Dyspepsia primary prevention

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Fahad Hasan, M.D.[2] Ajay Gade MD[3]]

Overview

The risk factors for dyspepsia fall into two broad and overlapping categories. For organic dyspepsia, the principal preventable risks are Helicobacter pylori infection, nonsteroidal anti-inflammatory drug (NSAID) use, cigarette smoking, and excessive alcohol consumption. For FD, preventable and modifiable contributors include dietary triggers (fatty foods, high-FODMAP foods, excessive caffeine and alcohol), physical inactivity, psychological stress, sleep disturbance, and post-infectious dysregulation of the gut-brain axis. Primary prevention thus encompasses a combination of infectious disease control, pharmacological gastroprotection, and sustained lifestyle modification.

Primary Prevention

Overview of Preventable Risk Factors

Risk Factor	Mechanism of Dyspepsia Risk	Primary Preventive Action
Helicobacter pylori infection	Causes peptic ulcer disease, gastritis, and contributes to FD symptoms	Test-and-treat in appropriate populations; population-based screen-and-treat programmes
NSAID use	Inhibits COX-1, reduces prostaglandin-mediated mucosal protection, causes ulcers	Lowest effective dose; PPI co-prescription in high-risk patients; prefer COX-2 selective agents when possible
Cigarette smoking	Increases gastric acid secretion, reduces mucosal defence, impairs ulcer healing	Smoking cessation
Excessive alcohol consumption	Erodes gastric mucosa; augments NSAID and H. pylori injury	Moderation or abstinence; ≤20 g/day threshold associated with elevated peptic ulcer risk
High body mass index (obesity)	Independently associated with gastric and duodenal ulcer risk via adiposity-driven inflammation	Weight normalisation; BMI reduction
High-fat and high-FODMAP diet	Delays gastric emptying, exacerbates visceral hypersensitivity, triggers postprandial symptoms	Dietary modification: smaller meals, low FODMAP, reduced fat intake
Physical inactivity	Associated with FD prevalence via gut motility and gut-brain axis disruption	Regular moderate aerobic exercise
Psychological stress / anxiety / depression	Disrupts gut-brain axis, exacerbates visceral hypersensitivity, precedes onset of DGBI	Stress management, psychological therapies, sleep hygiene
Post-infectious gastroenteritis	Triggers post-infectious FD via mucosal inflammation, immune activation, microbiome alteration	Prevention of enteric infections; food safety; hand hygiene

Helicobacter pylori Eradication as Primary Prevention

Helicobacter pylori is the most significant modifiable risk factor for peptic ulcer disease, gastric cancer, and H. pylori-associated dyspepsia. Infection causes progressive mucosal damage that, if left untreated, may culminate in gastric cancer through a sequence of atrophic gastritis, intestinal metaplasia, dysplasia, and carcinoma. H. pylori eradication before the development of precancerous histological changes has been demonstrated to significantly reduce gastric cancer incidence.

A 2022 updated systematic review and meta-analysis of 29 randomised controlled trials (6,781 patients) by Ford et al. demonstrated that H. pylori eradication therapy is superior to control for symptom cure in functional dyspepsia (relative risk [RR] of symptoms not being cured = 0.91; 95% CI 0.88 to 0.94; number needed to treat [NNT] = 14; 95% CI 11 to 21) and for symptom improvement (RR of symptoms not improving = 0.84; 95% CI 0.78 to 0.91; NNT = 9; 95% CI 7 to 17). Adverse events were more common with eradication therapy (RR = 2.19; 95% CI 1.10 to 4.37).

Eradication also prevents subsequent development of peptic ulcers in H. pylori-infected individuals and is highly cost-effective when considered in the context of downstream prevention of gastric cancer, peptic ulcer disease, and recurrent dyspepsia-related healthcare utilisation. Population-based H. pylori screen-and-treat strategies are estimated to reduce dyspepsia-related clinician consultations substantially, helping offset programme costs, and modelling studies indicate additional savings from prevented dyspepsia cases could substantially improve cost-effectiveness of H. pylori eradication in lower-prevalence settings.

The 2024 ACG Clinical Guideline on Treatment of H. pylori recommends a "test-and-treat" strategy as the initial management approach for patients under 60 years presenting with uninvestigated dyspepsia and without alarm features (vomiting, gastrointestinal bleeding, unexplained iron deficiency, or weight loss). A lower age threshold of 50 years for the test-and-treat strategy may be appropriate in populations at higher risk of gastric cancer (e.g., immigrants from high-incidence regions, those with a family history of gastric cancer). For treatment-naive patients with H. pylori infection, bismuth quadruple therapy (BQT) for 14 days is the preferred empiric regimen when antibiotic susceptibility is unknown; rifabutin triple therapy or potassium-competitive acid blocker (PCAB) dual therapy for 14 days are suitable empiric alternatives in patients without penicillin allergy.

NSAID-Related Gastroprotection

Nonsteroidal anti-inflammatory drugs (NSAIDs) are a leading preventable cause of peptic ulcer disease, upper gastrointestinal bleeding, and dyspeptic symptoms. NSAIDs contribute to over 100,000 deaths annually due to peptic ulcer and related complications globally. Primary prevention strategies include:

• Risk stratification: High-risk patients include those aged >65 years, those with a history of peptic ulcer disease or GI bleeding, those on high-dose NSAID therapy, and those concomitantly using aspirin, corticosteroids, or anticoagulants.

• PPI co-prescription: The ACG recommends long-term proton pump inhibitor co-therapy as prophylaxis for patients at moderate to high risk of NSAID-associated upper GI bleeding based on the above risk factors. NICE guidelines similarly advocate offering gastroprotective treatment (such as PPI at the lowest effective dose for the shortest period necessary) to persons receiving NSAIDs for chronic conditions such as osteoarthritis and rheumatoid arthritis, particularly for those aged over 45 years on long-term therapy.

• COX-2 selective inhibitors: For patients with a history of upper GI bleeding who require NSAIDs, an international consensus recommends a selective COX-2 inhibitor together with PPI co-prescription. COX-2 inhibitors carry a lower risk of upper GI mucosal injury but do not protect against lower GI NSAID enteropathy, and are associated with increased cardiovascular risk in susceptible individuals.

• H. pylori testing before initiating long-term NSAIDs: Testing for H. pylori infection and eradicating the infection if positive is recommended in patients requiring long-term NSAID therapy, as H. pylori infection independently increases the risk of NSAID-related GI complications. Whether PPI co-therapy is needed after successful eradication depends on individual GI risk assessment.

• Misoprostol: A synthetic prostaglandin E1 analogue that prevents NSAID-related ulcers; however, its use is limited by gastrointestinal side effects (diarrhoea, cramping). It remains an option for patients in whom PPIs are not tolerated or available.

Dietary and Lifestyle Modification

Dietary Patterns

Dietary modification is the first step in the management algorithm for FD and is central to primary prevention of dyspeptic symptoms. Evidence from randomised controlled trials and observational studies identifies the following as preventable dietary triggers:

• High-fat foods: Dietary fat delays gastric emptying and exacerbates postprandial symptoms in FD. Reducing fat content is among the earliest and most consistently recommended dietary changes.

• High-FODMAP foods: A randomised controlled trial by Goyal et al. (2022), enrolling 105 FD patients (Rome IV), showed that both a low-FODMAP diet (LFD) and traditional dietary advice (TDA) produced significant symptom improvement at 4 weeks versus baseline, with the low-FODMAP diet showing a higher response in patients with associated bloating on multivariate analysis. A subsequent Belgian study (2019–2022) demonstrated that a 6-week low-FODMAP diet, guided by a dietitian, reduced postprandial distress syndrome (PDS) symptom scores (Leuven Postprandial Distress Scale [LPDS] scores falling from 1.8 at baseline to 1.0; P < 0.001) in more than 70% of FD patients, with associated improvements in quality of life, depression, and somatic symptom scores.

• Traditional dietary advice: Clinical practice guidelines recommend eating smaller, more regular meals; reducing intake of caffeine, alcohol, carbonated drinks, fatty foods, processed foods, spicy foods, and excess dietary fibre. Almost 80% of patients with FD report meal-related symptoms; this subset (PDS subtype) is most likely to respond to dietary modification.

• Mediterranean dietary pattern: Moderate-quality evidence from systematic reviews indicates that high versus low adherence to the Mediterranean diet — a pattern rich in fibres, mono- and polyunsaturated fatty acids, antioxidants, and polyphenols — is associated with a reduced likelihood of FD. The 2022 ACG evidence-based dietary review for upper gastrointestinal disorders endorses a personalised dietary approach rather than universal food restriction, recognising the low quality of available evidence for individual food avoidance recommendations.

• Meal frequency and timing: Eating behaviour, including meal frequency and the timing of meals, is associated with FD risk. A study among young Japanese adults found that irregular meal patterns were independently associated with FD prevalence.

