Helicobacter pylori infection increases the risk of dyslipidemia in Chinese non-obese and non-diabetic population from the perspective of age category: a retrospective cross-sectional study

Abstract

Background/Objectives

Currently, the increased prevalence of Helicobacter pylori (H. pylori) infection and elevated levels of dyslipidemia pose a major public health challenge. We aimed to investigate the association between dyslipidemia and H. pylori infection from the perspective of age category.

Methods

A retrospective cross-sectional study was conducted on 3530 non-obese and non-diabetic individuals who underwent a physical examination at the 991st Hospital of the Joint Logistics Support Force of People’s Liberation Army from January to December 2024. Physical measurements, hematological markers, and detection of H. pylori were gathered from all patients. According to the results of the detection of H. pylori, the subjects were divided into the H. pylori-positive group and the H. pylori-negative group. The correlation between H. pylori infection and blood lipid levels was compared between the two groups according to age category. Binary Logistic regression analysis was used to analyze the factors influencing H. pylori infection.

Results

Among 3530 healthy subjects, 1176 cases (33.31%) were in the H. pylori-positive group and 2354 cases (66.69%) were in the H. pylori-negative group. In the 30–59 age group, low-density lipoprotein cholesterol (LDL-c), triglycerides (TG), and total cholesterol (TC) levels were significantly higher in H. pylori-positive individuals compared to H. pylori-negative individuals (P < 0.05), with no significant differences in other age groups (P > 0.05). Binary Logistic regression showed that H. pylori infection was associated with elevated LDL-c [OR = 2.100, 95%CI (1.771–2.491), P < 0.001], elevated TC [OR = 2.844, 95%CI (2.232–3.623), P < 0.001], male gender [OR = 1.267, 95%CI (1.054–1.524), P < 0.05], ages 40–49 [OR = 1.602, 95%CI (1.181–2.173), P < 0.05].

Conclusions

H. pylori infection is associated with dyslipidemia in non-obese and non-diabetic people, especially those aged 30–59. In men aged 40–49, H. pylori positivity was more strongly related to elevated TC and LDL-c, highlighting the importance of routine H. pylori screening in this age group.

Introduction

Helicobacter pylori (H. pylori) is a gram-negative bacterium that is strongly associated with the occurrence of chronic gastritis (90%), peptic ulcers (5-10%), and gastric cancer (1%) [1, 2]. The global population exhibits a general susceptibility to H. pylori infection, which is prevalent across various regions and ethnic groups, with infection rates reaching up to 50%. China, in particular, has a high prevalence of H. pylori infection and a high incidence of gastric cancer [3]. Eradication of H. pylori can significantly reduce the risk of gastric cancer [4]. In 1994, H. pylori was classified as a Group I carcinogen, and in 2022, the US Department of Health and Human Services formally recognized H. pylori as carcinogen [5, 6]. Recent studies have broadened the understanding of H. pylori infection, revealing its association not only with gastrointestinal disease but also with hematological, neurological, and cardiovascular diseases, underscoring the importance of early detection and treatment [7, 8]. Furthermore, extensive research has shown an association between H. pylori infection and dyslipidemia [9, 10], meanwhile, a meta-analysis found no significant association between H. pylori seropositivity and TC or TG levels [11]. The relationship between H. pylori infection and dyslipidemia in different age groups remains underexplored, particularly in the context of age-specific metabolic changes.

This study, a retrospective cross-sectional survey, aims to assess the association of H. pylori infection with dyslipidemia in the Chinese non-obese and non-diabetic population from the perspective of age category.

