not show up in the bare NNT. These substances are prescription only, and some of them have received restrictions on use that have to do with heart rhythm and the nervous system. So the same applies here as to everything else in this section: start, duration and end belong in medical hands, not in a self experiment.

Neuromodulators: the biggest misunderstanding

When a low dose antidepressant is suggested after several attempts, many people hear something other than what is meant. They hear: you are depressed, and your gut is imagined.

Something else is meant. At low doses, tricyclic substances intervene in pain processing, at the nerve pathways between gut and brain. That is why they are called neuromodulators here.

RCT, n=292 53 against 40 against 38 percent

Nicholas Talley and eight North American centres randomised 292 people with functional dyspepsia over ten weeks to placebo, amitriptyline 50 milligrams or escitalopram 10 milligrams. People with depression and people on antidepressants were excluded.

Adequate relief was reported by 40 percent on placebo, 53 percent on amitriptyline and 38 percent on escitalopram. In the pain predominant type, amitriptyline was more than three times superior to placebo (odds ratio 3.1). Those with delayed gastric emptying responded less well (odds ratio 0.4). Gastric emptying itself did not change under either substance.

Two limitations belong with this. The primary endpoint sat exactly on the significance threshold at P equals 0.05. And the trial ran on the older Rome II criteria, so its pain predominant type is not identical with epigastric pain syndrome under Rome IV.

For you this means: the substance was not aimed at mood here, because people with depression were not even included. And the 40 percent on placebo explain why anecdotal reports say so little in this field.

Talley NJ, Locke GR, Saito YA et al. Gastroenterology. 2015;149(2):340-349. PMID: 25921377 · DOI: 10.1053/j.gastro.2015.04.020 [RCT, n=292]
The frame that belongs with these substances

Prescription only, outside the licence, and with real risks

Amitriptyline and escitalopram are prescription only. The milligram figures named above are trial data and not a recommendation.

In functional dyspepsia these substances are used in Germany outside their licence, that is off label. This requires particular medical explanation and makes reimbursement uncertain.

Tricyclics such as amitriptyline can cause dry mouth, constipation, tiredness, a drop in blood pressure on standing and heart rhythm disturbances including QT prolongation. They do not fit with narrow angle glaucoma, with an enlarged prostate with residual urine or urinary retention, or with certain heart conditions. In older age the risk of falls and confusion can rise. Combined with other serotonergic agents, interactions are possible. Pregnancy and breastfeeding call for a separate judgement.

Whether such an attempt fits for you is decided by a medical examination, not by this text.

The meta-analysis of 13 trials with 1,241 people names an NNT of 6, with the benefit limited to tricyclics and antipsychotics. And it is honest: looking only at the trials that had excluded people with an accompanying affective disorder, no benefit remained. Side effects were more frequent, with a number needed to harm of 21.

Reframe

In this condition a neuromodulator is not a verdict on your psyche. It is an attempt to lower the volume of the message described further above.

I say this so plainly because this misunderstanding keeps many people away from an option that is among the better documented ones in studies. Whether it fits in an individual case is decided by a medical judgement with an eye on side effects, other medications and comorbidities. It is neither started nor stopped on its own.

Plants: several studies, small effects, honest limitations

Two plant routes have been studied in randomised form. One is the set combination of peppermint oil and caraway oil in enteric coated capsules. In a trial with 96 people, pain intensity fell by 40 percent after 28 days compared with 22 percent on placebo. In a newer trial with 114 people the combination was better than placebo in both subgroups.

A note that belongs with this combination

It is not suitable for everyone

With gallstones, with an obstruction of the bile ducts, with inflammation of the gallbladder and with severe liver disease it should not be used. It is not intended for children, and for pregnancy and breastfeeding solid data are missing. Peppermint oil can make heartburn worse in some people.

That matters particularly here. Gallstones can press on the same upper abdomen as functional dyspepsia, and they sit further up in the differential list. So the workup belongs before the attempt and not after it.

The other route is herbal combination preparations made from several extracts. In a multicentre trial with 315 people the difference from placebo was significant but small: 6.9 versus 5.9 points in the symptom score. In a smaller trial with 120 people and a six plant variant, after eight weeks 43.3 percent on the active preparation and 3.3 percent on placebo reported symptom freedom.

