TyG plus biological age and cardiometabolic multimorbidity in CHARLS
In a prospective CHARLS cohort of 8,767 adults aged 45 and older without cardiometabolic multimorbidity at baseline, higher TyG and faster biological aging were each independently associated with later cardiometabolic multimorbidity; combined TyG-biological-age scores improved prediction beyond clinical factors but not beyond models keeping the two measures separate. [1]
Automatic summary · not editorially reviewed
The key findings
The prospective CHARLS cohort included 8,767 participants aged 45 and older without cardiometabolic multimorbidity at baseline, and baseline assessments included the TyG index and two biological age algorithms. [1]
Over a median follow-up of 108 months, 873 participants were newly diagnosed with cardiometabolic multimorbidity; TyG and biological age were independently associated with it. [1]
Adding TyG-biological-age composites to the clinical model improved the C-index by 0.015–0.024 but did not improve discrimination beyond models with TyG and biological age as separate covariates. [1]
The source at a glance
- Study type / format
- Prospective cohort study (abstract)
- Population / context
- 8,767 CHARLS participants aged 45 and older without cardiometabolic multimorbidity at baseline
- Summary based on
- Study abstract
- Publication status
- Preprint · peer-review status not confirmed
- Original publication
- August 26, 2026
CHARLS cohort without baseline multimorbidity
This prospective cohort study followed 8,767 participants aged 45 and older from the China Health and Retirement Longitudinal Study who did not have cardiometabolic multimorbidity at the start. Cardiometabolic multimorbidity means having two or more conditions such as type 2 diabetes, stroke and coronary heart disease. At baseline the researchers measured the triglyceride-glucose (TyG) index and calculated biological age with two algorithms, Light-BA and KDM-BA. Biological age acceleration was derived from the residual of biological age regressed on chronological age. Combined TyG-biological-age indices were the products of TyG and biological age.
Supporting source [1]
Higher TyG and faster aging linked to later CMM
During a median follow-up of 108 months, 873 participants were newly diagnosed with cardiometabolic multimorbidity. TyG and biological age were independently associated with this outcome, with mutually adjusted hazard ratios of 1.23–1.27 and 1.39–1.44 per standard-deviation increase. People with elevated TyG and rapid biological aging had the greatest risk, with hazard ratios of 2.37 for Light-BA and 2.26 for KDM-BA, although there was no significant multiplicative interaction. Continuous TyG-biological-age composites were associated with 49%–62% higher risk per standard-deviation increase, and the highest versus lowest quartile showed more than threefold higher risk. Higher cumulative exposure and elevated two-wave trajectory levels were linked to hazard ratios of 3.93–5.17 comparing highest and lowest exposure groups.
Supporting source [1]
Prediction gain and limits of the composite
Multi-state analyses showed consistent associations of the composites with transitions across the cardiometabolic disease continuum and with mortality. Adding TyG-biological-age composites to the prespecified clinical model raised the C-index by 0.015–0.024 and improved net clinical benefit, but did not improve discrimination beyond models containing TyG and biological age as separate covariates. Associations were stronger in younger and non-frail participants in exploratory subgroup analyses. The authors describe the two dimensions as complementary and say the composites should not be interpreted as superior to models retaining TyG and biological age separately. They call for external validation, particularly for earlier stages of cardiometabolic disease. This summary is based on the abstract; the full text was not reviewed.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. This is a prospective cohort study in Chinese adults aged 45 and older, so associations are not causal and external validation is needed, especially for earlier disease stages.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Yang B, Chen Q, Yang S. · europepmc.org · August 26, 2026