Materials and methods

Research object

A total of 3530 patients met the inclusion criteria in a physical examination at the 991st Hospital of the Joint Logistics Support Force of People’s Liberation Army from January to December 2024. All personnel were required to maintain a stable diet and body weight for at least 2 weeks before blood collection, avoid overeating, avoid strenuous physical activity for 24 h, overnight fast for 8–12 h, and rest for at least 5 min in a seated position. Clinical information was collected and analyzed, including medical history, age, gender, body mass index (BMI), serum lipid parameters [total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-c), high-density lipoprotein cholesterol (HDL-c)], and ¹⁴C-urea breath test results. Inclusion criteria: ① Patients aged 20–70 years, regardless of gender, completed ¹⁴C-urea breath test and serum lipid parameters; ② complete clinical data; ③ no previous or current H. pylori eradication therapy and dyslipidemia therapy [12]; ④ non-obese and non-diabetic population. Exclusion criteria: ① patients with a history of malignancy, abnormal liver or kidney function, mental illness, and obesity or diabetes; ② patients with severe cardiopulmonary dysfunction; ③ patients receiving H. pylori eradication therapy and dyslipidemia therapy; ④ BMI ≥ 30 kg/m², glycated hemoglobin A1c (HbA1c ≥ 6.5); ⑤ incomplete clinical data. The incomplete data were deleted. The incomplete data were serum lipid parameters (TG, TC, LDL-c, or HDL-c), and the proportion of missing data was 4.59%, which was less than 5%. Deletion and mean-filling methods were used to handle the missing data. The results of the statistical analysis showed that the conclusions drawn from the two methods of handling missing data were consistent.

Determination of sample size

The sample size was calculated using PASS 21, based on a presumed 50% infection rate, 95% confidence level, and 5% CI width. Post-hoc power analysis was not conducted; however, the large sample size (n = 3,530) ensures sufficient statistical power for detecting meaningful associations.

Definition of H. pylori infection

Subjects fasted for at least 6 h before testing and completed the ¹⁴C-urea breath test. The entire ¹⁴C-urea capsule was swallowed during the examination. The patient was instructed to remain seated quietly and to as little as possible after taking the medicine. Within 15–25 min, the patient was instructed to take a long inhalation followed by a slow exhalation, and forced exhalation was prohibited. The test was performed immediately after exhalation. Samples were then analyzed using a 14 C-urea breath analyzer. To account for the possibility of false-positive and false-negative results near the critical value, a value ≥ 75 is considered positive [13].

Definition of dyslipidemia

Dyslipidemia was defined as meeting one of the following criteria: HDL-c level < 0.9 mmol/L; LDL-c level ≥ 3.4 mmol/L, TG level ≥ 1.7 mmol/L, TC level ≥ 5.2 mmol/L, according to the Chinese guidelines for Lipid Management (2023) [14]. Dyslipidemia was defined as either “borderline high LDL-c, TC, TG " or “low HDL-c,” whichever occurred first [15].

Observation target

The main observations were as follows: (1) To understand the overall H. pylori infection rate; (2) The included researchers were divided into 20–29 ages, 30–39 ages, 40–49 ages, 50–59 ages, and ≥ 60 ages, and the situation of H. pylori infection in different age groups was compared; (3) The patients were divided into H. pylori-positive group and H. pylori-negative group, and the four indicators of blood lipids were compared between the two groups according to age category; (4) one-way ANOVA was used to analyze the correlation between H. pylori infection and four indicators of blood lipids; (5) binary Logistic regression model was used to analyze the factors influencing H. pylori infection.

Ethical considerations

This study was conducted by the ethical principles of the Medical Ethics Committee of the 991st Hospital of the Joint Logistics Support Force of People’s Liberation Army (No. 991YJ-202316). Data were anonymized using numerical coding to maintain patient confidentiality, and all data collected were used only for this research.

Statistical data analysis

SPSS 22 software was used for statistical analysis. Continuous and categorical variables were presented as mean ± standard deviation (x̅±s) and counts or percentages, using Student’s t-test or one-way ANOVA and chi-square test for comparisons between the two groups. A binary Logistic regression model was used to estimate odds ratios (OR) and 95% confidence intervals (CI) associated with H. pylori infection. The dependent variable was the presence of H. pylori infection, and the variables included in the analysis were analyzed using one-way ANOVA or chi-square tests for statistical significance. Confounders were controlled using the forward stepwise method. P < 0.05 was considered statistically significant.