What the efficacy figures do not replace

Herbal does not mean free of side effects

The nine plant mixture tested in that trial contains greater celandine. Whether your own preparation contains it is stated in the package leaflet. For preparations containing greater celandine, liver injury has been described. The German medicines agency BfArM ran a graduated plan procedure on this and ordered warnings in 2018.

If you take such a preparation and notice tiredness, dark urine, pale stools or a yellowing of skin or eyes, stop taking it and have your liver values checked. Whether such a remedy fits for you belongs in a medical conversation beforehand, particularly if you take other medicines or a liver condition is known.

Why a mixture can act in opposite ways at two sites of the stomach has been shown by a tissue study: in guinea pig preparations the mixture relaxed the upper part of the stomach and at the same time increased movement in the outlet region. That is tissue in the laboratory, not a human being. Such findings explain, they document nothing for your everyday life.

Why the caution elsewhere has good reasons

German guideline and European consensus disagree here

The German S1 guideline places phytotherapeutics further forward than the American guideline and the European consensus do. In the European Delphi round with 41 experts, no therapy other than acid blockers and eradication reached agreement above 80 percent.

This is not an ideological dispute. The reasons for the caution are understandable: the trials are mostly manufacturer linked, the effect sizes small, and the preparations differ in their composition. Anyone who knows these reasons can make their own decision instead of having to choose between two camps.

Psychological approaches and the microbiome hint

Nine small randomised trials on psychological approaches give a standardised mean difference of minus 1.33. That looks large. Only three had a sham treatment arm, the risk of bias is correspondingly high, and the Lancet seminar explicitly calls the role of these approaches uncertain.

Best studied is gut directed hypnosis. In a trial with 126 people, the symptom score fell in the long term by a median of 73 percent under hypnosis, and by 43 percent under standard drug treatment. That is the size of the change, not the proportion of people who got better. And of the 126 randomised, only 79 completed all phases, which puts the numbers into perspective further. Striking: in the hypnosis group nobody started medication during follow up, in the comparison groups 82 and 90 percent did. Something like this can hardly be blinded. More under gut directed hypnotherapy.

And a single finding on the microbiome: in a study from Hong Kong with 86 people meeting Rome III criteria, after eight weeks 78 percent on rifaximin compared with 52 percent on placebo reported adequate relief, more markedly in women than in men. One centre, no replication.

The frame belongs with it: rifaximin is prescription only and licensed in Germany for hepatic encephalopathy and travellers diarrhoea, not for functional dyspepsia. Use here would be off label. And every course of antibiotics brings its own risks, among them diarrhoea caused by Clostridioides difficile and the development of resistance. So this is a hint, not a recommendation, and nothing for a self experiment. On small intestinal bacterial overgrowth in general: SIBO.

The core sentence of this section

All the tested approaches together give an honest picture: small, real effects and a high placebo rate. And now you know why treatment here means guided trial and error, not an off the shelf prescription.

What everyday life can contribute, without building yourself a list of bans

At some point almost everyone reaches the moment when the list of deleted foods is longer than the list of allowed ones. And the belly is still not quiet.

I consider this path one of the most damaging in functional complaints. It costs joy, social life and nutrients and often brings less than one single targeted change. What do the data say? Less than the guidebooks suggest.

Systematic review, k=16 Fat is the best supported trigger

Kerith Duncanson and colleagues searched six databases and found 16 of 6,451 screened studies that had examined the connection between food and functional dyspepsia.

Dietary fat was linked to symptoms in all three studies that examined it specifically. Wheat containing foods were involved in six studies. Caffeine was associated in four studies. The connection with alcohol remained explicitly unclear. The authors call for randomised trials on gluten, FODMAP and fat.

For you this means: if you can only change one thing, the fat content of the meal is the best supported lever. Not giving up everything.

And one rule of sequence about wheat, before you try anything: if coeliac disease has not been assessed yet, the testing comes before the avoidance. A gluten free diet before the test can make the coeliac diagnosis impossible, because antibodies and tissue sample may then come out normal although the condition is present.

