Hypertension constitutes a major global determinant of cardiovascular and chronic kidney disease burden, driving elevated rates of mortality and disability [1]. Childhood hypertension is a significant predictor of adult-onset hypertension and the occurrence of serious cardiovascular complications later in life [2]. Children exhibiting elevated blood pressure are at heightened risk of transitioning into adulthood with clinically persistent hypertension [3]. A prevalence of 4.00% for hypertension and 9.67% for prehypertension has been documented in the population of individuals aged 19 and below [1]. Children and adolescents with overweight or obesity exhibit a markedly elevated prevalence of hypertension compared to their normal-weight peers [1]. The important risk factors for hypertension in these individuals are high body mass index (BMI), sedentary lifestyles, high-sodium diets, and family history of hypertension [4].

The gut microbiota demonstrates a significant correlation with the progression of hypertension [5]. A compromised gut barrier, resulting from microbiota dysregulation, permits the systemic entry of pathogenic microbes and their metabolites, leading to the induction of chronic inflammation and endothelial damage, which are recognized as key contributors to the pathogenesis and clinical worsening of hypertension [5]. Diet is an important external factor affecting the gut microbiota [6]. Some safe live microbes are present in fermented foods and other types of foods (e.g., yogurt, raw fruits/vegetables) and are influenced by food type and processing level. Evidence suggests that food-derived microbial components affect the gut microbiota composition and can improve gastrointestinal health and enhance immune responses [7]. Probiotic intake may be linked to lower blood pressure in the general population [8]. Furthermore, dietary microbial consumption is significantly related to a decreased risk of obesity in children and adolescents [9] and a lower risk of mortality in adults with hypertension [10]. Multiple studies have also shown that diet and BMI interact in metabolic disorders, specifically that a healthy diet may antagonize the risk of overweight/obesity-related diseases [11]. Thus, the authors intended to evaluate the association between dietary live microbial consumption and hypertension risk in children and adolescents, as well as the combined influence of microbial consumption and BMI on hypertension risk, to provide a basis for dietary management and hypertension prevention.

The 2009–2023 NHANES surveys comprised 12,641 individuals aged 8–17 years. Through the screening process, 3299 participants were excluded, resulting in 9342 participants for final analysis (Figure 1). Of these 9342 children and adolescents, 433 had hypertension, and 8909 did not. Participant characteristics are displayed in Table 1. The mean age was 12.52 (±0.04) years, and 5296 (60.36%) individuals were at least 12 years old. Among all participants, 4620 (49.67%) were female, and 2828 (53.27%) were non-Hispanic Whites. Overweight/obesity was identified in 4012 (40.36%) children and adolescents, with 5330 (59.64%) participants classified as non-overweight/obesity. The mean consumption of MedHi live microbial food was 0.93 (±0.03) 100 g/day. There were 6738 (69.76%) participants in the low-MedHi consumption group and 2604 (30.24%) in the high-MedHi consumption group. Significant differences emerged in gender, overweight/obesity, BMI percent, and MedHi consumption between the hypertension and non-hypertension groups (P < 0.05).

Fig. 1.

Flowchart for screening the study population. NHANES, the National Health and Nutrition Examination Survey; BMI, body mass index.

Figure 2 lists the RCS curve of the association between MedHi food consumption and the odds of hypertension. As dietary microbial consumption increases, the odds of hypertension decrease, but no significant nonlinear association was observed (Poverall = 0.004, Pnonlinear = 0.199).

Fig. 2.

The restricted cubic splines (RCS) curve of the relationship between MedHi live microbial consumption and hypertension odds among children and adolescents. MedHi, foods containing medium and high live microbes; OR, odds ratio.

