Abstract
Background and objectives
Helicobacter pylori (H. pylori) has been increasingly linked to extragastric conditions. However, the relationship between H. pylori infection and cardiovascular diseases (CVD) remains controversial. This study aims to investigate the association between H. pylori infection and 10-year cardiovascular risk.
Methods
A total of 1,398 subjects who underwent health examinations at Beijing Tongren Hospital were included in this study. H. pylori infection was determined using 13C-breath test. The 10-year cardiovascular risk was assessed using the Framingham score. Insulin resistance was evaluated through the triglyceride-glucose (TyG) index and its derivatives. Logistic regression and subgroup analyses were performed to evaluate associations.
Results
Individuals with H. pylori infection exhibited significantly higher TyG index and its derivatives (all P < 0.001), indicating increased insulin resistance. All TyG-related indices were strongly correlated with 10-year CVD risk, with TyG-WHR showing the strongest association (R = 0.745, P < 0.001). The estimated 10-year CVD risk was significantly higher in the H. pylori-infected group (P = 0.003). After adjusting for potential confounders, H. pylori infection remained independently associated with high cardiovascular risk (OR = 2.552, 95% CI: 1.312–4.963, P = 0.006). Notably, this association was more pronounced in females, individuals younger than 50 years, non-smokers, non-diabetics, and those without hypertension.
Conclusions
H. pylori infection is associated with increased insulin resistance and elevated 10-year cardiovascular risk, particularly among individuals without traditional risk factors. These findings suggest that H. pylori infection may represent a non-traditional contributor to cardiovascular risk and warrants further investigation.
Supplementary Information
The online version contains supplementary material available at 10.1186/s12872-026-06099-8.
Keywords: Helicobacter pylori, Insulin Resistance, 10-year cardiovascular risk
Introduction
Helicobacter pylori (H. pylori) infection is one of the most common bacterial infections worldwide, affecting more than half of the global population. In China, the prevalence of H. pylori infection remains notably high, with significant regional variations and an overall prevalence rate exceeding 50% [1]. This widespread infection poses a substantial public health burden. Traditionally, H. pylori has been associated with gastrointestinal diseases, including chronic gastritis, peptic ulcers, and gastric cancer. However, recent research has broadened the scope of diseases linked to H. pylori to include extragastric conditions such as hyperglycemia, hyperlipidemia, and cardiovascular diseases (CVDs), which have garnered significant attention [2–4].
CVDs, including cerebrovascular disease, peripheral vascular disease, coronary heart disease, and heart failure, are leading causes of morbidity and mortality worldwide [5]. The Framingham score is a well-established tool used to estimate the 10-year risk of cardiovascular events [6], and its widespread applicability across diverse populations underscores its importance in cardiovascular risk stratification. Insulin resistance (IR) is a key factor in the pathogenesis of various diseases, including CVD. The triglyceride-glucose (TyG) index serves as an important marker for evaluating insulin resistance. While the hyperinsulinemic-euglycemic clamp remains the gold standard, the TyG index offers greater sensitivity and specificity [7, 8]. Recent studies suggest that the TyG index and its derivatives—such as TyG × waist-to-hip ratio (TyG-WHR), TyG × waist-to-height ratio (TyG-WHtR), and TyG × body mass index (TyG-BMI)—outperform the TyG index alone in predicting cardiovascular-related mortality [9].
Despite numerous studies exploring the relationship between H. pylori infection and cardiovascular events, the findings have been inconsistent. Some research suggests a significant association, while other studies propose that the observed link may be coincidental or confounded by other factors [10–12]. Importantly, most previous studies have focused on populations with established cardiovascular risk factors, such as diabetes or hypertension, potentially obscuring the impact of H. pylori infection in otherwise low-risk individuals. In addition, insulin resistance has been proposed as a potential mechanistic link between H. pylori infection and cardiovascular risk, yet this relationship has not been fully characterized using sensitive surrogate markers such as the TyG index and its derivatives.
Therefore, this study aimed to investigate the association between H. pylori infection, insulin resistance, and 10-year cardiovascular risk, with a particular focus on stratified populations, especially individuals without traditional cardiovascular risk factors.