Duncanson KR, Talley NJ, Walker MM, Burrows TL. J Hum Nutr Diet. 2018;31(3):390-407. PMID: 28913843 · DOI: 10.1111/jhn.12506 [Systematic Review]

The alcohol finding is remarkable. Almost every guidebook names it as a trigger, the systematic review classifies the data as unclear. That does not mean alcohol is harmless. It only means the studies do not carry that statement. What else it can do in the gut is described under alcohol and the gut.

And why are dietary statements in functional complaints so wobbly? A second paper by the same group examined 40 studies for whether the recording period for food and the one for symptoms match at all. In 10 percent they did not match at all. And only 12 of 40 studies used a validated instrument for symptom recording.

So the problem often lies in the methodology, not on the plate. That is why I consider your own carefully kept diary more informative than a general list. This has not been compared, it is my conclusion from the criticism of the survey methods.

Six directions, not instructions

  • Portion size before food selection. Distension is the most direct stimulus. Smaller portions act exactly where accommodation and sensitivity sit.
  • Watch the fat content. The best supported association in the systematic review. It is about the amount per meal, not about fat as an enemy.
  • Eating pace. Eating fast may fill the space faster than the fundus can open it. I did not come across studies on eating pace in functional dyspepsia in this search, the thought follows from what we know about accommodation. Trying it costs nothing.
  • Test coffee, do not delete it. Associated in four studies. Whether it applies to you is shown better by two weeks of observation than by any rule.
  • Sleep. Solid intervention trials on this in functional dyspepsia are missing. Sleep and gut in general: sleep and the microbiome.
  • Load. Not as an accusation, but as a factor influencing sensitivity. Mind body approaches stand next to the medications in the German guideline.
Reframe

A dietary change in functional complaints has two possible outcomes. Either you find your triggers. Or you find out that it is not the food.

Both are a result. The second is often the more relieving one, because it releases you from an endless search. And now you know why I am reluctant to start with a deletion list and prefer to start with two weeks of honest observation.

Common questions about functional dyspepsia

These are the questions I hear most often, in the consultation room and in letters. The answers draw on the sources at the end of this article.

I had a gastroscopy and everything was fine. Why do I still have symptoms?

Because endoscopy looks for what is visible: ulcers, inflammation, tumours. Functional dyspepsia sits in the control of distension, sensitivity and mucosal barrier. Around 80 percent of people with dyspepsia have no structural explanation, according to the 2020 Lancet review. So a normal result does not mean nothing is there. It means the dangerous causes have been ruled out.

What is the difference between functional dyspepsia and gastritis?

Gastritis means inflammation of the stomach lining that can be seen under the microscope. In functional dyspepsia the stomach lining looks unremarkable on routine assessment. In everyday language the two terms blur, because many reports contain the word gastritis without a tissue sample backing it up. If no biopsy is mentioned in the report, it is worth asking.

What is the difference between functional dyspepsia and irritable bowel syndrome, and can you have both?

Functional dyspepsia sits in the upper abdomen, irritable bowel syndrome revolves around abdominal pain linked to bowel movement. Having both is common. In the Rome IV survey, irritable bowel syndrome and functional heartburn were particularly closely linked to the overlap variant. And in the same Swedish sample, functional dyspepsia came with more eosinophils, irritable bowel syndrome with more mast cells.

How do I tell whether I have the meal related type or the pain type?

The rule of thumb is the meal. Fullness after eating and early satiation point towards postprandial distress syndrome. Pain or burning independent of eating points towards epigastric pain syndrome. In the Rome IV survey, 61 percent had the first type, 18 percent the second, 21 percent both.

Why am I full after only a few bites?

The upper part of the stomach, the fundus, normally relaxes while you eat and makes room. In around 40 percent of people with functional dyspepsia examined with a barostat, this happened measurably too little, and early satiation in particular was linked to that finding. This is not a question of willpower, it is a reflex that comes out too quietly.

What does my duodenum have to do with it if my stomach is what hurts?

In a Swedish population sample, a high eosinophil count in the first part of the duodenum was linked to non ulcer dyspepsia with an odds ratio of 11.7. Belgian researchers measured a more permeable duodenal lining in biopsies. The duodenum helps steer gastric emptying, satiation and pain signalling. When it falls out of rhythm, the upper abdomen speaks up.

Can I have duodenal eosinophilia tested?

No, at least not as a routine examination. There is no accepted counting threshold for everyday clinical work, the findings come from study biopsies with standardised counting, and one Mayo Clinic cohort did not find the cell differences at all. This is a research finding, not a lab form you can order.

