<?xml version="1.1" encoding="utf-8"?>
<article xsi:noNamespaceSchemaLocation="http://jats.nlm.nih.gov/publishing/1.1/xsd/JATS-journalpublishing1-mathml3.xsd" dtd-version="1.1" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance"><front><journal-meta><journal-id journal-id-type="publisher-id">JMDS</journal-id><journal-title-group><journal-title>Journal of Medicines Development Sciences</journal-title></journal-title-group><issn>2382-6363</issn><eissn>2382-6371</eissn><publisher><publisher-name>Bio-Byword Scientific Publishing Pty. Ltd.</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.18063/JMDS.v11i1.1367</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title>Predictive Value of the C-Reactive Protein–Triglyceride–Glucose Composite Index for All-Cause Mortality in General Population: A Dual-Cohort Study Based on NHANES and CHARLS</title><url>https://artdesignp.com/journal/JMDS/11/1/10.18063/JMDS.v11i1.1367</url><author>HeAnxin,LuoMiao</author><pub-date pub-type="publication-year"><year>2026</year></pub-date><volume>11</volume><issue>1</issue><history><date date-type="pub"><published-time>2026-03-16</published-time></date></history><abstract>Background: Metabolic dysregulation and chronic inflammation coexist commonly, synergistically increasing cardiovascular and all-cause mortality. Single biomarkers fail to comprehensively assess metabolism-inflammation imbalance.&amp;nbsp;This study first validates the dose-response relationship between CTI (a novel dual-pathway composite biomarker) and all-cause mortality across two cross-continental cohorts.&amp;nbsp;Methods: Data from NHANES (n&amp;nbsp;=&amp;nbsp;7, 752) and CHARLS (n&amp;nbsp;=&amp;nbsp;9, 352) were integrated. CTI was calculated for all participants.&amp;nbsp;Statistical methods including multivariable Cox model, propensity score overlap weighting, RCS regression, and competing risk model analyzed CTI-mortality correlation.&amp;nbsp;Sensitivity analysis and external validation ensured result robustness.&amp;nbsp;Results: Median follow-ups: 11.3 years (NHANES, 1, 260 deaths) and 9 years (CHARLS, 236 deaths).&amp;nbsp;Fully adjusted Model 3: Each 1-unit CTI increase linked to 21% (NHANES: HR&amp;nbsp;=&amp;nbsp;1.21, 95%&amp;nbsp;CI: 1.12&amp;ndash;1.31) and 56% (CHARLS: HR&amp;nbsp;=&amp;nbsp;1.56, 95%&amp;nbsp;CI: 1.34&amp;ndash;1.82) higher all-cause mortality.&amp;nbsp;All-cause mortality surged when CTI&amp;nbsp;&amp;gt;&amp;nbsp;9.77 (NHANES) or &amp;gt;&amp;nbsp;7.54 (CHARLS) (P&amp;nbsp;&amp;lt; 0.001).&amp;nbsp;Highest CTI quartile had 37% (NHANES) and 221% (CHARLS) higher mortality vs. lowest; effect pronounced in middle-aged and elderly (CHARLS, median age 58).&amp;nbsp;CTI (AUC&amp;nbsp;=&amp;nbsp;0.61) outperformed TyG or CRP alone.&amp;nbsp;Conclusions: CTI, integrating inflammatory and metabolic indicators, effectively identifies high-risk individuals across populations.&amp;nbsp;With population-specific thresholds, it is promising for routine health screening risk stratification, guiding early intervention.</abstract><keywords>C-reactive protein–triglyceride–glucose index (CTI), All-cause mortality, Cardiopulmonary mortality, NHANES, CHARLS, Propensity score overlap weighting, Competing risk model.</keywords></article-meta></front><body/><back><ref-list><ref id="B1" content-type="article"><label>1</label><element-citation publication-type="journal"><p>[1] Chong D, et al., 2024, Global Burden of Cardiovascular Diseases: Projections from 2025 to 2050.&amp;nbsp;European Journal of Preventive Cardiology, zwae281.[2] Ostrominski JW, et al., 2023, Prevalence and Overlap of Cardiac, Renal, and Metabolic Conditions in US Adults, 1999-2020.&amp;nbsp;JAMA Cardiology, 8(11): 1050&amp;ndash;1060.[3] Wheatcroft SB, et al., 2003, Pathophysiological Implications of Insulin Resistance on Vascular Endothelial Function.&amp;nbsp;Diabetic Medicine, 20(4): 255&amp;ndash;268.[4] DeFronzo RA, et al., 2015, Type 2 Diabetes Mellitus.&amp;nbsp;Nature Reviews Disease Primers, 1: 15019.[5] Hill MA, et al., 2021, Insulin Resistance and Cardiovascular Disease.&amp;nbsp;Metabolism, 119: 154766.[6] Li S, et al., 2024, Triglyceride-Glucose Related Indices and Mortality.&amp;nbsp;Cardiovascular Diabetology, 23(1): 286.[7] Hu H, et al., 2024, Diabetes Risk Prediction Models.&amp;nbsp;BMJ Open Diabetes Research &amp;amp; Care, 12(1): e003680.[8] Tang S, et al., 2024, C-Reactive Protein-Triglyceride Glucose Index Predicts Stroke in Hypertensive Population.&amp;nbsp;Diabetology &amp;amp; Metabolic Syndrome, 16(1): 277.[9] Koenig W, 2013, High-Sensitivity C-Reactive Protein and Atherosclerotic Disease.&amp;nbsp;International Journal of Cardiology, 168(6): 5126&amp;ndash;5134.[10] Wang A, et al., 2017, Cumulative High-Sensitivity C-Reactive Protein Exposure Predicts Cardiovascular Disease Risk.&amp;nbsp;Journal of the American Heart Association, 6(10): e005610.[11] Simental-Mend&amp;iacute;a LE, et al., 2008, Fasting Glucose and Triglyceride Product as Insulin Resistance Surrogate.&amp;nbsp;Metabolic Syndrome and Related Disorders, 6(4): 299&amp;ndash;304.[12] Cui C, et al., 2024, Triglyceride Glucose Index and Modified Indices in Cardiovascular Disease Prediction.&amp;nbsp;Cardiovascular Diabetology, 23(1): 185.&amp;nbsp;[13] Xia X, et al., 2024, Triglyceride-Glucose Index and Atherosclerotic Cardiovascular Disease.&amp;nbsp;Cardiovascular Diabetology, 23(1): 208.[14] Cui C, et al., 2024, TyG Index and High Sensitivity C-Reactive Protein Joint Association with Cardiovascular Disease.&amp;nbsp;Cardiovascular Diabetology, 23(1): 156.[15] Shoelson SE, et al., 2006, Inflammation and Insulin Resistance.&amp;nbsp;Journal of Clinical Investigation, 116(7): 1793&amp;ndash;1801.</p><pub-id pub-id-type="doi"/></element-citation></ref></ref-list></back></article>
