News|Articles|September 15, 2026

Study Links H. pylori Exposure to Greater Global Colorectal Cancer Burden

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Key Takeaways

  • Pooled data across 43 studies (48.7 million) associated H. pylori exposure with 1.6-fold higher CRC risk; attributable fraction estimates were highly sensitive to study design.
  • Restricting to 14 population-based/cohort studies reduced estimated global attributable burden from 22% to 12%, highlighting confounding and selection bias risks.
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Helicobacter pylori exposure could be associated with approximately 22% of colorectal cancer cases worldwide.

Colorectal cancer (CRC) remains a significant source of cancer morbidity and mortality, with approximately 1.9 million new cases and more than 900,000 deaths reported worldwide in 2022.1 Although established risk factors include age, genetics, diet, and lifestyle, researchers are examining whether Helicobacter pylori—a bacterium best known for its causal relationship with gastric cancer—could also contribute to CRC development.2

An exploratory risk-attribution modeling study published in eGastroenterology estimated that H. pylori exposure could be associated with more than 1 in 5 CRC cases worldwide.2

However, the estimate varied substantially according to the evidence included, underscoring the need for prospective studies before H. pylori can be considered a causal or modifiable CRC risk factor.2

Analysis Estimates a Potential 22% Attributable Burden

The study’s investigators combined CRC risk estimates from systematic reviews and pooled analyses with 2022 incidence data from the Global Cancer Observatory. Analyses were stratified by geographic region, sex, age, diagnostic method, availability of a national CRC screening program, and use of H. pylori eradication therapy.2

Across 43 studies that included 48,694,403 individuals, exposure to H. pylori was associated with a 1.6-fold greater risk of CRC compared with no exposure. The resulting population-attributable fraction suggested that approximately 22% of CRC cases worldwide could be related to H. pylori exposure.2

That figure should be interpreted cautiously. When investigators restricted the analysis to 14 population-based and cohort studies, the estimated attributable proportion fell to 12%. This difference demonstrates how study selection, design, and population characteristics can influence burden estimates.2

The analysis did not identify statistically significant differences according to sex, age above or below 60 years, method used to detect H. pylori, or access to a national CRC screening program. Regional variation was more pronounced. The Western Pacific had the highest regional estimate, at approximately 25%, whereas Mongolia had the highest country-level estimate, at 36%. China had the largest estimated absolute burden, with 139,619 CRC cases potentially associated with exposure.2

Exploratory birth-cohort findings also suggested that the attributable fraction increased among individuals born more recently. It rose from 9.5% among those born before 1947 to approximately 15% among individuals born from 1963 through 1977. The researchers emphasized that these patterns require confirmation.2

Findings Build on Earlier Observational Evidence

Previous research has also identified an association between H. pylori and CRC. A nationwide Veterans Health Administration cohort included 812,736 individuals who underwent H. pylori testing, of whom 205,178 tested positive. Over as many as 15 years of follow-up, positivity was associated with an 18% higher risk of CRC and a 12% higher risk of CRC-related mortality.3

Among patients who tested positive, remaining untreated was associated with greater CRC incidence and mortality compared with receiving treatment.3 More recent analyses of 2 randomized trial cohorts also produced mixed but potentially supportive findings. In one cohort, treatment was associated with a reduced CRC risk over 29.4 years, whereas the second cohort showed no overall benefit after 13.8 years. Benefit in the second cohort appeared limited to participants with high genetic susceptibility or antibodies against particular H. pylori antigens.4

Collectively, these findings strengthen the rationale for further investigation but do not prove that eradication prevents CRC. Observational associations can be affected by diet, socioeconomic conditions, health care access, and other exposures that vary alongside H. pylori prevalence.

Implications for Pharmacy Practice and Prevention

Current H. pylori treatment recommendations focus on established gastrointestinal indications and gastric cancer prevention—not CRC prevention.

The American College of Gastroenterology recommends optimized bismuth quadruple therapy for 14 days as the preferred empiric regimen for many treatment-naïve adults. Clarithromycin-based triple therapy should be avoided unless susceptibility testing confirms clarithromycin sensitivity. Confirmation of eradication is recommended at least 4 weeks after antibiotic therapy ends.5

Pharmacists can support appropriate regimen selection, identify drug interactions, counsel patients through complex dosing schedules, and reinforce the importance of completing treatment and confirming eradication. These responsibilities are especially important as clarithromycin and levofloxacin resistance reduce the effectiveness of commonly used empiric regimens.5

The new analysis does not support population-wide H. pylori eradication solely to prevent CRC. Broad treatment programs could increase antibiotic use, adverse effects, and antimicrobial resistance.2 CRC screening should also continue according to established recommendations regardless of H. pylori status.

REFERENCES
  1. Global Cancer Observatory. Colorectum fact sheet. International Agency for Research on Cancer. Accessed September 15, 2026.https://gco.iarc.who.int/today/en/fact-sheets-cancers/41/colorectum
  2. Li Y, Cui C, Sun D, et al. Global and regional burden of colorectal cancer potentially related to Helicobacter pyloriexposure: a risk attribution modelling study. eGastroenterology. 2026;4(3):e100436. doi:10.1136/egastro-2026-100436. https://egastroenterology.bmj.com/content/egastro/4/3/e100436.full.pdf
  3. Shah SC, Camargo MC, Lamm M, et al. Impact of Helicobacter pylori Infection and Treatment on Colorectal Cancer in a Large, Nationwide Cohort. J Clin Oncol. 2024;42(16):1881-1889. doi:10.1200/JCO.23.00703
  4. Han X, Xu H, Liu Z, et alHelicobacter pylori infection, treatment and colorectal cancer risk by genetic predisposition: evidence from two randomised trialsGut Published Online First: 30 June 2026. doi: 10.1136/gutjnl-2026-338156
  5. Chey WD, Howden CW, Moss SF, et al. ACG Clinical Guideline: Treatment of Helicobacter pylori Infection. Am J Gastroenterol. 2024;119(9):1730-1753. doi:10.14309/ajg.0000000000002968

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