The associations between microbial food consumption and hypertension odds are presented in Table 2. When grouped according to the types of microbial content in food, the medium- (P = 0.354) and high-live microbial groups (P = 0.323) (vs. the low group) were not significantly associated with the odds of hypertension. When the analysis was based on MedHi food consumption, a 100 g/day increase in MedHi food intake [OR = 0.88 (0.76–1.00), P = 0.053] showed a marginally significant association with the odds of hypertension. Individuals in the high-MedHi food consumption group (vs. low-MedHi) [OR = 0.70 (0.50–0.98), P = 0.039] were associated with lower odds of hypertension, and this association persisted after further adjustment for overweight/obesity [OR = 0.71 (0.51–0.99), P = 0.046]. The association between MedHi food consumption and hypertension odds was further analyzed based on overweight/obesity subgroups (Table 3). High-MedHi food consumption was associated with lower odds of hypertension only in overweight/obese individuals [OR = 0.61 (0.39–0.95)], but not in non-overweight/obese individuals (P = 0.859).

When analyzing the joint effect between MedHi food consumption (low-MedHi, high-MedHi) and overweight/obesity (no, yes) (Table 4), individuals in the high-MedHi and overweight/obesity group [OR = 0.60 (0.39–0.92)], the low-MedHi and non-overweight/obesity group [OR = 0.29 (0.20–0.42)], and the high-MedHi and non-overweight/obesity group [OR = 0.28 (0.16–0.49)] were linked to lower odds of hypertension versus the low-MedHi and overweight/obesity group, and there was a significant trend in these joint effect terms (Ptrend = 0.019).

Table 5 shows the results of the additive interaction between MedHi food consumption and overweight/obesity on hypertension odds. The RERI for the additive interaction was −1.33 (−2.62, −0.04), the AP was −0.65 (−1.41, 0.10), and the SI was 0.44 (0.19, 1.00), indicating that the additive interaction was not significant. However, high microbial consumption may exert an antagonistic trend on the odds of hypertension associated with overweight/obesity. Figure 3 visualizes the interaction of microbial consumption and BMI on the odds of hypertension. With the increase of MedHi microbial consumption, the slope of BMI relative to hypertension odds gradually decreases, indicating that high levels of microbial consumption may exert an antagonistic trend on the odds of BMI-related hypertension. As BMI increases, the impact of microbial consumption on hypertension also increases. Furthermore, multiplicative interaction analysis revealed no significant multiplicative interaction between MedHi microbial consumption and overweight/obesity in relation to the odds of hypertension (P for likelihood‑ratio test = 0.470) (Supplementary Table 2).

Figure 3.

The visualization of the interaction between dietary live microbial consumption and BMI on the odds of hypertension. BMI, body mass index; MedHi, foods containing medium and high live microbes; OR, odds ratio.

The present study explored the association between microbial consumption and the odds of hypertension in children and adolescents. The findings indicated that high MedHi microbial consumption was associated with lower odds of hypertension among children and adolescents. Moreover, live microbial intake and overweight/obesity exhibited a joint effect on the odds of hypertension.

Hypertension prevalence increases steadily with advancing age. Childhood blood pressure status correlates closely with that in early middle age, and this status can persist from childhood into adulthood [14]. The gut microbiota has been reported to regulate blood pressure through various mechanisms, encompassing the renin-angiotensin-aldosterone, autonomic nervous, and immune systems [5]. Diet is regarded as one of the most influential modifiable factors shaping gut microbial diversity and function [15]. The present findings revealed that high MedHi microbial food consumption was associated with lower odds of hypertension. A meta-analysis also showed that probiotic intervention significantly reduced blood pressure, BMI, and glucose levels in hypertension patients [16]. In addition, these findings indicated that high microbial consumption may exert an antagonistic trend on the odds of overweight/obesity-related hypertension. Overweight/obesity is an important factor influencing hypertension. Hypertension has a prevalence of 15.3% among children with obesity, while it is 1.9% among children of normal weight [1]. Hill et al. reported that a diet rich in live microbes is linked to reduced systolic blood pressure, BMI, C-reactive protein, blood glucose, and triglyceride levels [17]. A meta-analysis demonstrated that probiotic consumption has a significant effect on reducing weight, BMI, fat mass, and insulin [18]. These studies demonstrated the reducing effect of high dietary live microbial consumption on the characteristics related to childhood obesity.

