, Available online , doi: 10.3967/bes2026.051
, Available online , doi: 10.3967/bes2026.052
Yanyan Zhou,
Keyi Yu,
Ming Liu,
Zhenzhou Huang,
Yanqing Che,
Mengyu Shi,
Zhenpeng Li,
Xiaoli Du,
Duochun Wang,
Liyan Ma,
Li Yu
, Available online , doi: 10.3967/bes2026.068
, Available online , doi: 10.3967/bes2026.056
, Available online , doi: 10.3967/bes2026.054
This population-based cross-sectional study aimed to examine the associations of unhealthy diet and insufficient physical activity (PA) with anxiety and depressive symptoms among Chinese adults aged 18–60 years. Data were derived from the 2022–2023 Psychology and Behavior Investigation of Chinese Residents (PBICR) Project, a large cross-sectional survey conducted in China. After exclusions, 14 358 adults were included in this study. Dietary risk factors were summed into a 0–5 score. PA was measured by the International Physical Activity Questionnaire (IPAQ-7, short form). Anxiety and depressive symptoms were defined as the Generalized Anxiety Disorder Scale(GAD-7) ≥ 10 and Patient Health Questionnaire-9(PHQ-9) ≥ 10, respectively. Adjusted odds ratios (aORs) and 95% confidence intervals(CIs) were estimated using ordered logistic regression; dose-response was examined with restricted cubic splines. Overall, 1 879 participants (13.09%) self-reported anxiety and 3,084 (21.48%) self-reported depressive symptoms. A monotonic dose-response relationship was observed between the number of unhealthy dietary behaviors and both outcomes. Compared with participants reporting no unhealthy dietary behaviors, those reporting 1, 2, 3, 4, and 5 behaviors had progressively higher odds of anxiety (aOR = 1.47, 2.03, 2.75, 4.59, and 8.37) and depression (aOR = 1.53, 2.14, 2.84, 5.59, and 16.46). Physical activity level was not significantly associated with either anxiety or depressive symptoms after adjustment for covariates. The strong relationship between cumulative unhealthy dietary behaviors and mental health symptoms highlights the potential importance of dietary interventions for preventing anxiety and depression.
, Available online , doi: 10.3967/bes2026.053
, Available online , doi: 10.3967/bes2026.055
, Available online , doi: 10.3967/bes2026.024
Huihuan Luo,
Yuanting Xie,
Xinyi Fang,
Bin Pan,
Yalan Xiao,
Jingyu Li,
Xiaoqing Hong,
Dongyang Han,
Wenyue Tu,
Haidong Kan,
Yanyi Xu,
Renjie Chen
, Available online , doi: 10.3967/bes2026.059
Objective Prior epidemiological research demonstrated an association between short-term exposure to fine particulate matter (PM2.5) and acute diabetic events, specifically diabetic ketoacidosis (DKA). However, mechanistic investigations remain lacking to substantiate biological link. Methods Twenty 18-week-old male BKS db/db mice were randomly assigned to two groups (n = 10 per group). Ambient PM2.5 suspension (5 mg/kg in 50 μL) or an equal volume of phosphate-buffered saline was intratracheally instilled once daily for three consecutive days. Within 24 hours after the final instillation (Day 3), serum β-hydroxybutyrate was quantified, and liver tissues were collected for transcriptomic profiling (RNA-seq) to explore potential mechanisms linking PM2.5 to ketone body levels (i.e., β-hydroxybutyrate). Results The PM2.5 group exhibited higher 3-hydroxybutyric acid levels than controls. The liver transcriptome differed significantly between groups. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses indicated differentially expressed genes were primarily associated with lipid metabolism. Further, 43 genes exhibited moderate-to-strong correlations with 3-hydroxybutyric acid (16 positive, 27 negative; coefficients 0.56 – 0.76). These genes are involved in fatty acid oxidation, lipogenesis, lipid transport, glucose metabolism, and inflammation. Conclusion PM2.5 exposure may enhance ketogenesis through disruption of hepatic glucolipid metabolism, providing mechanistic insight into its potential role in acute diabetic metabolic decompensation.