Results

Part 1

Baseline status of H. pylori infection

The baseline characteristics of all enrolled participants are shown in Table 1. Of 3530 individuals, 1176 (33.31%) were infected with H. pylori, and 2354 (66.69%) were not infected with H. pylori. The infection rate was 35.18% (914/2598) in males and 28.11% (262/932) in females. There was no significant difference in mean age between the H. pylori-positive group and the H. pylori-negative group (P > 0.05). To further explore the relationship between the two was examined by age category. The overall infection rate was highest in those 30–39 ages (35.59% (567/1593)) and lowest in those 20–29 ages (15.83% (19/120)). The infection rate was higher in those aged 40–49 and 50–59 than in those aged > 60. There was no significant difference in age between the two groups, but there were significant differences in gender and age category between the two groups (P < 0.05). Figure 1 shows the abnormal proportions of H. pylori infection, HDL-c, TG, LDL-c, and TC in each age category. The proportion of H. pylori infection was higher in the age category of 30–59 years, which was more than 30%. The proportion of abnormal HDL-c was stable in all age groups, lower than 7%; the proportion of abnormal LDL-c was different in different age groups, and the abnormal proportion increased with increasing age, but the abnormal proportion was highest in the 50–59 age group, reaching 40.22%. The proportion of TG and TC also increased with age, but the abnormal proportion of TG was higher than that of TC in all age groups, and the abnormal proportion was highest in people aged > 60 years (38.75% vs. 16.97%). Figure 2 shows the abnormal proportions of LDL-c, TC, TG, and HDL-c in the H. pylori-positive and H. pylori-negative groups. The abnormal proportion of LDL-c, TC, TG, and HDL-c in H. pylori-positive and H. pylori-negative groups were (48.72% vs. 24.34%), (23.13% vs. 6.66%), (38.52% vs. 29.95%), and (6.80% vs. 5.65%). There was no significant difference in HDL-c between the two groups (P > 0.05), but the comparison of LDL-c, TC, and TG between the two groups was significant (P < 0.05).

Table 1.

General data of patients in the two groups (using student’s t test or chi-square test)

Variable		H. pylori-positive group n = 1176(%)		H. pylori-negative group n = 2354(%)	t/X2	p
Gender					15.43	0.00
	male	914(77.72)		1684(71.54)
	Female	262(22.28)		670(28.46)
Average		42.19 ± 10.56		42.66 ± 10.76	1.22	0.22
age/year
Age category/year					23.27	0.00
	20–29 30–39 40–49 50–59 ≥ 60	19(15.83) 567(35.59) 270(33.54) 243(32.79) 77(28.41)		101(84.17) 1026(64.41) 535(66.46) 498(67.21) 194(71.59)

Fig. 1.

The proportion of H. pylori positive, HDL-c, TG, LDL-c, and TC abnormality in each age category. H. pylori infections were marked in red, TG abnormal in green, HDL-c abnormal in yellow, TC abnormal in blue, and LDL-c abnormal in purple

Fig. 2.

Abnormal proportions of LDL-c, TC, TG, and HDL-c in the H. pylori-positive group and the H. pylori-negative group. “Positive” represents the proportion of H. pylori-positive patients with abnormal LDL-c, TC, TG, and HDL-c, marked in red, and “Negative” represents the proportion of H. pylori-negative patients with abnormal LDL-c, TC, TG, and HDL-c, marked in blue. *** indicates significance <0.01, ns indicates significance >0.05