Smoking Cessation

Cigarette smoking increases gastric acid secretion, reduces mucosal defence mechanisms, impairs ulcer healing, and raises the risk of complications from peptic ulcer disease, including bleeding and perforation. A 2023 two-sample Mendelian randomization study (Liu et al., 452,264 participants from the Gene ATLAS) confirmed a causal role for smoking initiation (SmkInit; ever/never) in the development of both gastric ulcer and duodenal ulcer, using 325 identified genetic variants as a proxy. In contrast, age of smoking initiation, smoking cessation, number of cigarettes per day, and alcohol consumption did not demonstrate causal relationships with peptic ulcer disease risk in this analysis, suggesting that preventing smoking initiation is the key preventive target. Similarly, genetically predicted BMI had a confirmed causal relationship with both gastric and duodenal ulcer development.

From a clinical standpoint, smoking cessation remains a strongly recommended primary preventive intervention for dyspepsia and peptic ulcer disease. All available smoking cessation interventions — pharmacological (varenicline, nicotine replacement therapy, bupropion) and behavioural — should be offered to patients who smoke and present with dyspeptic symptoms.

Alcohol Moderation

Excessive alcohol consumption erodes the gastric mucosa, exacerbates NSAID- and H. pylori-related mucosal injury, and increases the risk of upper GI bleeding. In a large prospective cohort study, alcohol consumption greater than 15 g/day (approximately one standard drink or more per day) was associated with an increased risk of upper GI bleeding, particularly secondary to peptic ulcer. Patients should be counselled that alcohol moderation — not necessarily total abstinence — is recommended, with heavier drinking (defined as ≥20 g/day in cohort studies) specifically associated with elevated peptic ulcer and bleeding risk.

Physical Activity

Physical inactivity is associated with higher FD prevalence. In a population-based study, individuals with FD reported significantly less walking (57% versus 63%, P = 0.04) and lower frequency of exercising, particularly for walking (P = 0.008) and moderate (P = 0.03) and vigorous intensity activity, compared with those without FD. Among patients with the PDS subtype specifically, lower vigorous exercise levels were documented.

A 2021 randomised controlled trial (Rane et al.) enrolling 72 FD patients (Rome IV criteria) demonstrated that aerobic exercise at moderate intensity — 30 minutes per session, 5 sessions per week for 6 weeks — combined with conventional treatment, significantly improved Glasgow Dyspepsia Severity Score (GDSS), Depression Anxiety Stress Scales-42 (DASS-42), and visual analogue scale (VAS) scores compared with conventional treatment alone. Additionally, a 2025 meta-analysis of 15 randomised controlled trials (1,359 FD patients) confirmed that exercise therapy improved key dyspeptic symptoms including epigastric fullness and pain, and additionally enhanced quality of life, sleep quality, and reduced depression compared with conventional treatment. Regular moderate aerobic physical activity should be encouraged in individuals with or at risk of FD as part of primary preventive strategy.

Psychological Stress Management and Sleep Hygiene

Functional dyspepsia is a disorder of gut-brain interaction in which psychological factors exert a substantial modulatory role. The initial diagnosis of disorders of gut-brain interaction (DGBI) is preceded by a diagnosis of stress-related psychiatric disorders in up to 60% of patients in prospective cohort data. Individuals with FD experience more psychological stress than healthy controls, and higher stress levels are associated with more severe dyspeptic symptoms.

Primary prevention strategies for FD targeting the gut-brain axis include:

• Stress identification and management (cognitive behavioural techniques, mindfulness, relaxation therapy)
• Maintaining regular sleep schedules and addressing sleep disorders, which are independent predictors of clinical outcomes in FD
• Addressing anxiety and depression, which are strongly associated with FD onset and perpetuation
• Gold-standard management of DGBI, as recognised by contemporary guidelines, comprises a biopsychosocial approach involving lifestyle and dietary changes in conjunction with psychological treatment to manage stress and mental health

The BSG 2022 guideline recommends that FD be introduced to the patient as a disorder of gut-brain interaction, with a simple account of the gut-brain axis and how it is impacted by diet, stress, and cognitive, behavioural, and emotional responses to symptoms, as part of the initial explanatory framework.

Prevention of Post-Infectious Functional Dyspepsia

Acute enteric infection — including gastroenteritis due to bacterial, viral, or protozoal pathogens — is a recognised trigger of post-infectious FD. Standard public health measures to prevent enteric infections include:

• Attention to food hygiene and safe food preparation
• Hand hygiene with soap and water before eating and after using the toilet
• Safe drinking water access
• Appropriate management and antibiotic treatment of acute bacterial gastroenteritis where indicated
• Travel precautions and prophylaxis when visiting high-risk regions

Initial Management

For individuals presenting with uninvestigated dyspepsia, the following primary preventive and early management steps are recommended:

• Alarm feature assessment: Dysphagia, unexplained weight loss, progressive symptoms, evidence of GI bleeding, iron deficiency anaemia, epigastric mass, or family history of upper GI malignancy mandate prompt upper gastrointestinal endoscopy rather than empirical management. The BSG 2022 guideline recommends urgent evaluation for all patients aged ≥55 years with new-onset dyspepsia. The 2024 ACG H. pylori guideline recommends a lower age threshold of ≥50 years for endoscopy-first strategy in populations at higher risk of gastric cancer.

