DNA Methylation-derived biological age and long-term mortality risk in subjects with type 2 diabetes
Authors' conclusion
These findings suggest that biological aging, as estimated through existing epigenetic tools, is associated with mortality risk in individuals with T2D, independently of common risk factors and that increased DNAm-surrogates of inflammatory protein levels characterize deceased T2D patients. Replication in larger cohorts is needed to assess the potential of this approach to refine mortality risk in T2D.
Study context
- Population
- Patients with T2D from a cohort of 568 followed for 16.8 years, balanced for all risk factors after propensity score matchingPS-matched subgroup
- Participants
- 50 patients
- Comparison
- Deceased vs survived T2D patients
- Deceasedn = 23
- Survivedn = 27reference
- Outcome
- Epigenetic age (DNAmPhenoAge)
Methodological detailspropensity score matching, nested in cohort of 568 T2D patients followed 16.8 years
- Propensity score matching
- Nested in cohort of 568 T2D patients followed 16.8 years
Main finding
As reported in the abstract
P = 0.012
- DNA methylation (DNAm) PhenoAge association with mortality, independent of canonical risk factors: HR
- 1.16 (95% CI 1.05-1.28; p = 0.004)
Observational data: associations, not effects.
Further findings
Median
| Outcome | Deceased | Survived | P value |
|---|---|---|---|
| DunedinPoAm pace of agingAccelerated in deceased | 1.05 (IQR 1.02–1.11) | 1.02 (IQR 0.98–1.06) | P = 0.012 |
- DunedinPoAm pace of aging — DunedinPoAm association with mortality, independent of canonical risk factors: HR
- 3.65 (95% CI 1.43-9.35; p = 0.007)
DNAm-estimated inflammatory proteins and cell counts
- Epigenetic predictors of CXCL10, CXCL11 and enRAGE, CRP methylation risk score and DNAm-based exhausted CD8 + T cell counts higher in deceased vs survived
Original publication
DNA Methylation-derived biological age and long-term mortality risk in subjects with type 2 diabetes. Cardiovasc Diabetol. Published 13 July 2024. doi:10.
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