Why the study?
Elevated systolic blood pressure and resting heart rate contribute to diabetic complications and inflammation that upregulate LRG1, but the relationship between double product and cognitive function in type 2 diabetes remains to be clarified.
Is double product associated with cognitive decline in patients with type 2 diabetes?
Is double product associated with cognitive decline in patients with type 2 diabetes?
Elevated double product (systolic blood pressure × resting heart rate) is longitudinally associated with cognitive decline in patients with type 2 diabetes, partially mediated by LRG1.
Answers are grounded in this paper and cite their sources.
May warrant monitoring double product in type 2 diabetes; hypothesis-generating for causal effects and interventions.
BackgroundElevated systolic blood pressure (SBP) and resting heart rate (RHR) contribute to pathogenesis of diabetic complications. They increase inflammation which can upregulate leucine-rich α-2-glycoprotein 1 (LRG1), an emerging biomarker of cognitive decline.ObjectiveTo examine association between double product (DP, derived from multiplying SBP and RHR) and cognitive function in type 2 diabetes (T2D), with possible mediation by plasma LRG1.MethodsIn this prospective cohort of 1319 patients (mean age 62.5 ± 7.3), plasma LRG1 was measured with enzyme-linked immunosorbent assay. Cognitive function was assessed using Repeatable Battery for Assessment of Neuropsychological Status (RBANS). Cross-lagged panel analysis was done to examine temporal relationship between DP and cognitive function.ResultsBaseline DP was associated with lower baseline RBANS total score (adjusted coefficient = -2.43; 95%CI -4.76, -0.10; p = 0.041). 586 patients were followed up to 8.6 years. Baseline DP was associated with follow-up RBANS total score (adjusted coefficient = -3.80; 95%CI -6.51, -1.10; p = 0.006). It was also associated with lower follow-up RBANS scores in immediate memory and delayed memory with adjusted coefficients -4.38 (95%CI -8.49, -0.28; p = 0.036) and -5.12 (95%CI -9.88, -0.35; p = 0.035) respectively. In cross-lagged panel analysis, standardized effect size of baseline DP on follow-up RBANS total score (β = -0.08; p = 0.002) was larger than that of baseline RBANS total score on follow-up DP (β = -0.04; p = 0.266). LRG1 accounted for 14.7% of the association in mediation analysis (p = 0.035).ConclusionsDP was independently associated with cognitive function with possible mediation by LRG1. DP preceded decline in cognitive function. DP may be potential intervention and monitoring target for prevention of cognitive impairment and possibly Alzheimer's disease in T2D.
No takes yet. Share an insight, caveat, or question.
Low et al. (2025) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: