Bidirectional Associations Between Blood Glucose and Blood Pressure: A Data-Driven Causal Analysis Using Structural Equation Modelling and Granger Causality on NHANES Longitudinal Data

Background and Objectives: Whether hyperglycaemia causes hypertension, hypertension worsens glycaemic control, or both conditions arise from shared metabolic drivers remains clinically consequential yet unresolved. This study applies a triangulated causal inference framework to large-scale population data to quantify the direction, magnitude, and robustness of the glucose–blood pressure relationship. The primary objective is to test for bidirectional causal effects between glycaemic status and blood pressure; secondary objectives include quantifying effect magnitudes by multiple complementary methods and assessing robustness to unmeasured confounding. Materials and Methods: We analysed 55,386 adults from the National Health and Nutrition Examination Survey (NHANES, 1999–2023). Multiple causal inference techniques were integrated: directed acyclic graph (DAG) testing, structural equation modelling (SEM) with latent constructs, propensity score matching (PSM), inverse probability weighting (IPW), doubly robust augmented IPW (AIPW), and E-value/Rosenbaum Γ sensitivity analyses, with external replication in the Framingham Heart Study data (n = 4240). Results: All of the methods used confirmed the bidirectional effects. PSM showed that hyperglycaemia increased systolic BP by 1.76 mmHg (95% CI: 0.58–2.96, p = 0.005), and hypertension increased fasting glucose by 6.55 mg/dL (95% CI: 4.61–8.58, p < 0.001), revealing a marked asymmetry favouring the BP → glucose direction. AIPW confirmed both effects (3.51 mmHg and 6.15 mg/dL, both p < 0.001). SEM identified significant bidirectional structural paths between latent glycaemic and blood-pressure constructs, with the Glycaemic → BPState path showing a negative coefficient (β = −0.15, p = 0.043), a sign reversal attributable to conditioning on the shared latent metabolic-syndrome factor. Sensitivity analyses indicated that an unmeasured confounder would need associations of RR ≥ 1.40–1.64 with both exposure and outcome to nullify these estimates, representing moderate robustness. Conclusions: The BP → glucose pathway is the dominant causal direction, suggesting that prioritisation of hypertension control may yield underappreciated benefits for glycaemic regulation. These findings support integrated cardiometabolic management strategies.