Methods
Study population
This study recruited adults from the Tongren Health Care Study [13] who underwent physical examinations at Beijing Tongren Hospital, Capital Medical University. The study was approved by Beijing Tongren Hospital Ethics Committee (TRECKY2018-033). Clinical trial number is not applicable. Collected data comprised demographic information (age, sex), smoking status, medical history (diabetes and hypertension), laboratory measurements, and carbon breath test results. Individuals with a history of cancer, severe cardiovascular disease, or gastrointestinal surgery were excluded. A total of 1,398 participants met the inclusion criteria.
Anthropometric and laboratory measurements
Body mass index (BMI) was calculated as weight (kg) divided by height (meters) squared (kg/m2). Waist circumference (WC) was measured at the midpoint between the lower margin of the last palpable rib and the top of the iliac crest using a flexible measuring tape. Hip circumference was measured at the widest part of the buttocks. Blood pressure (BP) was recorded as the average of three measurements taken while the participant was seated. Blood samples were collected after an overnight fast to measure plasma glucose, glycosylated hemoglobin A1c (HbA1c), total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), direct bilirubin, total bilirubin, total bile acids, alkaline phosphatase (ALP), alanine transaminase (ALT), aspartate transaminase (AST), γ-glutamyl transpeptidase (γ-GT), blood urea nitrogen (BUN), serum creatinine (SCr), and uric acid (UA) concentrations. H. pylori infection was detected using the [13] C-breath test, conducted either on an empty stomach or 2 h post-meal, with a positive result defined as a measurement greater than 4.
Assessment of TyG index and its derivatives
The TyG index was calculated using the formula: Ln [fasting TG (mg/dL) × fasting glucose (mg/dL)/2] [8, 14]. The following derivatives were calculated:
TyG-WHR = TyG × WC/Hip circumference
TyG-WHtR = TyG × WC/Height
TyG-BMI = TyG × [Body weight (kg)/Height2 (m)]
Estimation of 10-year CVD risk
The 10-year CVD risk was estimated using the Framingham risk score, which considers factors such as age, gender, total cholesterol (TC), HDL cholesterol, systolic blood pressure (SBP), treatment for hypertension, smoking status, and diabetes status [6]. Although the Framingham risk score was originally developed in Western populations, it has been widely applied in Asian populations for cardiovascular risk estimation. The score assigns points based on these factors, which are then summed to estimate the 10-year risk of developing cardiovascular events. Cardiovascular risk was categorized as low risk (≤ 10%) or high risk (> 10%).
Statistical analysis
Continuous variables are presented as mean ± standard deviation, while categorical variables are expressed as percentages. Statistical significance between H. pylori-infected and non-infected subjects was assessed using independent Student’s t-tests and Chi-square tests. Trend Chi-square tests were applied to compare the distribution of variables grouped into quartiles. Spearman correlation analysis was performed to evaluate correlations between TyG indices and 10-year CVD risk. Binary logistic regression analysis was conducted to estimate crude and adjusted odds ratios (ORs) with 95% confidence intervals (CIs) for the 10-year CVD risk and TyG-related indices associated with H. pylori infection. All P values were two-tailed, with P < 0.05 considered statistically significant. Statistical analyses were conducted using SPSS software, version 24.0 (SPSS Inc., Chicago, IL, USA).
Results
Clinical characteristics of the study population
A total of 1,398 subjects were enrolled in this study, with 658 females (47.07%). The prevalence of H. pylori infection was 24.03% (336 subjects). Table 1 presents the clinical characteristics of subjects with and without H. pylori infection. Notably, the percentage of males was higher in the H. pylori-infected group compared to the non-infected group. The infected group also exhibited significantly larger waist and hip circumferences, higher BMI, and a greater proportion of smokers. Furthermore, subjects with H. pylori infection had poorer blood glucose and lipid profiles, as well as elevated levels of serum creatinine and uric acid (all P < 0.05). Interestingly, no significant age difference was observed between the H. pylori-positive and -negative groups in the present study. This finding may be related to the characteristics of the study population. Our cohort consisted of individuals undergoing routine health examinations at a tertiary hospital in central Beijing, representing a relatively homogeneous urban population with similar socioeconomic status, hygiene conditions, and living environments. These factors may have attenuated age-related differences in H. pylori prevalence that are commonly observed in broader community-based populations [15].