Does Helicobacter treatment do anything for functional dyspepsia?

Yes, and the effect is honestly small. 29 randomised trials with 6,781 people gave a number needed to treat of 9 for improvement and 14 for symptom freedom, and 4.5 where eradication actually succeeded. Side effects were more frequent. The decision belongs in medical hands, and a course of antibiotics that has been started is not stopped on your own.

Why do acid blockers do so little for me even though it burns?

The Cochrane review evaluated 25 trials with 8,453 participants. For the direct placebo comparison, 18 of those trials with 6,172 people were available, and there a real but small advantage showed up with a number needed to treat of 11. Low and standard doses worked so similarly that the authors combined them, and no difference by subgroup showed up. An ongoing therapy is not changed on your own but discussed with your doctor.

Why am I being offered an antidepressant when my problem is my stomach?

Because low dose tricyclics are used here as neuromodulators, that is as dampeners of pain processing, not as a mood medication. In the meta-analysis of 13 trials the number needed to treat was 6. In the large amitriptyline trial, people with depression were excluded, and the effect still showed. Whether this fits is a medical judgement.

Do peppermint oil and caraway oil help in functional dyspepsia, and what do the studies say?

Two randomised trials with 96 and 114 participants showed advantages over placebo. In the older one, pain intensity fell by 40 percent compared with 22 percent on placebo, in the newer one the combination was better in both subgroups. Enteric coated capsules are not a detail here: the oil is meant to be released only beyond the stomach. The other side matters too: with gallstones, bile duct obstruction, gallbladder inflammation or severe liver disease the combination should not be used, it is not intended for children, and peppermint oil can make heartburn worse.

What about the herbal combination preparations made of several plants?

For the well known nine plant preparation there are several randomised trials. In a multicentre trial with 315 people the difference from placebo was significant but small. A smaller trial with a six plant variant showed clearer numbers. Part of the picture: mostly manufacturer linked trials, differing compositions, no European consensus. And herbal does not mean free of side effects. For preparations containing greater celandine, liver injury has been described, and the German medicines agency BfArM ordered warnings on this. So use belongs in a medical conversation.

My symptoms started after a stomach bug. Is that a coincidence?

Probably not. A meta-analysis of 19 studies found functional dyspepsia in 9.55 percent of people after acute gastrointestinal infection, with an odds ratio of 2.54 compared with controls from the same population. The pathogens named were salmonella, campylobacter, giardia and norovirus. So your pattern has a number behind it.

Is functional dyspepsia psychological?

It is neither purely psychological nor purely physical. In a Swedish ten year cohort, marked anxiety at baseline predicted new onset functional dyspepsia, with an odds ratio of 7.61 and a very wide confidence interval. In a separate analysis of the same work, the link with anxiety showed up only for the meal related type. In an Australian twelve year cohort the path ran the other way round in a subset. Both directions are described, and neither is an accusation.

Functional dyspepsia or gastroparesis: how do you tell them apart?

Through gastric emptying, and the border is more permeable than many think. In a registry of 944 people, after 48 weeks 42 percent of those initially classified as gastroparesis were reclassified as functional dyspepsia, and 37 percent the other way round, without a matching change in symptoms. Both groups showed the same loss of pacemaker cells. More in the separate article on gastroparesis.

What should I change about eating first, if I can only change one thing?

According to the systematic review, dietary fat is the best supported trigger: in all three studies that examined it specifically, it was linked to symptoms. Portion size comes right after. And one firm precaution: eating gluten free before coeliac disease testing has been done can make the diagnosis impossible.

How long does functional dyspepsia last?

The course is usually chronic, with better and worse phases. The European consensus panel states explicitly that long term prognosis and life expectancy are favourable. That is not a way of playing it down, it is a relief: the condition can be very tiresome without being dangerous.

When do I definitely need to see a doctor?

With blood in the bowel movement, black tarry stool, vomiting blood, unintentional weight loss, fever, night time symptoms that wake you up, repeated vomiting, difficulty swallowing, a new persistent change in bowel habit from around 45 to 50 years of age, anaemia or a family history of bowel cancer, stomach cancer or inflammatory bowel disease. These red flags need medical assessment. And a recommended examination is not postponed and not replaced by anything in this text.

