Epigenetic biological age and type 2 diabetes risk in older German adults
In the ESTHER cohort, a previous type 2 diabetes diagnosis was associated with higher baseline biological age on two clocks, and accelerated biological aging predicted higher later diabetes risk. [1]
Automatic summary · not editorially reviewed
The key findings
The ESTHER cohort included 1915 adults aged 50–75 at baseline, followed up to 21 years, with repeat biological age measurements in 894 participants at 8-year follow-up. [1]
A previous type 2 diabetes diagnosis was associated with higher baseline biological age on the PCPhenoAge and PCGrimAge clocks. [1]
Steeper biological age trajectories over 8 years were associated with 51% to 85% higher subsequent type 2 diabetes risk per standard deviation across all five clocks. [1]
The source at a glance
- Study type / format
- Population-based cohort study (abstract only).
- Population / context
- 1915 adults aged 50–75 years at baseline in the German population-based ESTHER cohort.
- Summary based on
- Study abstract
- Publication status
- Preprint · peer-review status not confirmed
- Original publication
- August 20, 2026
ESTHER cohort: 1915 adults aged 50–75
The abstract describes a German population-based cohort, ESTHER, with 1915 participants aged 50–75 years at baseline, followed for up to 21 years. Five epigenetic biological age clocks based on DNA methylation were estimated. In 894 participants, biological age was measured again from blood samples taken at the 8-year follow-up. The study examined links between a history of type 2 diabetes and biological age at baseline, and between biological age levels and trajectories and later diabetes cases.
Supporting source [1]
Higher baseline biological age with prior diabetes
A previous type 2 diabetes diagnosis was associated with higher biological age at baseline, as measured by the PCPhenoAge and PCGrimAge clocks. In the survival analysis, accelerated PCGrimAge predicted a higher overall type 2 diabetes risk over a median follow-up of 13.5 years (interquartile range 7.8–16.7). The fully adjusted hazard ratio was 1.65 per standard deviation of PCGrimAge (95% confidence interval 1.25–2.17). These are associations, not evidence that biological age causes diabetes.
Supporting source [1]
Steeper 8-year age trajectories and later diabetes
Steeper biological age trajectories between baseline and the 8-year follow-up were associated with 51% to 85% higher subsequent type 2 diabetes risk per standard deviation increase across all five clocks. Linear trends were confirmed in restricted cubic spline models. The abstract reports consistent associations between these 8-year trajectories and diabetes incidence over the subsequent 9 years. The authors suggest biological age measures may help identify older adults at elevated risk and inform targeted prevention. The abstract does not report the number of diabetes cases or adjustment details.
Supporting source [1]
How to interpret this
This explainer is based only on the abstract; the full text was not reviewed. The abstract does not report the number of diabetes cases, detailed adjustment variables or the exact composition of the five clocks. The findings are observational associations and do not show that biological age causes diabetes.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Yin Q, Stevenson-Hoare J, Holleczek B, Schöttker B, Brenner H. · europepmc.org · August 20, 2026