Biological aging and incident cardiovascular diseases in individuals with diabetes: insights from a large prospective cohort study
Authors' conclusion
Biological aging significantly increases CVD risk and reduces life expectancy in diabetic population, with effects modified by CHIP status. Targeting biological aging mechanisms may help prevent CVDs and premature mortality in diabetic population.
Study context
- Population
- Individuals with diabetes in UK Biobank
- Participants
- 12,828 individuals
- Exposure
- Accelerated vs non-accelerated biological aging
- Outcome
- Incident CVDs (CHD, atrial fibrillation (AF), HF, stroke, degenerative valvular heart disease) and life expectancy loss
- Follow-up
- Median 13.1 years
Methodological detailsUK Biobank, Cox proportional hazard models, causal mediation analysis
- UK Biobank
- Cox proportional hazard models
- Causal mediation analysis
Main finding
As reported in the abstract
Incident cardiovascular diseases (CVDs) documented
3794
Phenotypic age (PhenoAge) accelerated aging significantly associated with all CVD subtypes, HRs ranging
1.23 to 1.62
Accelerated biological aging associated with life expectancy loss
over 2 years
Observational data: associations, not effects.
Further findings
Interaction with clonal hematopoiesis of indeterminate potential (CHIP)
- CHIP and PhenoAge accelerated aging had a significant synergistic effect on coronary heart disease (CHD), heart failure (HF) and valvular heart disease (VHD)
Mediation
- Inflammatory activation contributed significantly to accelerated aging-associated CHD and HF
Original publication
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