Where the upper abdomen connects to the rest of the body

Functional dyspepsia rarely stands alone. It hangs on nutrition, on sleep, on load, on other intolerances and on how the immune system in the gut is currently working. If you want to read further, these are the next sensible steps.

SJ

Shukri Jarmoukli

Physician · Area of focus: integrative medicine · ViveCura Berlin

I work in my private practice at the intersection of conventional medicine, functional medicine and clinical psychoneuroimmunology. In functional dyspepsia I am less interested in which preparation gets tried next, and more in which question stayed open before the next attempt.

My position in two sentences: functional dyspepsia does not mean that nothing was found, it means that the routine examination is not the tool with which this disturbance is seen. And before I give anything, two things get clarified: whether the red flags have been cleanly ruled out, and whether there is enough stomach acid up there.

This article does not replace medical advice and does not replace a recommended examination. It is meant to help you ask better questions. One more thing, because this text touches on mood and drive: if low mood will not let go of you, or you have thoughts of not wanting to live any more, please get medical or psychotherapeutic help soon. In Germany, Telefonseelsorge is available around the clock, free and anonymous, on 0800 111 0 111 or 0800 111 0 222. In an emergency, call 112.

ViveCura, Privatpraxis Shukri Jarmoukli, Skalitzer Straße 137, 10999 Berlin

Scientific sources

  1. Stanghellini V, Chan FKL, Hasler WL, Malagelada JR, Suzuki H, Tack J, Talley NJ. Gastroduodenal Disorders. Gastroenterology. 2016;150(6):1380-1392. PMID: 27147122 · DOI: 10.1053/j.gastro.2016.02.011 [Guideline]
  2. Storr M, Andresen V, Frieling T et al. S1-Leitlinie der Deutschen Gesellschaft für Neurogastroenterologie und Motilität (DGNM) zur funktionellen Dyspepsie (Reizmagen), einer Disorder of Gut-Brain Interaction (DGBI). Z Gastroenterol. 2025;63(4):403-422. AWMF register 175-001. PMID: 40199346 · DOI: 10.1055/a-2518-1430 [Guideline]
  3. Wauters L, Dickman R, Drug V et al. United European Gastroenterology (UEG) and European Society for Neurogastroenterology and Motility (ESNM) consensus on functional dyspepsia. United European Gastroenterol J. 2021;9(3):307-331. PMID: 33939891 · DOI: 10.1002/ueg2.12061 [Guideline]
  4. Moayyedi P, Lacy BE, Andrews CN, Enns RA, Howden CW, Vakil N. ACG and CAG Clinical Guideline: Management of Dyspepsia. Am J Gastroenterol. 2017;112(7):988-1013. PMID: 28631728 · DOI: 10.1038/ajg.2017.154 [Guideline]
  5. Ford AC, Mahadeva S, Carbone MF, Lacy BE, Talley NJ. Functional dyspepsia. Lancet. 2020;396(10263):1689-1702. PMID: 33049222 · DOI: 10.1016/S0140-6736(20)30469-4 [Mechanism Review]
  6. Aziz I, Palsson OS, Törnblom H, Sperber AD, Whitehead WE, Simrén M. Epidemiology, clinical characteristics, and associations for symptom-based Rome IV functional dyspepsia in adults in the USA, Canada, and the UK. Lancet Gastroenterol Hepatol. 2018;3(4):252-262. PMID: 29396034 · DOI: 10.1016/S2468-1253(18)30003-7 [Cohort, n=5,931]
  7. Ford AC, Marwaha A, Sood R, Moayyedi P. Global prevalence of, and risk factors for, uninvestigated dyspepsia: a meta-analysis. Gut. 2015;64(7):1049-1057. PMID: 25147201 · DOI: 10.1136/gutjnl-2014-307843 [Meta-analysis, k=100]
  8. Sperber AD, Bangdiwala SI, Drossman DA et al. Worldwide Prevalence and Burden of Functional Gastrointestinal Disorders, Results of Rome Foundation Global Study. Gastroenterology. 2021;160(1):99-114. PMID: 32294476 · DOI: 10.1053/j.gastro.2020.04.014 [Cohort, n=73,076]