Qingyin Bu,
Qian Wang,
Gang Zhang,
Yifan Wang,
Longhu Sun,
Shuang Liang,
Fan Yang,
Zhazheng He,
Honggang Yi,
Zhening Pu,
Juncheng Dai
, Available online , doi: 10.3967/bes2026.069
Objective To investigate the effects of metabolic syndrome (MetS) and its interaction with genetic factors on lung cancer incidence and mortality. Methods The cohort analysis included 355,344 participants from the UK Biobank. MetS was defined using the modified National Cholesterol Education Program Adult Treatment Panel III criteria. Cox proportional hazards models were used to evaluate the associations between MetS-related variables, their interactions with genetic factors, and lung cancer outcomes (incidence and mortality). Results MetS was associated with increased risks of lung cancer incidence (hazard ratio [HR]: 1.31, 95% confidence interval [CI]: 1.22–1.42) and mortality (HR: 1.35, 95% CI: 1.24–1.48). Risk increased proportionally to the number of metabolic abnormalities. Increased waist circumference, reduced high-density lipoprotein cholesterol, and elevated glycated hemoglobin were independently associated with both outcomes. Participants with both high genetic risk and MetS had the highest risk of lung cancer incidence (HR: 2.07, 95% CI: 1.82–2.35) and mortality (HR: 2.12, 95% CI: 1.83–2.45) compared with those with low genetic risk and no MetS. A significant positive additive interaction was observed between waist circumference and genetic risk. Conclusion Metabolic abnormalities are important modifiable risk factors for lung cancer. Integrating metabolic health assessment with genetic risk profiling may improve risk stratification and targeted prevention of lung cancer.
, Available online , doi: 10.3967/bes2026.057
Objective This study aimed to comprehensively characterize the genomic diversity, evolutionary dynamics, pathogenic potential, antimicrobial resistance, and secondary metabolite capacity of the Nocardia genus using whole-genome analyses. Methods We analyzed 751 publicly available Nocardia genomes using genome-based species delineation, phylogenomics, pangenome analysis, and comparative functional profiling to assess taxonomy, virulence, antibiotic resistance genes (ARGs), and biosynthetic gene clusters (BGCs). Results Phylogenomic analyses resolved five major clades: N. farcinica, N. carnea, N. asteroides, N. transvalensis, and N. otitidiscaviarum groups. The pangenome is open, comprising 467,566 gene clusters and reflecting extensive genomic diversity. Virulence factors and ARGs exhibit clade-specific patterns: the N. farcinica group harbors the most complete virulence repertoire and diverse resistance determinants, whereas the N. carnea and N. asteroides groups carry fewer genes. Analysis of 10,196 BGCs across 46 classes revealed conserved clusters of non-ribosomal peptide synthetases, terpenes, and type I polyketide synthases, with higher biosynthetic potential in the N. farcinica, N. transvalensis, and N. otitidiscaviarum groups. Several genomes encode BGCs associated with antibacterial or anticancer compounds. Conclusion This comprehensive genome analysis of Nocardia, representing the most complete sampling to date, clarifies phylogeny, reclassifies misassigned strains, identifies potential novel species, and reveals clade-specific patterns of virulence, resistance, and secondary metabolism.