Correlation between H. pylori infection status and dyslipidemia

The comparison of mean ± standard deviation (SD) of LDL-c, TC, TG, and HDL-c levels at the age categories in the H. pylori-positive and H. pylori-negative groups is shown in Table 2. Statistically significant differences in H. pylori infection status were assessed by comparing H. pylori-positive and H. pylori-negative individuals. In the total category of participants, the levels of LDL-c (3.133 ± 0.810), TC (5.319 ± 1.062), and TG (1.905 ± 1.746) were higher in the H. pylori-positive group than in the negative group (2.768 ± 0.690, 4.885 ± 0.888, 1.645 ± 1.186). The HDL-c level in the positive group was lower than that in the negative group (1.276 ± 0.294 vs. 1.308 ± 0.345, both P < 0.05). Figure 3 Age category shows the mean ± SD of LDL-c, TC, TG, and HDL-c in H. pylori-positive and H. pylori-negative groups. The median (IQR) levels of LDL-c (Fig. 4a), TG (Fig. 4b), HDL-c (Fig. 4c), and TC (Fig. 4d) by H. pylori-infection status are shown in Fig. 4. The median (IQR) levels of LDL-c, TG, and TC in the H. pylori-positive group were higher than those in the H. pylori-negative group in the 30–39, 40–49, and 50–59 age groups, and the differences were statistically significant (P < 0.05), whereas there was no significant difference in blood lipid levels between the H. pylori-positive and H. pylori-negative groups in the < 30 and ≥ 60 age groups (P > 0.05).

Table 2.

Comparative the mean ± sd of LDL-c, TC, TG, and HDL-c levels at the age categories in H. pylori-positive and H. pylori-negative groups (using one-way ANOVA)

Overall Participants
Variable			H. pylori-positive group (mean ± SD)		H. pylori-negative group (mean ± SD)		p
LDL-c TC			3.133 ± 0.810 5.319 ± 1.062		2.768 ± 0.690 4.885 ± 0.888		0.00 0.00
TG HDL-c			1.905 ± 1.746 1.276 ± 0.294		1.645 ± 1.186 1.308 ± 0.345		0.00 0.00
Age category (Age < 30)
LDL-c TC TG HDL-c			2.602 ± 0.569 4.627 ± 0.744 1.410 ± 0.771 1.328 ± 0.284		2.664 ± 0.719 4.739 ± 0.816 1.452 ± 0.905 1.357 ± 0.379		0.72 0.58 0.85 0.76
Age category (Age 30–39)
LDL-c TC TG HDL-c			3.075 ± 0.767 5.172 ± 1.008 1.792 ± 1.485 1.227 ± 0.273		2.713 ± 0.686 4.739 ± 0.824 1.533 ± 1.060 1.267 ± 0.283		0.00 0.00 0.00 0.07
Age category (Age 40–49)
LDL-c TC TG HDL-c			3.182 ± 0.765 5.407 ± 0.972 2.107 ± 1.920 1.273 ± 0.290		2.777 ± 0.672 4.924 ± 0.873 1.692 ± 1.226 1.333 ± 0.437		0.00 0.00 0.00 0.04
Age category (Age 50–59)
LDL-c TC TG HDL-c			3.328 ± 0.889 5.696 ± 1.179 2.057 ± 2.267 1.375 ± 0.312		2.846 ± 0.634 5.077 ± 0.877 1.785 ± 1.302 1.341 ± 0.332		0.00 0.00 0.04 0.18
Age category (Age ≥ 60)
LDL-c TC TG HDL-c			2.900 ± 0.901 5.082 ± 1.077 1.667 ± 1.850 1.317 ± 0.318		2.889 ± 0.826 5.136 ± 1.140 1.844 ± 1.429 1.343 ± 0.353		0.93 0.73 0.31 0.58

Fig. 3.

Age category showed the mean ± SD of LDL-c, TC, TG, and HDL-c in H. pylori-positive and H. pylori-negative groups. H. pylori-positive groups were marked in red, and H. pylori-negative groups were marked in blue. *** indicates significance <0.01, * indicates significance <0.05. a: LDL-c level and Helicobacter pylori infection status in each age group; b: TG level and Helicobacter pylori infection status in each age group; c: HDL-c level and Helicobacter pylori infection status in each age group; d: TC level and Helicobacter pylori infection status in each age group

Fig. 4.