  9. Tack J, Piessevaux H, Coulie B, Caenepeel P, Janssens J. Role of impaired gastric accommodation to a meal in functional dyspepsia. Gastroenterology. 1998;115(6):1346-1352. PMID: 9834261 · DOI: 10.1016/s0016-5085(98)70012-5 [Cohort, n=75]
  10. Tack J, Caenepeel P, Fischler B, Piessevaux H, Janssens J. Symptoms associated with hypersensitivity to gastric distention in functional dyspepsia. Gastroenterology. 2001;121(3):526-535. PMID: 11522735 · DOI: 10.1053/gast.2001.27180 [Cohort, n=240]
  11. Vijayvargiya P, Jameie-Oskooei S, Camilleri M, Chedid V, Erwin PJ, Murad MH. Association between delayed gastric emptying and upper gastrointestinal symptoms: a systematic review and meta-analysis. Gut. 2019;68(5):804-813. PMID: 29860241 · DOI: 10.1136/gutjnl-2018-316405 [Meta-analysis, k=25]
  12. Pasricha PJ, Grover M, Yates KP et al. Functional Dyspepsia and Gastroparesis in Tertiary Care are Interchangeable Syndromes With Common Clinical and Pathologic Features. Gastroenterology. 2021;160(6):2006-2017. PMID: 33548234 · DOI: 10.1053/j.gastro.2021.01.230 [Cohort, n=944]
  13. Talley NJ, Walker MM, Aro P et al. Non-ulcer dyspepsia and duodenal eosinophilia: an adult endoscopic population-based case-control study. Clin Gastroenterol Hepatol. 2007;5(10):1175-1183. PMID: 17686660 · DOI: 10.1016/j.cgh.2007.05.015 [Cohort, n=1,001]
  14. Walker MM, Talley NJ, Prabhakar M et al. Duodenal mastocytosis, eosinophilia and intraepithelial lymphocytosis as possible disease markers in the irritable bowel syndrome and functional dyspepsia. Aliment Pharmacol Ther. 2009;29(7):765-773. PMID: 19183150 · DOI: 10.1111/j.1365-2036.2009.03937.x [Cohort, n=1,001]
  15. Vanheel H, Vicario M, Vanuytsel T et al. Impaired duodenal mucosal integrity and low-grade inflammation in functional dyspepsia. Gut. 2014;63(2):262-271. PMID: 23474421 · DOI: 10.1136/gutjnl-2012-303857 [Cohort, n=30]
  16. Puthanmadhom Narayanan S, O'Brien DR, Sharma M et al. Duodenal Mucosal Barrier in Functional Dyspepsia. Clin Gastroenterol Hepatol. 2022;20(5):1019-1028. PMID: 34607017 · DOI: 10.1016/j.cgh.2021.09.029 [Cohort, n=64]
  17. Huyghe P, Ceulemans M, Keita ÅV et al. The Duodenal Microenvironment in Functional Dyspepsia. J Neurogastroenterol Motil. 2025;31(2):186-198. PMID: 40205896 · DOI: 10.5056/jnm24176 [Mechanism Review]
  18. Wauters L, Talley NJ, Walker MM, Tack J, Vanuytsel T. Novel concepts in the pathophysiology and treatment of functional dyspepsia. Gut. 2020;69(3):591-600. PMID: 31784469 · DOI: 10.1136/gutjnl-2019-318536 [Mechanism Review]
  19. Futagami S, Itoh T, Sakamoto C. Systematic review with meta-analysis: post-infectious functional dyspepsia. Aliment Pharmacol Ther. 2015;41(2):177-188. PMID: 25348873 · DOI: 10.1111/apt.13006 [Meta-analysis, k=19]
  20. Koloski NA, Jones M, Kalantar J, Weltman M, Zaguirre J, Talley NJ. The brain-gut pathway in functional gastrointestinal disorders is bidirectional: a 12-year prospective population-based study. Gut. 2012;61(9):1284-1290. PMID: 22234979 · DOI: 10.1136/gutjnl-2011-300474 [Cohort, n=1,775]
  21. Aro P, Talley NJ, Johansson SE, Agréus L, Ronkainen J. Anxiety Is Linked to New-Onset Dyspepsia in the Swedish Population: A 10-Year Follow-up Study. Gastroenterology. 2015;148(5):928-937. PMID: 25644097 · DOI: 10.1053/j.gastro.2015.01.039 [Cohort, n=703]
  22. Vakil N, Moayyedi P, Fennerty MB, Talley NJ. Limited value of alarm features in the diagnosis of upper gastrointestinal malignancy: systematic review and meta-analysis. Gastroenterology. 2006;131(2):390-401. PMID: 16890592 · DOI: 10.1053/j.gastro.2006.04.029 [Meta-analysis, k=15]