, Available online , doi: 10.3967/bes2026.049
Objective This study aimed to investigate the association between exposure to mixtures of environmental endocrine-disrupting chemicals (EDCs) and metabolic dysfunction-associated steatotic liver disease (MASLD) and to assess the potential mediating role of iron metabolism. Methods A total of 6,989 adults from the China Health and Nutrition Survey (2015 cycle) were included. The serum concentrations of 22 EDCs were measured. Logistic regression, weighted quantile sum (WQS) regression, and Bayesian kernel machine regression (BKMR) models were used to evaluate the association between EDC exposure and risk of MASLD. Mediation analyses were performed to assess the mediating role of serum ferritin (SF). Results Eight EDCs were positively associated with MASLD. The WQS regression model identified six major contributors, including β-hexachlorocyclohexane, p,p’-DDT, monoethyl phthalate, acenaphthene, perfluorooctanoic acid, and perfluoro-n-pentanoic acid, in mixture effects. The BKMR model demonstrated that higher levels of EDC mixture were associated with an increased risk of MASLD. Subgroup analyses suggested stronger correlations in males and in individuals aged <65 years. SF was estimated to mediate 11.2%–32.1% of the association between key EDCs and MASLD. Conclusion Exposure to EDC mixtures was associated with an increased risk of MASLD, with iron metabolism playing a notable mediating role. Reducing the exposure to key EDCs may help alleviate the burden of MASLD.
, Available online , doi: 10.3967/bes2026.048
Objective This study aimed to investigate the role of circulating inflammatory cytokines in the pathway linking cerebral small vessel disease (CSVD) to cognitive impairment (CI), and to further elucidate the neuroimaging mechanism of CSVD-driven inflammatory cytokines on cognitive function. Methods We conducted a two-step, two-sample Mendelian randomization (MR) analysis to evaluate the causal effect of CSVD on circulating inflammatory cytokines and CSVD-driven inflammatory cytokines on the risk of CI. Using a separate two-sample MR analysis, we explored the potential mechanisms by which these inflammatory cytokines affect cognition, with cytokines identified as mediators between CSVD and CI treated as exposure and brain structural imaging as outcomes. Results Genetically predicted CSVD was causally associated with the levels of 11 circulating inflammatory cytokines. Among these CSVD-driven inflammatory cytokines, growth-regulated oncogene alpha (GROα) was associated with poorer verbal and numerical reasoning, stem cell factor (SCF) was associated with better working memory, and tumor necrosis factor-alpha (TNF-α) was associated with reduced processing speed. SCF mediated the association between small-vessel ischemic stroke and numeric memory performance, with a mediation effect of 10%. Furthermore, circulating SCF levels showed causal relationships with the volumes of multiple brain regions within the default mode network and with the integrity of seven white matter tracts. Conclusion SCF, GROα, and TNF-α play important roles in the pathway linking CSVD to CI. Circulating SCF may influence cognitive function by modulating brain volume and white matter integrity.
Bingqing Kou,
Yifan Zang,
Bisen Liu,
Yijin Pei,
Chong Shen,
Jianxin Li,
Fangchao Liu,
Jie Cao,
Shufeng Chen,
Jianfeng Huang,
Dongfeng Gu,
Tong Wang,
Keyong Huang,
Xiangfeng Lu
, Available online , doi: 10.3967/bes2026.044
Objective Dyslipidemia has been linked to increased arterial stiffness. However, few studies have comprehensively assessed the cumulative effects of lipid profiles on arterial stiffness. Methods Based on the initial recruitment of 7,134 participants from the China-PAR cohort, we finally included 6,717 participants with up to four repeated lipid measurements between baseline (1998–2008) and the most recent follow-up (2018–2020). Cumulative exposure to total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), non-HDL-C, and remnant cholesterol (RC) was estimated using the area under the curve method. Arterial stiffness was measured in 2018–2020 using the arterial pressure-volume index (API) and the arterial velocity-pulse index (AVI), which reflect the stiffness of peripheral and central arteries, respectively. Results Participants (mean age: 51.4 ± 10.3 years) included 2,598 men (38.68%), with a mean cumulative lipid exposure duration of 14.02 years. Cumulative TG, HDL-C, and RC were significantly associated with API levels, with adjusted βs (95% confidence intervals [CIs]) of 2.31 (1.53, 3.08), −1.14 (−2.24, −0.04), and 2.39 (1.52, 3.25), respectively, for the highest quartile compared with the lowest quartile. Restricted cubic splines showed nonlinear associations of cumulative TG and RC with API and a linear association for HDL-C (all P < 0.05). For AVI, only cumulative HDL-C showed a significant inverse association, with an adjusted β (95% CI) of −1.16 (−2.12, −0.21) for the highest quartile, and a nonlinear association was observed (P < 0.05). Conclusion Long-term cumulative TG and RC were associated with increased peripheral arterial stiffness but not central arterial stiffness, and cumulative HDL-C was negatively associated with both peripheral and central arterial stiffness. These findings underscore the importance of long-term TG and RC control along with maintaining adequate HDL-C levels.