Table 1.
Comparison of clinical characteristics classified by H. pylori infection
| H. Pylori negative (n = 1062) | H. pylori positive (n = 336) | P value | |
|---|---|---|---|
| Age(years) | 42.01 ± 12.64 | 42.45 ± 13.07 | 0.575 |
| Waist circumference (cm) | 79.31 ± 11.13 | 82.00 ± 11.72 | 0.000 |
| Hip circumference (cm) | 95.82 ± 6.16 | 96.94 ± 6.36 | 0.004 |
| BMI (kg/m2) | 23.56 ± 3.54 | 24.33 ± 3.64 | 0.001 |
| SBP (mmHg) | 124.46 ± 16.29 | 127.38 ± 17.27 | 0.005 |
| DBP (mmHg) | 76.49 ± 10.56 | 77.77 ± 11.83 | 0.061 |
| Female (%) | 526 (49.53) | 132 (39.29) | 0.001 |
| Hypertension (%) | 118 (11.11) | 43 (12.80) | 0.399 |
| Smoke (%) | 162 (12.26) | 79 (23.51) | 0.000 |
| Diabetes (%) | 50 (4.71) | 25 (7.44) | 0.053 |
| Fasting blood glucose (mmol/l) | 5.33 ± 1.06 | 5.63 ± 1.67 | 0.001 |
| HbA1c (%) | 5.65 ± 0.60 | 5.74 ± 0.95 | 0.063 |
| Total cholesterol (mmol/l) | 5.01 ± 0.88 | 5.15 ± 1.03 | 0.029 |
| Triglycerides (mmol/l) | 1.25 ± 1.02 | 1.51 ± 1.39 | 0.001 |
| HDL-C (mmol/l) | 1.53 ± 0.40 | 1.45 ± 0.40 | 0.003 |
| LDL-C (mmol/l) | 2.99 ± 0.78 | 3.12 ± 0.95 | 0.024 |
| ALT (U/L) | 22.22 ± 16.85 | 22.93 ± 16.39 | 0.542 |
| AST (U/L) | 22.40 ± 13.92 | 21.52 ± 7.72 | 0.322 |
| γ-GT (U/L) | 27.90 ± 29.60 | 28.53 ± 25.88 | 0.754 |
| BUN (mmol/L) | 4.85 ± 1.25 | 4.97 ± 1.31 | 0.176 |
| Serum creatinine (μmol/L) | 71.59 ± 14.23 | 75.03 ± 15.52 | 0.001 |
| Uric acid (μmol/L) | 331.32 ± 85.16 | 351.28 ± 95.80 | 0.001 |
Bold values indicate statistical significance (P< 0.05)
To further evaluate the potential confounding effect of sex imbalance between groups, sex-stratified analyses were additionally performed. Baseline clinical characteristics in male and female participants are presented in Supplementary Tables S1 and S2, respectively. Overall, the trends observed in the sex-stratified analyses were generally consistent with those in the combined cohort. In both males and females, participants with H. pylori infection tended to exhibit higher adiposity, less favorable glucose and lipid profiles.
Higher TyG index and its derivatives in H. pylori infected subjects
As shown in Table 2, subjects with H. pylori infection had significantly higher values for the TyG index and its derivatives (TyG-WHR, TyG-WHtR, and TyG-BMI) compared to non-infected subjects (all P < 0.001). To further evaluate the potential confounding effect of sex imbalance between groups, sex-stratified analyses were additionally performed. As shown in Supplementary Tables S1 and S2, male and female subjects with H. pylori infection tended to exhibited higher TyG-related indices compared with non-infected subjects, although some differences appeared more pronounced in males.
Table 2.