  23. Ford AC, Tsipotis E, Yuan Y, Leontiadis GI, Moayyedi P. Efficacy of Helicobacter pylori eradication therapy for functional dyspepsia: updated systematic review and meta-analysis. Gut. 2022;71(10):1967-1975. PMID: 35022266 · DOI: 10.1136/gutjnl-2021-326583 [Meta-analysis, k=29]
  24. Pinto-Sanchez MI, Yuan Y, Hassan A, Bercik P, Moayyedi P. Proton pump inhibitors for functional dyspepsia. Cochrane Database Syst Rev. 2017;11(11):CD011194. PMID: 29161458 · DOI: 10.1002/14651858.CD011194.pub3 [Meta-analysis, k=25]
  25. Pittayanon R, Yuan Y, Bollegala NP et al. Prokinetics for Functional Dyspepsia: A Systematic Review and Meta-Analysis of Randomized Control Trials. Am J Gastroenterol. 2019;114(2):233-243. PMID: 30337705 · DOI: 10.1038/s41395-018-0258-6 [Meta-analysis, k=29]
  26. Ford AC, Luthra P, Tack J, Boeckxstaens GE, Moayyedi P, Talley NJ. Efficacy of psychotropic drugs in functional dyspepsia: systematic review and meta-analysis. Gut. 2017;66(3):411-420. PMID: 26567029 · DOI: 10.1136/gutjnl-2015-310721 [Meta-analysis, k=13]
  27. Talley NJ, Locke GR, Saito YA et al. Effect of Amitriptyline and Escitalopram on Functional Dyspepsia: A Multicenter, Randomized Controlled Study. Gastroenterology. 2015;149(2):340-349. PMID: 25921377 · DOI: 10.1053/j.gastro.2015.04.020 [RCT, n=292]
  28. von Arnim U, Peitz U, Vinson B, Gundermann KJ, Malfertheiner P. STW 5, a phytopharmacon for patients with functional dyspepsia: results of a multicenter, placebo-controlled double-blind study. Am J Gastroenterol. 2007;102(6):1268-1275. PMID: 17531013 · DOI: 10.1111/j.1572-0241.2006.01183.x [RCT, n=315]
  29. Madisch A, Holtmann G, Mayr G, Vinson B, Hotz J. Treatment of functional dyspepsia with a herbal preparation. A double-blind, randomized, placebo-controlled, multicenter trial. Digestion. 2004;69(1):45-52. PMID: 14755152 · DOI: 10.1159/000076546 [RCT, n=120]
  30. May B, Köhler S, Schneider B. Efficacy and tolerability of a fixed combination of peppermint oil and caraway oil in patients suffering from functional dyspepsia. Aliment Pharmacol Ther. 2000;14(12):1671-1677. PMID: 11121917 · DOI: 10.1046/j.1365-2036.2000.00873.x [RCT, n=96]
  31. Rich G, Shah A, Koloski N, Funk P, Stracke B, Köhler S, Holtmann G. A randomized placebo-controlled trial on the effects of Menthacarin, a proprietary peppermint- and caraway-oil-preparation, on symptoms and quality of life in patients with functional dyspepsia. Neurogastroenterol Motil. 2017;29(11):e13132. PMID: 28695660 · DOI: 10.1111/nmo.13132 [RCT, n=114]
  32. Schemann M, Michel K, Zeller F, Hohenester B, Rühl A. Region-specific effects of STW 5 (Iberogast) and its components in gastric fundus, corpus and antrum. Phytomedicine. 2006;13 Suppl 5:90-99. PMID: 16765572 · DOI: 10.1016/j.phymed.2006.03.020 [In vitro]
  33. Rodrigues DM, Motomura DI, Tripp DA, Beyak MJ. Are psychological interventions effective in treating functional dyspepsia? A systematic review and meta-analysis. J Gastroenterol Hepatol. 2021;36(8):2047-2057. PMID: 34105186 · DOI: 10.1111/jgh.15566 [Meta-analysis, k=9]
  34. Calvert EL, Houghton LA, Cooper P, Morris J, Whorwell PJ. Long-term improvement in functional dyspepsia using hypnotherapy. Gastroenterology. 2002;123(6):1778-1785. PMID: 12454833 · DOI: 10.1053/gast.2002.37071 [RCT, n=126]
  35. Tan VPY, Liu KSH, Lam FYF, Hung IFN, Yuen MF, Leung WK. Randomised clinical trial: rifaximin versus placebo for the treatment of functional dyspepsia. Aliment Pharmacol Ther. 2017;45(6):767-776. PMID: 28112426 · DOI: 10.1111/apt.13945 [RCT, n=86]