Lu Yu,
Zheng Li,
Peijie Sun,
Shuyang Yan,
Wanying Shi,
Wenqi Hao,
Wanling Li,
Mingkun Yu,
Dejin Yang,
Yingli Qu,
Saisai Ji,
Wenli Zhang,
Feng Zhao,
Yawei Li,
Haocan Song,
Jiayi Cai,
Ying Zhu,
Song Tang,
Feng Tan,
Yuebin Lv,
Xiaoming Shi
, Available online , doi: 10.3967/bes2026.045
Objective To investigate associations between heavy metals and metalloids (HMMs) exposure and hepatic fibrosis risk, and to explore the modifying role of thyroid hormones. Methods Using nationally representative data of 9,543 adults from the China National Human Biomonitoring, hepatic fibrosis risk was assessed with the Fibrosis-4 index (FIB-4). Weighted logistic and linear regression models evaluated links between 13 HMMs and fibrosis outcomes. Dose-response relationships were modeled with restricted cubic splines, and subgroup analyses explored potential effect modification. Results Blood cobalt (Co) (OR = 1.613, 95% CI: 1.126-2.310) and blood manganese (Mn) (OR = 1.699, 95% CI: 1.238-2.331) showed nonlinear positive associations with hepatic fibrosis risk, while urinary tin (Sn) (OR = 0.888, 95% CI: 0.797-0.990) was inversely associated. Low triiodothyronine (T3) levels increased Co-induced fibrosis risk and may enhance the protective effect of Sn, while high T3 levels exacerbated Mn-related risk. Stratified analysis by thyroxine (T4) levels showed directionally consistent associations with the main findings. Conclusion Blood Co and Mn nonlinearly increased hepatic fibrosis risk, urinary Sn reduced it. T3 levels modulated these metal-specific risks, highlighting thyroid hormones as potential modifiers in HMMs-induced hepatotoxicity.
, Available online , doi: 10.3967/bes2026.043
Objective Immunoglobulin G (IgG) N-glycosylation is associated with mild cognitive impairment through the regulation of inflammatory balance; however, the underlying mechanisms remain unclear. Methods Our study utilized a post-genome-wide association studies (GWAS) method that integrated GWAS data for cognitive function with gene expression quantitative trait loci (eQTL), protein QTL (pQTL), and IgG N-glycan-QTL data. Results Mendelian randomization (MR) analyses suggested bidirectional causalities between glycan peaks (GPs) and cognitive function, with GP7, GP12, and GP19 showing a causal effect on cognitive function, while cognitive function conversely showed a causal effect on GP1 and GP8. Two proteins and 10 genes were implicated in the regulation of IgG N-glycosylation. Furthermore, multivariable MR results suggested complex causalities between genes/proteins and IgG N-glycans, which jointly promote or independently affect cognitive function. Conclusion Our study reveals a novel mechanism by which genes, proteins, and modified IgG N-glycans converge to pathologically affect cognitive function.