TyG index and its derivatives in subjects with or without H.pylori infection
|
H. Pylori negative (n = 1062) |
H. pylori positive (n = 336) |
P value | |
|---|---|---|---|
| TyG | 8.37 ± 0.65 | 8.54 ± 0.76 | 0.000 |
| TyG-WHR | 6.92 ± 1.08 | 7.21 ± 1.28 | 0.000 |
| TyG-WHtR | 3.96 ± 0.72 | 4.17 ± 0.81 | 0.000 |
| TyG-BMI | 197.72 ± 40.35 | 208.85 ± 46.79 | 0.000 |
Bold values indicate statistical significance (P< 0.05)
To further explore these differences, the TyG index and its derivatives were divided into quartiles (Q1-Q4), with Q1 representing the lowest values and Q4 the highest. Figure 1 illustrates the distribution of these quartiles between the H. pylori-infected and non-infected groups. In the H. pylori-infected group, a significantly higher proportion of subjects fell into the highest quartile (Q4) for TyG and its derivatives, while a significantly lower proportion fell into the lowest quartile (Q1) (all P trend < 0.05). To further account for the potential confounding effect of sex imbalance, logistic regression analyses adjusted for age and sex were additionally performed. As shown in Table 3, H. pylori infection remained independently associated with increased odds of being in the highest quartile (Q4) of TyG-related indices after adjustment for age and sex. These findings suggest that H. pylori infection is associated with elevated TyG-related indices, indicating increased insulin resistance among infected individuals.
Fig. 1.
Distribution of TyG index and its derivatives by H. pylori infection status. Distribution of the TyG index (A), TyG-WHR (B), TyG-WHtR (C), and TyG-BMI (D) divided into quartiles (Q1-Q4) among H. pylori infected and non-infected subjects
Table 3.
Association between H. Pylori infection and elevated TyG-related indices by logistic regression analysis
| H. Pylori infection | ||
|---|---|---|
| Odds ratio | 95% CI | |
| TyG | 1.398 | 1.016–1.924 |
| TyG-WHR | 1.618 | 1.138–2.301 |
| TyG-WHtR | 1.671 | 1.198–2.331 |
| TyG-BMI | 1.862 | 1.350–2.567 |
Participants were categorized into low- and high-index groups using the highest quartile of each TyG-related index as the cutoff. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using logistic regression analysis after adjustment for age and sex
TyG and its derivatives are highly correlated with 10-year cardiovascular disease risk
The TyG index is a key indicator of insulin sensitivity and plays a significant role in assessing CVD risk. We analyzed the correlation between the TyG index and its derivatives with the 10-year CVD risk calculated using the Framingham risk score. As shown in Fig. 2, the TyG index and its derivatives were all highly correlated with the 10-year CVD risk. Among these, TyG-WHR (R = 0.745, P < 0.001) and TyG-WHtR (R = 0.701, P < 0.001) exhibited the strongest correlations. These findings demonstrate that higher TyG indices, indicating greater insulin resistance, are associated with an increased 10-year CVD risk.
Fig. 2.
Correlation between TyG index and its derivatives with 10-year CVD risk. Scatter plots showing the correlation between the TyG index (A), TyG-WHR (B), TyG-WHtR (C) and TyG-BMI (D) with 10-year CVD risk, calculated using the Framingham risk score
Higher 10-year CVD risk in H. pylori infected subjects
We further compared the 10-year CVD risk between H. pylori-infected and non-infected groups. As shown in Fig. 3A, the 10-year CVD risk was significantly higher in the H. pylori-infected group (P = 0.003). Additionally, when the 10-year CVD risk was divided into quartiles, the distribution differed notably between the two groups (Fig. 3B). A significantly higher proportion of individuals in the H. pylori-infected group fell into the highest quartile for CVD risk compared to the non-infected group (P = 0.002). This finding indicates that H. pylori infection is associated with an elevated 10-year CVD risk.
Fig. 3.
Comparison of 10-year CVD risk between H. pylori infected and non-infected subjects. A Box plot showing the 10-year CVD risk scores between H. pylori infected and non-infected groups. Data are presented as mean ± 95% CI. B Quartile distribution of 10-year CVD risk scores between H. pylori infected and non-infected groups
H. pylori infection is independently associated with high CVD risk
Using the Framingham risk score, we classified subjects into low-risk and high-risk groups with a threshold of 10%. Logistic regression analysis was conducted to determine whether H. pylori infection was independently associated with high CVD risk. As shown in Table 4, H. pylori infection was significantly associated with high CVD risk. After adjusting for age and sex (Model 2), and further adjusting for diabetes, smoking, and hypertension (Model 3), followed by additional adjustment for BMI and WHR (Model 4), the odds ratios (ORs) remained significant (Model 4: OR = 2.552, 95% CI = 1.312–4.963, P = 0.006).
