A 10 mg/dL increase in fasting plasma glucose was associated with a 0.32 mmHg increase in systolic blood pressure (95% CI: 0.26-0.38, p<0.001), with a nonlinear breakpoint at 122.1 mg/dL.
Cross-Sectional (n=54,881)
Fasting plasma glucose exhibits a nonlinear, dose-response relationship with systolic blood pressure that is modulated by adiposity and plateaus above 122.1 mg/dL.
Effect estimate: 0.32 mmHg increase in SBP per 10 mg/dL FPG (95% CI 0.26-0.38)
p-value: p=<0.001
The relationship between blood glucose levels and blood pressure is well established in clinical literature, yet its precise quantitative characterization, including nonlinear effects, threshold phenomena, and demographic modifiers, remains incompletely understood. In this study, we conducted a comprehensive cross-sectional analysis of the National Health and Nutrition Examination Survey (NHANES) spanning 11 survey cycles (1999–2023), comprising 54,881 adult participants with at least one glycemic marker and standardized blood pressure measurements. Of these, 26,981 had valid fasting plasma glucose (FPG) measurements, and 49,327 had valid glycated hemoglobin (HbA1c) measurements. We employed restricted cubic splines (RCS), generalized additive models (GAMs), and segmented regression to characterize the dose–response relationship between glycemic markers and both systolic (SBP) and diastolic blood pressure (DBP). A 10 mg/dL increase in FPG was associated with a 0.32 mmHg increase in SBP (95% CI: 0.26–0.38, p < 0.001) after adjusting for age, sex, and body mass index (BMI). Nonlinearity was statistically significant for all exposure–outcome combinations (p < 10−7 for Wald tests). Segmented regression identified a FPG breakpoint at 122.1 mg/dL (95% CI: 119.5–125.6), below which SBP increased at 0.39 mmHg per mg/dL and above which the association was essentially flat. Stratified analyses revealed that the glucose–BP association was strongest in females (β = 0.048 per mg/dL) compared with males (β = 0.021), and in prediabetic individuals (β = 0.065) compared with those with established diabetes (β = 0.014). In the statistical mediation decomposition, body mass index accounted for 23.5% of the total FPG–SBP association. A significant FPG × BMI interaction (p < 0.001) indicated that the glucose–BP relationship is modulated by adiposity. These findings provide a large-scale population-level analysis of the glucose–blood pressure dose–response relationship and identify potential thresholds warranting further investigation for integrated cardiometabolic risk management (95% bootstrap CI: 19.3–28.9%; 1000 resamples); given the cross-sectional design and BMI’s plausible role as a shared upstream determinant of glucose and blood pressure, this proportion is reported as a confounding decomposition rather than as evidence of causal mediation. Insulin resistance (HOMA-IR) and C-reactive protein did not contribute significantly as additional decomposition pathways.:
Kolev et al. (Thu,) reported a cross-sectional. Fasting plasma glucose and HbA1c was evaluated on Systolic and diastolic blood pressure (0.32 mmHg increase in SBP per 10 mg/dL FPG, 95% CI 0.26-0.38, p=<0.001). A 10 mg/dL increase in fasting plasma glucose was associated with a 0.32 mmHg increase in systolic blood pressure (95% CI: 0.26-0.38, p<0.001), with a nonlinear breakpoint at 122.1 mg/dL.