Stress hyperglycemia ratio and incident hypertension in chinese middle-aged and older adults: mediating roles of lipids in a prospective cohort

Although dysglycemia and dyslipidemia contribute to hypertension, the role of stress hyperglycemia ratio (SHR), a dynamic glycemic marker, and its interaction with lipids remain unclear. Currently, the independent and synergistic effects of these factors on hypertension in older adults have not been fully elucidated in a large cohort. This study investigated the SHR-lipid interplay and quantified the mediating pathways, addressing a critical gap in understanding the metabolic drivers of hypertension. The analysis included 4,546 adults (aged ≥ 45 years, normotensive) from the 2011 to 2015 China Health and Retirement Longitudinal Study. Missing data were subjected to multiple imputations. Cox models were used to assess the association of SHR with incident hypertension, and Kaplan–Meier curves depicted disparities in risk accumulation across SHR quartiles. Restricted cubic splines were used to evaluate the dose–response relationships. The subgroup analyses included age, sex, smoking status, and comorbidities. Causal mediation analysis measured lipid-mediated (total cholesterol [TC] and triglyceride [TG]) effects. Sensitivity analysis utilized methodologies including the exclusion of diabetic patients and the implementation of interval-censored COX multivariate analysis. Over the 4-year follow-up period, 1,717 participants (37.8%) developed hypertension. Multivariate Cox proportional hazards regression analyses indicated a significant increase in the risk of hypertension associated with elevated SHR, with the highest SHR quartile exhibiting a 16% greater risk than the lowest. Restricted cubic spline models corroborated a linear dose–response relationship between increments in SHR and hypertension risk. The Kaplan–Meier survival curves showed the highest cumulative incidence of hypertension in the highest SHR quartile group. Subgroup analyses stratified by age, sex, race, smoking status, and comorbidities, along with sensitivity analyses excluding individuals with diabetes, confirmed the robustness of the associations. Causal mediation models further revealed that TC and TG partially mediated the relationship between SHR and hypertension, suggesting that metabolic dysregulation may be a contributing mechanism. Elevated SHR are independently associated with a risk of hypertension in older adults, which is partially mediated by lipids. Integrating SHR into routine metabolic assessments and lipid management may enhance prevention of hypertension in high-risk groups.