Table 4.
Association between H. Pylori infection and elevated 10-year CVD risk by logistic regression analysis
| H. Pylori infection | ||
|---|---|---|
| Odds ratio | 95% CI | |
| Model 1 | 1.739 | 1.285–2.353 |
| Model 2 | 2.492 | 1.496–4.415 |
| Model 3 | 2.749 | 1.437–5.257 |
| Model 4 | 2.552 | 1.312–4.963 |
Participants were categorized into low-risk and high-risk groups using a 10% Framingham risk score threshold. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using logistic regression analysis after adjustment for age and sex. Model 1: crude; Model 2: adjust for age and sex; Model 3: adjust for age, sex, Diabetes, Smoke, Hypertension. Model 4: adjust for age, sex, Diabetes, Smoke, Hypertension, BMI, WHR
H. pylori infection is independently associated with 10-year cardiovascular risk in healthy, younger, non-smoking and female populations
To further explore the association between H. pylori infection and high CVD risk, the study population was stratified into subgroups based on sex, age, smoking status, hypertension, and diabetes. The analysis revealed that H. pylori infection was independently associated with high CVD risk in several subgroups, including females, individuals under 50 years of age, non-smokers, and those without diabetes or hypertension (Fig. 4). Notably, these associations were more evident in individuals without traditional cardiovascular risk factors, suggesting that the potential impact of H. pylori infection on cardiovascular risk may be more pronounced in otherwise low-risk populations.
Fig. 4.
Stratified analysis of H. pylori infection and high CVD risk. Logistic regression analysis of H. pylori infection and high CVD risk stratified by sex, age, smoking status, and presence of diabetes and hypertension
Discussion
In this study, we found that H. pylori infection was significantly associated with increased insulin resistance and elevated 10-year cardiovascular risk. Notably, this association was more pronounced in individuals without traditional cardiovascular risk factors, including younger, non-diabetic, non-hypertensive, and non-smoking populations. The TyG index and its derivatives are well-established markers of insulin resistance, which is a key factor in the development of cardiovascular events. Our findings demonstrate that all TyG indices are strongly correlated with 10-year CVD risk. Notably, subjects with H. pylori infection exhibited significantly higher levels of the TyG index and its derivatives, indicating greater insulin resistance. Moreover, the 10-year CVD risk, as measured by the Framingham score, was significantly higher in the H. pylori-infected group compared to the non-infected group. Stratified logistic regression analysis further confirmed that H. pylori infection is independently associated with a higher risk of cardiovascular events, particularly in subgroups such as females, younger individuals, non-smokers, non-diabetics, and those without hypertension. This finding suggests that H. pylori infection may act as a non-traditional or early contributor to cardiovascular risk, particularly in otherwise low-risk individuals.
Previous studies investigating the relationship between H. pylori infection and CVD risk have yielded conflicting results. Some studies have demonstrated a significant association between H. pylori infection and increased CVD risk [11, 16], while others have not found such a connection. For instance, a large cohort study did not observe a significant correlation between H. pylori seropositivity and ischemic heart disease [12]. Additionally, some studies suggest that the evidence for a direct causal link between H. pylori infection and CVDs is inconsistent and may be influenced by confounding factors [10, 17].
The inconsistencies in previous studies may be attributed to differences in study populations, methodologies, and the presence of confounding variables. Our study addresses some of these limitations by conducting a stratified analysis, which revealed that H. pylori infection is independently associated with high CVD risk, particularly in females, younger individuals, healthy individuals, and non-smokers. This stratified approach may explain why earlier studies failed to detect a significant association, as the impact of H. pylori infection on CVD risk might be more pronounced in these specific subgroups. Our findings suggest that while the influence of H. pylori infection on CVD risk might be less significant compared to traditional risk factors such as hypertension, diabetes, smoking, and age, it still poses a considerable risk in otherwise healthy populations. Therefore, the eradication of H. pylori could have meaningful implications for reducing CVD risk, particularly in these subgroups.
