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Association of the glucose-to-lymphocyte ratio with all-cause and cardiovascular disease mortality in U.S. adults: A population-based cohort study.

Created on 13 Oct 2026

Authors

Yongtong He, Qiyin Cai, Songbai Wang

Published in

Clinics (Sao Paulo, Brazil). Volume 81. Pages 101117. Sep 09, 2026. Epub Sep 09, 2026.

Abstract

The Glucose-to-Lymphocyte Ratio (GLR) reflects metabolic-immune status, but its association with mortality in the general population remains unclear.
We analyzed 22,120 adults from NHANES (1999-2016) with complete data on glucose, lymphocytes and mortality. Associations between log₂-transformed GLR and all-cause or Cardiovascular Disease (CVD) mortality were evaluated using multivariable Cox models. Nonlinear dose-response relationships were assessed with restricted cubic splines, and survival differences visualized with Kaplan-Meier curves. Model performance was compared using ROC curves and DCA for inflammatory markers, while NRI and IDI were calculated based on the Framingham risk model.
Higher GLR was associated with older age, comorbidities, and increased mortality over a median follow-up of 122-months. Fully adjusted models showed associations with all-cause (HR = 1.33, 95% CI 1.25-1.42) and CVD mortality (HR = 1.51, 95% CI 1.36-1.66). Dose-response analyses indicated J-shaped curves with exploratory, cohort-specific inflection points at GLR ≈46 (all-cause) and ≈49 (CVD). GLR showed comparable or slightly better discrimination (AUC 67.5%‒67.7%) than individual inflammatory markers. When added to the Framingham model, GLR provided modest improvements in reclassification indices (NRI and IDI). E-values, subgroup and sensitivity analyses, and competing risks models showed the model was robust.
In this study, elevated GLR was associated with higher all-cause and CVD mortality in a J-shaped manner. While these findings suggest GLR may be a composite metabolic-immune marker worthy of further investigation, its clinical utility remains uncertain and requires external validation.

PMID:
42715901
Bibliographic data and abstract were imported from PubMed on 13 Oct 2026.

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