  36. Wauters L, Ceulemans M, Frings D et al. Proton Pump Inhibitors Reduce Duodenal Eosinophilia, Mast Cells, and Permeability in Patients With Functional Dyspepsia. Gastroenterology. 2021;160(5):1521-1531. PMID: 33346007 · DOI: 10.1053/j.gastro.2020.12.016 [Cohort, n=75]
  37. Duncanson KR, Talley NJ, Walker MM, Burrows TL. Food and functional dyspepsia: a systematic review. J Hum Nutr Diet. 2018;31(3):390-407. PMID: 28913843 · DOI: 10.1111/jhn.12506 [Systematic Review]
  38. Duncanson K, Burrows T, Keely S et al. The Alignment of Dietary Intake and Symptom-Reporting Capture Periods in Studies Assessing Associations between Food and Functional Gastrointestinal Disorder Symptoms: A Systematic Review. Nutrients. 2019;11(11):2590. PMID: 31661839 · DOI: 10.3390/nu11112590 [Systematic Review]
Transparency on the evidence: where the data are thin
  1. Duodenal eosinophilia is not a clinical test. The associations from the Swedish sample are strong, but there is no standardised counting threshold for routine care, and a Mayo Clinic cohort did not find the cell differences at all.
  2. The causal chain is not proven. Acid, bile, microbiome and food antigens are regarded as candidates for the barrier defect. A causal connection to the symptoms has not been shown in humans.
  3. Prokinetics rest on very low evidence quality. NNT 7 sounds good, the heterogeneity of 91 percent and the unchanged quality of life put the number clearly in perspective.
  4. With the neuromodulators there is a hard limitation. Looking only at trials that had excluded people with an accompanying affective disorder, no benefit remained in the meta-analysis. The large single trial with amitriptyline still showed an effect in the pain predominant type.
  5. The phytotherapy trials are mostly manufacturer linked, the effect sizes small and the preparations not identical. The nine plant mixture and the six plant variant are two different things.
  6. Psychological approaches: nine small trials, only three with a sham arm. The hypnosis trial dates from 2002 and has not been repeated at this size.
  7. Rifaximin is a single finding from one centre with 86 participants, without replication and without guideline backing.
  8. Alcohol as a trigger is more weakly documented than almost every guidebook suggests. The systematic review explicitly classifies the association as unclear.
  9. On the role of digestive enzymes in functional dyspepsia I did not find usable randomised evidence in this search. What I write about the order stomach acid first is marked as a clinical observation and is not a study result.
  10. Individual details of the German S1 guideline, for instance on age thresholds and phytotherapy, come from secondary presentations and are deliberately phrased cautiously here.
  11. The link between anxiety and subgroup comes from two separate analyses of the same Swedish work. The odds ratio of 7.61 applies to new onset functional dyspepsia overall, while the restriction to the meal related type comes from the cross sectional associations.
  12. On eating pace I found no study in functional dyspepsia. What I write about it is a physiological consideration derived from accommodation, not a study result. The same applies to my view that your own diary says more than a general list.
  13. What deliberately does not appear here. No dosage recommendation, no treatment protocol, no meal plan and no advice to change or stop an existing medication. Study doses are literature figures, not a recommendation. Nothing in any section implies that a recommended endoscopy, colonoscopy or laboratory testing should be postponed or replaced.

Have questions or want to book an appointment?

We'd be happy to advise you personally at our practice.

Book appointment