In the present study, participants with H. pylori infection exhibited higher BMI and central adiposity indices. Although some previous meta-analyses have reported lower BMI in populations with higher H. pylori prevalence, the association between H. pylori infection and obesity remains controversial [18, 19]. Discrepant findings across studies may be attributable to differences in ethnicity, socioeconomic status, dietary habits, lifestyle factors, and study design. In addition, our study population consisted of urban Chinese individuals undergoing routine health examinations, whose metabolic characteristics and lifestyle patterns may differ from those of previously reported populations.
The increased CVD risk associated with H. pylori infection can be explained by several mechanisms. Chronic inflammation induced by the infection leads to endothelial dysfunction and atherosclerosis, as the inflammatory response generates reactive oxygen species (ROS) that cause oxidative stress and damage to endothelial cells [20, 21]. This process is further exacerbated by the immune response, which involves cytokines such as interleukin-6 (IL-6), cyclooxygenase (COX), and tumor necrosis factor-alpha (TNF-α), promoting atherosclerosis [22–25]. H. pylori infection also affects lipid metabolism, leading to dyslipidemia, characterized by elevated levels of total cholesterol and triglycerides, and reduced HDL cholesterol, all of which contribute to cardiovascular risk [3, 26]. These mechanisms collectively contribute to the development and progression of CVD in individuals infected with H. pylori.
There are several limitations to our study. First, the cross-sectional design precludes causal inference. Second, the study population was derived from a single center in Beijing, which may limit generalizability. Third, H. pylori virulence factors (e.g., CagA status) were not assessed. Fourth, residual confounding factors, such as lifestyle and dietary habits, could not be fully excluded. Finally, because individuals with severe cardiovascular disease, malignancy, or prior gastrointestinal surgery were excluded, the proportion of high-risk older participants may have been reduced. This may partly explain why the association between H. pylori infection and cardiovascular risk appeared less pronounced in subjects aged ≥ 50 years.
In conclusion, H. pylori infection is associated with increased insulin resistance and elevated cardiovascular risk, particularly in individuals without traditional risk factors. These findings highlight the potential role of H. pylori infection as a non-traditional cardiovascular risk factor and underscore the need for further prospective studies.
Supplementary Information
Authors’ contributions
XLZ, JKY and MMZ designed this study. DNC, JC, YL and RRX were involved in data collection. WL provided statistical expertise. MMZ analyzed the data and wrote the first draft of the manuscript. XLZ and MMZ contributed to the interpretation and discussion of this study. All authors approved the final version of the manuscript.
Funding
This work was supported by grants from Beijing Municipal Science &Technology Commission (Z151100004015021) to XLZ, the National Natural Science Foundation of China (82341076) to JKY, the National Natural Science Foundation of China (82300917) and the Beijing Municipal Administration of Hospitals Incubating Program (PX20240203) to MMZ.
Data availability
The data that support the findings of this study are available from the corresponding author upon reasonable request.
Declarations
Ethics approval and consent to participate
The study was approved by the Ethics Committee of Beijing Tongren Hospital, Capital Medical University (TRECKY2018-033). As this was a retrospective study using anonymized data obtained from routine health examinations and involved no additional interventions, the Ethics Committee waived the requirement for additional study-specific informed consent. In addition, as part of the hospital’s standard pre-examination procedure, all individuals undergoing health examinations had signed written informed consent prior to participation, authorizing their examination results and clinical data to be used for scientific research purposes. Therefore, all data used in the present study were covered by the informed consent previously provided by all participants. All procedures involving human participants were conducted in accordance with the ethical standards of the institutional research committee and with the Declaration of Helsinki.
Consent for publication
Not applicable.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s Note
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Contributor Information
Dong-Ning Chen, Email: 13501082964@mail.ccmu.edu.cn.
Jin-Kui Yang, Email: jkyang@ccmu.edu.cn.
Xue-Lian Zhang, Email: trxlzhang@126.com.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Data Availability Statement
The data that support the findings of this study are available from the corresponding author upon reasonable request.