• Modifiable risk factor review: A structured review of NSAID use, aspirin and anticoagulant use, smoking, alcohol consumption, dietary habits, stress, and sleep should be performed in all patients with new-onset dyspepsia.

• H. pylori test-and-treat: In patients <60 years without alarm features, a non-invasive test for H. pylori (urea breath test or stool antigen test, preferred over serology) is recommended, with eradication treatment if positive before empirical acid suppression.

• Explanation and reassurance: For patients with FD, providing a clear diagnostic explanation of FD as a disorder of gut-brain interaction, along with reassurance about the absence of organic disease, forms the foundation of patient education and is itself associated with symptom improvement.

Long-Term Management

Long-term primary preventive measures for dyspepsia include:

• Ongoing dietary counselling: Sustained adherence to low-trigger dietary patterns (small meals, limited fat and FODMAP content, reduced caffeine and alcohol) prevents symptom relapse. Dietitian-guided FODMAP reintroduction after an elimination phase allows identification of individual tolerance thresholds, avoiding unnecessarily restrictive long-term diets.

• Continued physical activity: Regular moderate aerobic exercise (30 minutes, at least 5 days per week) should be maintained as a long-term preventive strategy.

• H. pylori re-testing post-eradication: Universal post-treatment test-of-cure is recommended by the 2024 ACG guideline using a urea breath test or stool antigen test, performed at least 4 weeks after completing eradication therapy and at least 2 weeks after stopping PPI, to confirm successful eradication and prevent re-treatment delays.

• NSAID prescribing review: Long-term NSAID users should be regularly reviewed for continued necessity and for ongoing gastroprotective co-therapy, with reassessment of GI and cardiovascular risk at each review.

• Psychological comorbidity monitoring: Anxiety, depression, and somatisation increase the risk of FD relapse and poor outcomes. Long-term psychological support, including cognitive behavioural therapy (CBT) or other psychological interventions, should be accessible for patients at risk.

• Patient education and self-management: Structured patient education about FD as a gut-brain interaction disorder, triggers, and coping strategies improves long-term outcomes and reduces unnecessary healthcare utilisation.

Special Populations

• Elderly patients: Older individuals have a substantially higher prevalence of NSAID use and are at proportionally greater risk of NSAID-related ulceration and bleeding due to concurrent antiplatelet and anticoagulant use, reduced mucosal resilience, and comorbidities. PPI co-prescription with NSAIDs is especially important in patients aged >65 years. Alarm features in older patients warrant prompt endoscopic evaluation given the higher pre-test probability of malignancy.

• Pregnant patients: NSAIDs are contraindicated in the third trimester of pregnancy (risk of premature closure of the ductus arteriosus) and should be used with caution in the first and second trimesters. H. pylori eradication is generally deferred until after delivery. Dietary modifications and lifestyle changes remain the primary preventive approach. PPIs are used in pregnancy only when the benefit clearly outweighs risk.

• Patients taking aspirin or antiplatelet therapy: Low-dose aspirin use for cardiovascular prevention is a significant risk factor for peptic ulcer and upper GI bleeding. In patients with a history of ulcer disease requiring antiplatelet therapy for secondary cardiovascular prevention, long-term daily PPI therapy is recommended. H. pylori testing and eradication is recommended before initiating chronic antiplatelet therapy.

• Patients from high H. pylori prevalence regions: Individuals from or immigrating from high-incidence regions for gastric cancer (East Asia, Eastern Europe, parts of Latin America and Sub-Saharan Africa) represent a priority population for H. pylori test-and-treat strategies. The 2024 ACG guideline endorses a population-level approach, including opportunistic testing, for racial and ethnic minority and immigrant groups in the United States where gastric cancer burden is disproportionately high.

• Patients with anxiety or depression: Given that psychiatric diagnoses precede DGBI onset in a significant proportion of patients, addressing anxiety and depression through appropriate pharmacological and psychological interventions represents an upstream preventive strategy for FD. Sleep disorders are also independent predictors of FD clinical outcomes and should be actively managed.

• Healthcare workers and food handlers: Occupational exposure to potential enteric pathogens increases the risk of H. pylori acquisition and post-infectious FD. Appropriate hygiene practices, access to clean food and water, and occupational health surveillance represent targeted preventive measures in these groups.