Illustration of the median (IQR) of LDL-c, TC, TG, and HDL-c levels in H. pylori-positive and H. pylori-negative groups, respectively. Dyslipidemia in the H. pylori-positive group was marked in red, and dyslipidemia in the H. pylori-negative group was marked in green. a: level of LDL-c by H. pylori-infection status; b: level of TG by H. pylori-infection status; c: level of HDL-c by H. pylori-infection status; d: level of TC by H. pylori-infection status

Part 2

The influencing factors of H. pylori infection were analyzed by binary logistic regression

Using one-way ANOVA or Chi-square test to screen out two groups of significant factors. The results showed that age category, gender, LDL-c, TG, and TC were statistically significant. A binary Logistic regression model was used to screen out factors related to H. pylori infection. With H. pylori infection as dependent variable (0 = no, 1 = yes), age category (20–29 years = 0, 30–39 years = 1, 40–49 years = 2, 50–59 years = 3, ≥ 60 years = 4), gender (female = 0, male = 1), LDL-c (not elevated = 0, elevated = 1), TG (not elevated = 0, elevated = 1), TC (not elevated = 0, elevated = 1) were used as independent variables. P < 0.05 was considered statistically significant. After adjustment for confounders, binary logistic regression analysis showed that male gender, age 40–49 years, elevated LDL-c and TC were independent risk factors for H. pylori infection (P<0.05). Binary Logistic regression analysis revealed the following associations with H. pylori infection: (1) elevated LDL-c [OR = 2.100, 95%CI (1.771–2.491), P < 0.001] vs. normal levels; (2) elevated TC [OR = 2.844, 95%CI (2.232–3.623), P < 0.001] vs. normal levels; (3) male gender [OR = 1.267, 95%CI (1.054–1.524), P < 0.05] vs. female; (4) age 40–49 [OR = 1.602, 95%CI (1.181–2.173), P < 0.05] vs. other age groups. As shown in Table 3.

Table 3.

Influencing factors of H. pylori infection in binary logistic regression model

Variable	β	SE	Waldχ2	OR	95% CI	P
elevated LDL-c	0.742	0.087	72.692	2.100	1.771~2.491	0.000
elevated TC male 40–49 age	1.045 0.237 0.471	0.124 0.094 0.156	71.573 6.357 9.176	2.844 1.267 1.602	2.232~3.623 1.054~1.524 1.181~2.173	0.000 0.012 0.002

Discussion

H. pylori was first identified in 1982 by Australian researchers in gastric biopsy specimens from people with chronic gastritis. This bacterium typically colonizes the human stomach and causes chronic inflammation of the gastric mucosa, which can progress to atypical hyperplasia and even malignant lesions [16, 17]. The prevalence of H. pylori infection exceeds 50% in the general population [18–21], with marked differences between developed and developing countries, as well as regional variations within countries [22, 23]. The incidence of H. pylori infection is increasing every year, has a significant impact on both physical and mental health, imposes a substantial economic and healthcare burden, and has therefore become a focus of research in recent years [24–27]. As research progresses, it becomes clear that H. pylori infection may not only contribute to gastrointestinal disorders but may also be involved in diseases of the hematological, neurological, and cardiovascular systems [28–31].