Youjing Zhang,
Meiling Hu,
Ziyi Yang,
Jianxin Li,
Jie Cao,
Jichun Chen,
Fangchao Liu,
Keyong Huang,
Hongfan Li,
Chong Shen,
Dongsheng Hu,
Xiaoqing Liu,
Shujun Gu,
Ling Yu,
Jianfeng Huang,
Xiangfeng Lu,
Dongfeng Gu,
Shufeng Chen
, Available online , doi: 10.3967/bes2026.034
Objective To examine the associations of sleep duration and physical activity (PA) with central obesity among Chinese adults. Methods Based on the Prediction for Atherosclerotic Cardiovascular Disease Risk in China (China-PAR) project, 175,373 observations from 106,518 participants were included. Generalized estimating equations quantified the associations of sleep duration and PA with waist circumference (WC) and central obesity. Stratified and joint analyses were performed to evaluate combined effects, and an isotemporal substitution model was used to assess substitution effects. Results Suboptimal sleep duration (< 7 h/day or ≥ 9 h/day) and inadequate PA were associated with higher WC and an increased risk of central obesity. Compared with optimal sleep duration (7–< 9 h/day), both longer (≥ 9 h/day) and shorter (< 7 h/day) sleep durations were associated with increased WC (0.27 cm [95% confidence interval (CI): 0.18, 0.35] and 0.15 cm [95% CI: 0.04, 0.27], respectively) and a higher risk of central obesity (odds ratio, 1.09 [95% CI: 1.07, 1.12] and 1.05 [95% CI: 1.02, 1.08], respectively). Joint analyses revealed that individuals with inadequate PA and short sleep duration had the highest WC and highest risk of central obesity. Among individuals sleeping > 8 h/day, substituting 30 min/day of sleep with moderate-to-vigorous PA significantly reduced the risk of central obesity. Conclusion Suboptimal sleep duration has a detrimental effect on central obesity, and adequate PA can mitigate this effect. The impact of reallocating sleep duration varies by sleep duration, highlighting the need to optimize both PA and sleep patterns in China.
Yudong Wu,
Yongqiang Chen,
Chen Chen,
Liang Ding,
Linsen Yang,
Kai Zhang,
Xi Meng,
Wenhui Shi,
Yang Li,
Jiahao Chen,
Yue Chen,
Yingli Qu,
Wanying Shi,
Ziyu Hu,
Fanye Long,
Lijun Wang,
Luxi Wei,
Jinhui Zhou,
Feng Zhao,
Ying Zhu,
Maigeng Zhou,
Yuebin Lv,
Xiaoming Shi
, Available online , doi: 10.3967/bes2026.033
Objective To investigate the association between urinary cobalt levels and all-cause and cause-specific mortality in older Chinese adults. Methods This study enrolled older adults (≥ 60 years) from two cohorts. Urinary cobalt concentrations were quantified using inductively coupled plasma mass spectrometry. Mortality outcomes were ascertained by linking them to the Chinese Disease Surveillance Point System. Cox proportional hazards models were used to evaluate the association between urinary cobalt and mortality, and subgroup analyses were performed to identify vulnerable populations. Results A total of 9,727 participants were followed for an average of 4.754 years, during which 2,745 deaths were recorded. Participants with the highest urinary cobalt concentration had a 29% greater all-cause mortality risk (HR: 1.292, 95% CI: 1.155–1.445) than those in the lowest quartile, along with significantly elevated mortality from cardiovascular (24.8%), neurological (137.1%), and other causes (25.3%). Subgroup analyses revealed that female, Han Chinese individuals, and rural residents were more susceptible to the effects of cobalt. Conclusion Cobalt exposure was associated with elevated all-cause, cardiovascular, and neurological mortality in older adults, with female, Han ethnicity, and rural residents being vulnerable groups. These findings provide population-based evidence for clinical management and policy revisions regarding cobalt exposure.
