Related Experiment Video
Updated: Jan 9, 2026
Retinal and Choroidal Thickness Changes in Populations with Helicobacter pylori Infection by Swept-Source Optical Coherence Tomography
Published on: November 1, 2024
Association between Anti-Helicobacter pylori IgG seropositivity on coronary heart disease and potential pathogenesis:
Jing Wang1, Tianying Chang2, Yiqiang Wang3
1Changchun University of Chinese Medicine, Changchun, China.
Insights
This study found a causal link between Helicobacter pylori (H. pylori) infection and increased coronary heart disease (CHD) risk. H. pylori infection may influence CHD through effects on insulin response and cholesterol levels.
Area of Science:
- Cardiovascular Epidemiology
- Infectious Disease Research
- Genetic Epidemiology
Background:
- Observational studies suggest a link between anti-Helicobacter pylori (H. pylori) IgG seropositivity and coronary heart disease (CHD).
- Confounding factors in previous studies have made this causal relationship controversial.
- Mendelian randomization (MR) is a robust method to investigate potential causal links.
Purpose of the Study:
- To clarify the causal association between anti-H. pylori IgG seropositivity and CHD using a two-sample Mendelian randomization (MR) analysis.
- To explore potential mediating pathways, including metabolic factors, in the relationship between H. pylori infection and CHD.
Main Methods:
- Utilized genome-wide association studies (GWAS) summary data for exposure (anti-H. pylori IgG seropositivity), outcome (CHD), and mediators.
- Employed inverse variance weighting (IVW) as the primary analysis method, supplemented by weighted median and MR-Egger regression.
- Conducted sensitivity analyses, including leave-one-out, heterogeneity, and pleiotropy assessments, to ensure result validity.
Main Results:
- Anti-H. pylori IgG seropositivity was significantly associated with an increased risk of CHD (OR=1.003, P=0.048).
- Mediating factors showed significant associations: increased peak insulin response (β=0.214, P=0.026), decreased total free cholesterol (β=-0.031, P=0.045), and reduced waist circumference (β=-0.073, P=0.027) and waist-to-hip ratio (β=-0.069, P=0.044).
- No significant heterogeneity or pleiotropy was detected, supporting the robustness of the findings.
Conclusions:
- This MR study provides strong evidence for a causal relationship between anti-H. pylori IgG seropositivity and an increased risk of CHD.
- The observed association may be mediated by higher peak insulin response, lower total free cholesterol, and reduced central adiposity (waist circumference and waist-to-hip ratio).
- Further research is warranted to confirm these findings and elucidate the precise mechanisms involved.
Background:
Currently, observational studies and clinical trials have shown that the occurrence of coronary heart disease (CHD) is closely related to anti-Helicobacter pylori (H. pylori) IgG seropositivity, but these studies may be affected by confounding factors, resulting in a causal relationship that is still controversial.
Methods:
We conducted a Mendelian randomization analysis to clarify the association between anti-H. pylori IgG seropositivity and CHD and explore its potential pathogenesis. Exposure, outcome, and mediator data were obtained all from the genome-wide association studies (GWAS) summary data. The inverse variance weighting (IVW) analysis method under the fixed-effect model was used as our primary statistical method. Other statistical methods are supplements, such as IVW under the random-effects model, weighted median, and MR-Egger regression method. Causal estimates are presented as odds ratios (ORs) with 95% confidence intervals (CIs). To ensure the stability and reliability of the results, we also performed sensitivity and heterogeneity analysis.
Results:
This study shows that increases of anti-H. pylori IgG seropositivity was significantly associated with an increased risk of CHD (OR=1.003, 95% CI:1.0001.006, P = 0.048) and increases in peak insulin response (β = 0.214, 95% CI: 0.025-0.403, P = 0.026), decrease in total free cholesterol levels (β = ‒0.031, 95% CI: ‒0.061 to ‒0.000, P = 0.045), decreased waist circumference (β = ‒0.073, 95% CI: ‒0.138 to ‒0.008, P = 0.027) and waist-to-hip ratio (β = ‒0.069, 95% CI: ‒0.136 to ‒0.002, P = 0.044). The leave-one-out method proved inadequate in detecting instances where a single SNP exhibited a bias towards or dependency on the causation. Furthermore, our findings revealed no heterogeneity or pleiotropy.
Conclusion:
Our MR study provided strong evidence of a causal relationship between anti-H. pylori IgG seropositivity and related to an increased risk of CHD. The effect of anti-H. pylori IgG seropositivity on CHD may be related to a higher peak insulin response or lower total free cholesterol levels and a decrease in waist circumference and waist-to-hip ratio. However, further research is needed to prove the results.
Related Concept Videos
01:22Pathophysiology of Peptic Ulcer Disease: Injurious Factors
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
01:30Peptic Ulcer Disease I: Introduction
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
01:17Gastritis-II: Pathophysiology
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
01:30Coronary Artery Disease I: Introduction
01:24Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors
01:28Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies
Few clinical manifestations differentiate gastric ulcers from duodenal ulcers. Distinctions in the location, timing, and pain relief are crucial for healthcare providers in differentiating between gastric and duodenal ulcers during clinical assessments.