Cardiovascular disease (CVD) is the leading chronic non-communicable disease threatening human life and health worldwide. Epidemiological, genetic, and clinical intervention studies have fully confirmed that LDL-c is a pathogenic risk factor for atherosclerotic cardiovascular disease (ASCVD) [32]. TC levels often increase with age and are lower in young and middle-aged women than in men. TC levels are higher in postmenopausal women than in men of the same age [14]. The association between H. pylori infection and dyslipidemia was first identified in 1996 in a Finnish case-control study. H. pylori infection may exacerbate metabolic disorders through inflammatory processes and elevated TG, TC, and LDL-c, thereby increasing the risk of CVD [33]. H. pylori can cause chronic inflammation in the gastric mucosa, and the global effect of inflammation may be related to the mechanism of atherosclerosis [34]. In addition, studies show that high TG levels are an inflammatory and metabolic predictor in several conditions. These include CVD [35], type 2 diabetes mellitus (T2DM) [36], hypertension [37], chronic nephritis [38–40] and hepatic steatosis [41]. Low levels of HDL-c have also been reported in hypertension [42], non-alcoholic hepatic steatosis [43], T2DM [44], thyroiditis [45], metabolic syndrome [46], pre-diabetes [47], diabetic kidney disease [48], and even in new-onset diabetes [49].

The mechanisms by which H. pylori infection affects blood lipids are diverse: (1) H. pylori infection can lead to anorexia, dyspepsia, and malabsorption as a result of chronic gastritis and peptic ulcers, which in turn may affect food intake and energy metabolism, potentially contributing to the development of dyslipidemia [50]. (2) H. pylori infection affects lipid metabolism by activating pro-inflammatory cytokines that affect lipolysis, stimulate hepatic fatty acid synthesis, and activate lipoprotein lipase in adipose tissue. In addition, H. pylori infection induces the production of several pro-inflammatory mediators and vasoactive substances, thereby increasing oxidative stress and insulin resistance through autoimmune pathways. The local microenvironment can be altered by several factors. Abnormal blood lipid levels and insulin resistance have a bidirectional interaction. Insulin resistance contributes to dyslipidemia, typically characterized by elevated TC and TG. Hyperinsulinemia induces sympathetic activation, upregulates α1-adrenergic receptors and angiotensin II, decreases lipoprotein lipase activity, and impairs TG catabolism, thereby promoting lipid dysregulation and atherogenesis [51]. (3) H. pylori infection can induce oxidative stress in gastric epithelial cells, triggering various pathophysiological mechanisms and eliciting host responses [52, 53]. Oxidative stress alters HDL-c-associated enzymes, leading to reduced HDL-c levels and subsequent lipoprotein and lipid abnormalities. In addition, serum amyloid A (SAA), an inflammatory mediator, can be induced to replace key HDL components, further reducing HDL-c levels and affecting lipid distribution and blood lipid profiles [54]. (4) H. pylori infection alters the structure of the gastrointestinal flora, thereby reducing the diversity of the flora. H. pylori infection interferes with the homeostasis of the internal environment and lipid metabolism by the intestinal flora [55]. A large study confirmed that the gut microbiome plays an important role in blood lipid changes [56].

Our study population was a normal population without obesity and diabetes. The population was divided into H. pylori-positive and H. pylori-negative groups according to the results of the ¹⁴C-urea breath test. There was significant difference in gender between the two groups, but there was no difference in age. However, the infection rate was higher in those aged 30–59 ages than in those aged 20–29 ages and > 60 years. There was a significant difference in age category between the two groups (P < 0.05). This is in line with the results of Sun et al., who reported that more men than women tended to be infected with H. pylori, with the highest positive rate in the 30–39 age group and the lowest rate in the < 30 age group [57]. Compared with H. pylori-negative individuals, H. pylori-positive individuals had significantly higher LDL-c, TC, and TG levels and lower HDL-c levels (all P < 0.05). These differences remained significant in the 30–39, 40–49, and 50–59 age groups (P < 0.05). However, no significant differences in lipid profile were observed in the age groups < 30 or ≥ 60 years (P > 0.05). Binary logistic regression showed the odds of H. pylori infection were significantly higher in individuals with elevated LDL-c (OR = 2.100, 95% CI: 1.771–2.491) and elevated TC (OR = 2.844, 95% CI: 2.232–3.623) compared to those with normal levels. Similarly, males had 1.267-fold increased odds (OR = 1.267, 95% CI: 1.054–1.524) compared to females, and the 40–49 age group had 1.602-fold increased odds (OR = 1.602, 95% CI: 1.181–2.173) compared to other age groups (all p-values < 0.05). This was consistent with Izhari et al. study [58], who reported that one-unit increase in the level of TC, TG, and LDL-c increased the odds of being infected with H. pylori by 226.2% (AOR:3.26, 95%CI:1.778–6.258, p < 0.001), 30% (AOR:1.298, 95%CI:0.928–1.834, p > 0.05), and 67% (AOR:0.333, 95%CI:0.156–0.676, p < 0.01), respectively. A meta-analysis also showed that H. pylori infection was positively associated with LDL-c, TC, and TG [59].