Hypertension pathogenesis in children and adolescents is multifaceted, wherein activation of the immune and sympathetic nervous systems exerts key regulatory effects [19]. Multiple critical components of the immune system are thought to participate in the pathogenic process of hypertension, such as adipocytokines, matrix metalloproteinases, tissue inhibitors of metalloproteinases, and the adaptive immune responses driven by T cells [20]. Adiponectin, a type of adipocytokine, is negatively linked to hypertension risk, even in subjects with normal BMI, and this correlation increases with age [21]. Immune system cells secrete matrix metalloproteinases and tissue inhibitors to control extracellular matrix remodeling, and these molecules mediate cardiovascular remodeling in hypertension [20]. Adolescents with hypertension exhibit changes in the distribution of adaptive immune T cells, and the distribution pattern of T cell subsets is related to left ventricular hypertrophy and aortic stiffness [22]. Some speculative mechanisms may be applicable to the influence of dietary live microbial intake on hypertension in children and adolescents. Live microbial strains are able to augment immune responses by engaging with gut-associated lymphoid tissue, inducing the synthesis of anti-inflammatory cytokines, enhancing the functional activity of regulatory T cells, and restoring the homeostatic balance between pro- and anti-inflammatory mediators [17]. Increased sympathetic nervous activity also contributes to the development of hypertension [23]. The sympathetic nervous system regulates blood pressure levels by inducing peripheral vasoconstriction, managing renal water and sodium balance, and stimulating renin release from juxtaglomerular cells [19]. Communication between the gut and brain may activate sympathetic nerves, contributing to the development of hypertension [24]. Furthermore, probiotics may reduce blood pressure through angiotensin-converting enzyme-inhibitory peptide secretion and lipopolysaccharide signaling interference, ameliorating endothelial dysfunction [5,17]. The gut microbiota may also link to the pathological process of hypertension through the brain-gut-kidney axis, inflammatory factors, and metabolites (e.g., short-chain fatty acids) [25].

This study supplements evidence on the relationship between dietary live microbial consumption and the odds of hypertension among children and adolescents. Additionally, the authors further investigated the combined effect of dietary live microbial intake and BMI on hypertension incidence. The analysis data are sourced from the nationally representative NHANES database, with all data subjected to rigorous quality control for validity assurance. Nevertheless, some limitations of this study must be acknowledged. First, NHANES dietary data originates from 24-hour dietary recall interviews, which may introduce recall bias and may not accurately quantify dietary intake. Furthermore, this only reflects recent dietary intake levels. Second, since laboratory test indicators such as blood glucose are only measured in adolescents and older subjects, the metabolic status of children and adolescents has not been included in the analysis, which may affect the results. Third, it is not possible to determine the causal connection between microbial consumption and hypertension due to the cross-sectional design of this study. Fourth, the present study population consisted of children and adolescents in the U.S. Due to differences in dietary patterns, the applicability of the study results to other populations should be further verified. Fifth, single-day dietary recall, residual confounding factors, misclassification of microbial intake, and variability in blood pressure measurements in children may all affect the accuracy of the results.

In conclusion, high dietary live microbial intake shows a weak inverse association with hypertension in children and adolescents, but findings may be confounded. Furthermore, dietary live microbial intake and overweight/obesity exerted a joint effect on the odds of hypertension. Prospective studies are needed.

Not applicable, because NHANES belongs to public databases; the patients involved in the database have obtained ethical approval; users can download relevant data for free for research and publish relevant articles; the present study is based on open-source data, and the Hangzhou First People’s Hospital Affiliated to Westlake University School of Medicine does not require research using publicly available data to be submitted for review to their ethics committee, so there are no ethical issues and other conflicts of interest. The NCHS Institutional Review Board granted ethical approval for NHANES, requiring written informed consent from each participant.

Not applicable, because this paper did not reveal any personal information of patients.

This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

(1), Xiaowei Li and Xianmei Huang conceived and designed the study;

(2), Xiaowei Li, Xiaoli Li and Yong Han collected the data;

(3), Xiaowei Li, Xiaoli Li and Yong Han analyzed and interpreted the data;

(4), Xiaowei Li wrote the manuscript;

(5), Xianmei Huang provided critical revisions that are important for the intellectual content;

(6), All authors approved the final version of the manuscript.

The datasets used and/or analyzed during the current study were publicly available from the NHANES database, https://www.cdc.gov/nchs/nhanes/