ArticleBMC medicine2025
Association of accelerated phenotypic aging, genetic risk, and lifestyle with progression of type 2 diabetes: a prospective study using multi-state model.
Article in BMC medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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.
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.
Who cites it
15 citing papers in PubMed.
- Cellular Senescence and Aging: Mechanisms, Disease Convergence, and Therapeutic Frontiers.MedComm · 2026Review
- Association of accelerated phenotypic aging, lifestyle and genetic risk with progression of cardiometabolic multimorbidity: a multi-state model analysis.GeroScience · 2026Article
- Associations of Multiomics Biological Aging With Diabetic Retinopathy and Life Expectancy.Investigative ophthalmology & visual science · 2026Article
- Death cause and age at death among individuals with diabetes: a 40-year retrospective Brazilian study.Archives of endocrinology and metabolism · 2026Article
- Sofrito and Fruit Consumption Associated with Lower Risk of Type 2 Diabetes in an Urban Latin American Cohort.Nutrients · 2026Article
- Investigating the research trajectory and future trends in type 2 diabetes mellitus and aging: a bibliometric analysis from 2009 to 2025 based on big data.Frontiers in aging · 2026Review
- Proteomics mediates the effects of biological aging on the progression of cardio-renal-metabolic comorbidity: a UK biobank cohort study.Cardiovascular diabetology · 2025Article
- Combined association between phenotypic age acceleration and dietary fiber intake with mortality in middle-aged and elderly cancer survivors.Nutrition journal · 2025Article
- Association Between Lumbar Spinal Stenosis and Accelerated Biological Aging Estimated by PhenoAge.Journal of clinical medicine · 2025Article
- Baseline and longitudinal changes of body roundness index and incident type 2 diabetes: evidence from the UK Biobank cohort.BMJ open diabetes research & care · 2025Article
- Biological aging and incident cardiovascular diseases in individuals with diabetes: insights from a large prospective cohort study.Cardiovascular diabetology · 2025Article
- Medical laboratory data-based models: opportunities, obstacles, and solutions.Journal of translational medicine · 2025Review
- The Relationship between Visceral Fat Accumulation and Risk of Cardiometabolic Multimorbidity: The Roles of Accelerated Biological Aging.Nutrients · 2025Article
- Associations between Life's Crucial 9 and severity, all-cause mortality, and cardiovascular mortality in individuals with cardiovascular-kidney-metabolic syndrome: the mediating role of phenotypic age acceleration.Frontiers in nutrition · 2025Article
- Editorial: Epidemiology of diabetes in Asia.Frontiers in clinical diabetes and healthcare · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAging is a major risk factor for type 2 diabetes (T2D), but individuals of the same chronological age may vary in their biological aging rate. The associations of Phenotypic Age Acceleration (PhenoAgeAccel), a new accelerated biological aging indicator based on clinical chemistry biomarkers, with the risk of dynamic progression remain unclear. We aimed to assess these associations and examine whether these associations varied by genetic risk and lifestyle.
methodsWe conducted a prospective cohort study that included 376,083 adults free of T2D and diabetes-related events at baseline in UK Biobank. PhenoAgeAccel > 0 and ≤ 0 were defined as biologically older and younger than chronological age. The outcomes of interest were incident T2D, diabetic complications, and mortality. Hazard ratios (HRs) with 95% confidence intervals (CIs) and population attributable fractions (PAFs) for these associations were calculated using multi-state model.
resultsDuring a median follow-up of 13.7 years, 17,615 participants developed T2D, of whom, 4,524 subsequently developed complications, and 28,373 died. Being biologically older was associated with increased risks of transitions from baseline to T2D (HR 1.77, 95% CI 1.71-1.82; PAF 24.8 [95% CI 23.5-26.2]), from T2D to diabetic complications (1.10, 1.04-1.17; 4.4 [1.4-7.4]), from baseline to all-cause death (1.53, 1.49-1.57; 17.6 [16.6-18.6]), from T2D to all-cause death (1.14, 1.03-1.26; 7.4 [1.8-13.0]), and from diabetic complications to all-cause death (1.32, 1.15-1.51; 15.4 [7.5-23.2]) than being biologically younger. Additionally, participants with older biological age and high genetic risk had a higher risk of incident T2D (4.76,4.43-5.12;18.2 [17.5-19.0]) than those with younger biological age and low genetic risk. Compared with participants with younger biological age and healthy lifestyle, those with older biological age and unhealthy lifestyle had higher risks of transitions in the T2D trajectory, with HRs and PAFs ranging from 1.34 (1.16-1.55; 3.7 [1.8-5.6]) to 5.39 (5.01-5.79; 13.0 [12.4-13.6]).
conclusionsPhenoAgeAccel was consistently associated with an increased risk of all transitions in T2D progression. It has the potential to be combined with genetic risk to identify early T2D incidence risk and may guide interventions throughout T2D progression while tracking their effectiveness.
Indexed as
Identifiers
What Socratic holds
Registered trials
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 Socratic graph.