In this study, using age category, we found that H. pylori infection was more closely associated with dyslipidemia in the 30–59 age group and the possible reasons were as follows: (1) With increasing age, the basal metabolic rate gradually decreases, the rate of lipolysis slows down, lipase activity decreases, and there is a tendency for fat accumulation and abnormal lipid metabolism. (2) In postmenopausal women, decreasing estrogen levels can lead to decreased levels of HDL-c and increased levels of LDL-c [60]. (3) H. pylori infection can cause chronic inflammation of the stomach lining. With age, there may be a reduced ability to clear H. pylori, resulting in the persistence of this inflammatory response. Dyslipidemia may also exacerbate oxidative stress and inflammation, creating a vicious cycle. Oxidative stress caused by H. pylori infection affects the function of the immune system, which in turn has a greater impact on blood lipids and exacerbates cardiometabolic disease [61]. (4) Unhealthy lifestyle and eating habits also play a role. People in this age group often face greater work and life pressures, leading to irregular eating patterns, high-fat and high-calorie diets, and lack of exercise. These factors alone increase the risk of dyslipidemia, and H. pylori infection may interact with these adverse lifestyle factors to exacerbate dyslipidemia. In younger people, the metabolism is more active and H. pylori infection may be cleared more easily. However, in older adults with conditions such as hypertension and diabetes, the effects of H. pylori may be less evident. It is therefore important to monitor the relationship between H. pylori infection and dyslipidemia in this age group.

The pathogenesis of H. pylori is based on its ability to produce a variety of virulence factors [62]. Cytotoxic-associated protein (CagA) and vacuolated toxin (VacA) are the most important virulence factors of H. pylori [63]. Studies have confirmed an association between infection with CagA-positive strains and coronary heart disease [64]. Studies have shown that lipid metabolism can be effectively improved after H. pylori eradication treatment. Wang et al. [65] suggested that after adjustment for confounding factors, H. pylori eradication would alleviate the deterioration of lipid metabolism, and patients with low total protein (TP) would benefit more from lipid metabolism after eradication, suggesting the positive role of H. pylori in controlling and improving lipid metabolism. The results of Adachi et al. showed lower concentrations of TC, TG, and LDL-c and higher levels of HDL-c in successfully eradicated H. pylori subjects compared to those with persistent H. pylori infection [66]. Park Y et al. [15] reported that H. pylori infection might play a pathophysiological role in developing dyslipidemia, whereas H. pylori eradication may reduce the risk of dyslipidemia. A triple therapy regimen for H. pylori eradication in Egypt found that there was a significant association between treatment of H. pylori infection and reduction in LDL-c, TG, and TC with an increase in HDL-c in both the 7-day and 10-day groups [67].