Fengjie Wang,
Yutong Zhou,
Ri De,
Runan Zhu,
Yu Sun,
Dongmei Chen,
Liping Jia,
Qi Guo,
Yao Yao,
Zhen Zhu,
Naiying Mao,
Linqing Zhao
, Available online , doi: 10.3967/bes2026.032
Objective LLC-MK2/TMPRSS2 cells constitutively express TMPRSS2, eliminating the requirement for additional trypsin during HPIV3 culture. The efficiency of LLC-MK2/TMPRSS2 for isolating HPIV3 from respiratory specimens was evaluated in comparison with Madin-Darby Canine Kidney (MDCK). Methods HPIV3-positive respiratory specimens from children with acute respiratory infections (February-June 2025) were inoculated into LLC-MK2/TMPRSS2 and MDCK. The cytopathic effect (CPE) was monitored microscopically, and the proportion of positive cells was evaluated using direct immunofluorescence assay (DFA). Viral infection dynamics were assessed using the cycle threshold (Ct) values obtained by qPCR. Results Among 50 specimens, 35 strains (35/50, 70%) were successfully isolated using LLC-MK2/TMPRSS2, while 14 strains were isolated using MDCK (14/50, 28%). More pronounced CPE and a higher number of virus-infected positive cells were shown in LLC-MK2/TMPRSS2 compared to that in MDCK (P < 0.001 and P = 0.001, respectively). Among specimens with an initial Ct < 27, the isolation rate of LLC-MK2/TMPRSS2 was higher and the Ct values were lower (< 27) (82.6%, 19/23). Among specimens with an initial Ct of 23 ≤ Ct < 27, the number of specimens with a supernatant Ct ≥ 27 (63.6%, 7/11) was significantly less than that in MDCK (P = 0.003). Conclusion LLC-MK2/TMPRSS2 exhibits superior adaptability and replication efficiency in the isolation of HPIV3 from respiratory specimens.
, Available online , doi: 10.3967/bes2026.031
Objective The cardiovascular impact of earthquakes remains poorly understood, particularly regarding subclinical vascular diseases in women. This study examined the association between seismic exposure and the progression of carotid atherosclerosis in northern Chinese adults. Methods 7,412 individuals were enrolled, including survivors of the 1976 Tangshan earthquake (magnitude 7.8) and unexposed controls. Carotid atherosclerosis was assessed using bilateral ultrasonography. Multivariate logistic regression accounted for sociodemographic, clinical, and lifestyle covariates. Results Among females, earthquake exposure was associated with significantly higher atherosclerosis prevalence (44.9% vs. 33.1% in males), with elevated adjusted odds (OR = 2.32, 95% CI: 1.78–3.02, P < 0.001). No significant association was observed in males after full adjustment. In women, CVD risk increased twofold (95% CI: 1.66–2.55, P < 0.001), with gradients by age (≥ 65 years: HR = 3.98, P < 0.001), education (elementary: HR = 4.00, P < 0.001), and income (low-income: HR = 2.74, P < 0.001). Proximity to the epicenter further amplified the CVD risk (log-rank P < 0.0001). Conclusion Seismic exposure independently predicts accelerated carotid atherosclerosis and cardiovascular risk in women, underscoring the need to elucidate sex-specific mechanisms and develop targeted interventions for post-disaster populations.
Xiaoyan Ma,
Peiliang Chen,
Chen Chen,
Xi Meng,
Jinhui Zhou,
Shihao Lou,
Jian Zhang,
Yao He,
Li Qi,
Wenhua Zhao,
Yuebin Lv,
Chen Mao,
Xiaoming Shi
, Available online , doi: 10.3967/bes2026.050
With the rapid aging of China’s population, the number of adults aged ≥ 80 years is rising, and their nutritional status and weight management have attracted growing attention. Body mass index (BMI) is a commonly used indicator for assessing body weight and nutritional status. However, existing BMI standards were mainly developed for the general adult population, and their applicability to the oldest old population remains uncertain. To provide guidance for BMI evaluation and weight management among the oldest old population in China, the National Health Commission issued the standard “Appropriate body mass index range and weight management standards for the oldest old (WS/T 868—2025)”. Based on evidence from prospective cohort studies including the Chinese Longitudinal Healthy Longevity Survey and the Healthy Aging and Biomarkers Cohort Study, the standard recommends an appropriate BMI range of 22.0–26.9 kg/m2 for adults aged ≥ 80 years and provides recommendations regarding BMI measurement, weight monitoring, and individualized weight management. The implementation of this standard provides scientific evidence for weight evaluation and health management in the oldest old population and contributes to promoting healthy aging.
