Evidence map›Paper›PMID 40256801›Full record

ArticleThe journals of gerontology. Series A, Biological sciences and medical sciences2025

Association of Epigenetic Markers of Aging With Prevalent and Incident Type 2 Diabetes.

Danmeng Lily Li, Allison M Hodge, Melissa C Southey, Graham G Giles, Pierre-Antoine Dugué

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Article in The journals of gerontology. Series A, Biological sciences and medical sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Social relationships and epigenetic markers of aging in middle-aged and older adults: cross-sectional and prospective analyses.The journals of gerontology. Series B, Psychological sciences and social sciences · 2025
    Article
  6. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Danmeng Lily LiPrecision Medicine, School of Clinical Sciences at Monash Health, Monash University, Clayton, Victoria, Australia.
Allison M HodgeCancer Epidemiology Division, Cancer Council Victoria, Melbourne, Victoria, Australia.
Melissa C SoutheyPrecision Medicine, School of Clinical Sciences at Monash Health, Monash University, Clayton, Victoria, Australia.
Graham G GilesPrecision Medicine, School of Clinical Sciences at Monash Health, Monash University, Clayton, Victoria, Australia.
Pierre-Antoine DuguéPrecision Medicine, School of Clinical Sciences at Monash Health, Monash University, Clayton, Victoria, Australia.ORCID 0000-0003-2736-3023

Funding

Melbourne Collaborative Cohort StudyNational Health and Medical Research Council 1026892National Health and Medical Research Council 1027505National Health and Medical Research Council 1043616National Health and Medical Research Council 1050198National Health and Medical Research Council 1074383National Health and Medical Research Council 396414Wellcome Trust 209057
6 · The paper itself

Abstract

backgroundType 2 diabetes (T2D) is characterized by elevated levels of metabolic and inflammatory markers but less is known about other molecular alterations that occur with aging. We aimed to assess the associations of DNA methylation-based measures of aging (epigenetic aging) with prevalent and incident T2D in a large sample of middle-aged and older Australians.

methodsWe used data from 5 403 participants in the Melbourne Collaborative Cohort Study (mean age = 59 years). Five blood-based epigenetic aging measures: PCPhenoAge, PCGrimAge, DNAmFitAge, bAge, and DunedinPACE were calculated. T2D status was assessed at baseline (1990-1994, Ncases = 180) and 2 waves of follow-up (1995-1998, Ncases = 134; 2003-2007, Ncases = 244). Modified Poisson regression models were used to estimate risk ratios for the associations of epigenetic age with prevalent and incident T2D.

resultsA standard deviation increase in epigenetic age was associated with 1.11-fold (PCPhenoAge, 95%CI: 0.98-1.26) to 1.33-fold (bAge, 95%CI: 1.12-1.57) higher prevalence of T2D at baseline. Prospectively, DunedinPACE showed the strongest association with incident T2D at follow-up 2 (risk ratio = 1.22, 95%CI: 1.07-1.38). These estimates were slightly attenuated but consistent in sensitivity analyses reclassifying participants who reported being T2D-free but had high glucose concentrations (> 7 mmol/L for fasting glucose, > 11.1 mmol/L for nonfasting glucose). No evidence of increased epigenetic age was found for participants with pre-T2D (> 5.6 mmol/L for fasting glucose, > 7.8 mmol/L for nonfasting glucose). The positive associations between epigenetic age and fasting glucose levels appeared stronger in participants with T2D.

conclusionsIn middle-aged and older Australians, epigenetic age, in particular as assessed by bAge and DunedinPACE, was positively associated with prevalent and incident T2D. Our findings may have implications for understanding the etiology and management of T2D.

Indexed as

AgingDiabetes Mellitus, Type 2DNA MethylationEpigenesis, GeneticAgedAustraliaBiomarkersCohort StudiesFemaleHumansIncidenceMaleMiddle AgedPrevalenceBiomarkersBiological agingEpigenetic agingIncident type 2 diabetesRisk factors

Identifiers

PMID40256801
PMCPMC12198671

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.