Although this study was a cross-sectional survey of a large sample of non-diabetic and non-obese populations, it is imperative to acknowledge that certain limitations were also evident in this study. First, this study is limited to a single center in China, the source of patients is relatively single, which may cause selective bias. Due to factors such as diet and genetic polymorphism, which may limit generalizability to other populations or ethnic groups. To establish more reliable evidence, there is a need for prospective multicenter cohort or international studies that would improve external validity. Second, this is a cross-sectional study, and although it confirmed the association between H. pylori infection and dyslipidemia, it could not determine the sequence of H. pylori infection and dyslipidemia. Third, the effect of H. pylori eradication on blood lipids was not included in the study. Fourth, the H. pylori infection status was only determined by the ¹⁴C-urea test, and H. pylori virulence factors and the influence of different types on dyslipidemia were not analyzed. Fifth, confounding factors such as smoking, alcohol consumption, and socioeconomic status—which may affect both H. pylori infection and dyslipidemia—were not measured in this study. This limitation may have introduced residual confounding, potentially over- or underestimating the observed associations. Sixth, missing data (4.59%) were limited to lipid parameters (TG, TC, LDL-c, HDL-c) and were handled using both listwise deletion and mean imputation. Although results were similar across both methods, we acknowledge that mean imputation has methodological limitations, and no formal sensitivity analysis was performed, which may affect robustness. Further studies should be needed in the following areas: First, lifestyle and environmental factors will be further collected in people aged 30–59 to assess the impact of lifestyle and environmental factors on H. pylori infection and dyslipidemia. Second, long-term cohort studies should be conducted to follow the effects of H. pylori infection on dyslipidemia over a long period and to observe the effects of H. pylori infection on blood lipids in obese or diabetic populations, to improve the scalability of the study. Third, future prospective cohort studies should evaluate whether H. pylori eradication therapy improves LDL-c, TC, and TG levels over time. Fourth, H. pylori virulence factors will be further analyzed to determine whether certain strains are more strongly associated with dyslipidemia.

Conclusions

Our results show that H. pylori infection is associated with dyslipidemia in the non-obese and non-diabetic population, especially those aged 30–59. In men aged 40–49, H. pylori positivity was more strongly associated with elevated TC and LDL-c, highlighting the importance of routine H. pylori screening in this age group. The occurrence of dyslipidemia in H. pylori-positive individuals may trigger atherosclerosis, coronary heart disease, and cerebral infarction in the population. Given the statistically significant association of dyslipidemia with H. pylori-positive individuals, effective management of the lipid profile of H. pylori-positive patients would be beneficial to minimize the clinical impact of infection on CVD.

Abbreviations

H. pylori

Helicobacter pylori

TC

Total cholesterol

TG

Triglyceride

LDL-c

Low-density lipoprotein cholesterol

HDL-c

High-density lipoprotein cholesterol

PPI

Proton pump inhibitor

CVD

Cardiovascular disease

ASCVD

Atherosclerotic cardiovascular disease

BMI

Body mass index

HbA1c

Glycated hemoglobin A1c

OR

Odds ratios

CI

Confidence intervals

SD

Standard deviation

Author contributions

HHS played a pivotal role in shaping the conceptual framework, conceptualizing and designing this study, assisting in data collection, supervising data entry, carrying out the initial analysis, drafting the initial manuscript, and reviewing and revising the final manuscript. JWW and XYZ contributed to the composition of the manuscript. DLZ were responsible for collecting data and conducting data analysis. KY and SX drafted the initial manuscript, reviewed and revised the final manuscript. Furthermore, all ICMJE requirements for authorship have been met, and this work is original and honest. All authors have read and agreed to the published version of the manuscript.

Funding

This study was supported by grants from the 991st Hospital of Joint Logistic Support Force of People’s Liberation Army (991YJ-202316).

Data availability

Data is provided within the manuscript or supplementary information files.

Declarations

Ethics approval and consent to participate

The studies involving human participants underwent review and approval by the Ethics Committee of the 991st Hospital of the Joint Logistics Support Force of People’s Liberation Army (No. 991YJ-202316). Our study adhered to the Declaration of Helsinki. This retrospective study used de-identified historical medical records and did not involve any intervention or additional risk to participants. The Ethics Committee of the 991st Hospital of the Joint Logistics Support Force of the People’s Liberation Army waived informed consent.

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.