, Available online , doi: 10.3967/bes2026.016
Objective To investigate the association between occupational high-temperature exposure and accelerated biological aging. Methods A total of 140 male workers exposed to occupational high-temperatures and 207 male non-exposed control workers were selected as study subjects. Questionnaire surveys and health examinations were conducted. Biological age and organ-specific biological age were calculated using the Klemera–Doubal method. Generalized linear models were used to analyze the effects of occupational high-temperature exposure, body mass index (BMI), smoking, alcohol consumption, and sleep duration on biological age (BA) acceleration and organ-specific biological age. Results Significant differences were observed between the exposed and control groups in length of service, systolic blood pressure, red blood cell count, albumin levels, urea, creatinine, BA acceleration, and liver–kidney BA acceleration (P < 0.05). Compared with the control group, which showed a BA acceleration of 0.04 ± 1.34 years, the exposed group demonstrated significantly higher BA acceleration of 0.62 ± 1.31 years. After adjustment for covariates, workers exposed to high-temperatures exhibited significantly higher BA acceleration and liver–kidney BA acceleration than controls (P < 0.001). High-temperature exposure and BMI were associated with BA acceleration, with a significant interaction between the two factors (P < 0.05). High- temperature exposure, BMI, and smoking were identified as risk factors for BA acceleration, whereas sleep duration was a protective factor (P < 0.05). Conclusion Occupational high-temperature exposure may accelerate biological aging. An interaction exists between occupational high-temperature exposure and BMI in relation to BA acceleration.
Queyun Sun,
Cheng Cui,
Weiting Cai,
Lin Jiang,
Jingjing Xu,
Yi Yao,
Na Xu,
Xiaozeng Wang,
Zhenyu Liu,
Zheng Zhang,
Yongzhen Zhang,
Xiaogang Guo,
Zhifang Wang,
Yingqing Feng,
Qingsheng Wang,
Jianxin Li,
Xueyan Zhao,
Jue Chen,
Runlin Gao,
Lei Song,
Yaling Han,
Jinqing Yuan,
Ying Song
, Available online , doi: 10.3967/bes2026.015
Objective To investigate the joint effect of free fatty acid (FFA) and the triglyceride-glucose (TyG) index on the prognosis of overweight and obese coronary artery disease (CAD) patients. Methods A total of 5,887 patients were enrolled in this study. Restricted cubic spline analyses were used to assess the dose-response relationship of FFA and TyG with major adverse cardiovascular and cerebrovascular events (MACCE). Mediation analysis was used to examine whether TyG mediated the association between FFA and MACCE. Kaplan–Meier survival curves were used to compare the cumulative incidence of events. Multivariable Cox models were used to explore the independent association between Low-/High-FFA and Low-/High-TyG on outcomes. Results FFA and TyG were independent predictors of MACCE. TyG mediated 10.7% of the association between FFA and MACCE. Patients with high FFA and TyG levels exhibited a markedly higher MACCE risk (adjusted hazard ratio: 1.951, 95% confidence interval: 1.533–2.484; P < 0.001), with a significant interaction between FFA and TyG. Among patients with elevated FFA levels, MACCE increased progressively across higher TyG tertiles (P for trend = 0.001). Conclusions FFA and the TyG index independently predict adverse outcomes in overweight or obese CAD patients, with the TyG index mediating the relationship between FFA and MACCE. Their combined assessment enhances the risk stratification in this population.
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