ArticleClinical rheumatology2024
Associations of accelerated biological aging and metabolic heterogeneity of obesity with rheumatoid arthritis: a prospective cohort study.
Article in Clinical rheumatology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Association between Modified Cardiometabolic Index and rheumatoid arthritis: the mediating role of phenotypic age acceleration.Clinical rheumatology · 2026Article
- Association between biological aging and clinical mortality among patients with rheumatoid arthritis.Clinical rheumatology · 2026Article
- Association Between Neutrophil Percentage-Albumin Ratio and Biological Aging in Rheumatoid Arthritis in the United States: A Cross-Sectional Study of NHANES.Mediators of inflammation · 2026Article
- Crossing the metabolic homeostasis divide: panoramic decoding of therapeutic targets for metabolic-inflammatory crosstalk in rheumatoid arthritis.Frontiers in immunology · 2025Review
- Accelerated biological aging as potential mediator in the relationship between central obesity and lung cancer risk.Frontiers in aging · 2025Article
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8 authors.
Funding
Abstract
objectiveTo evaluate the associations between biological aging, metabolic heterogeneity of obesity, and rheumatoid arthritis (RA).
methodsThis prospective cohort study analyzed 268,184 individuals from the UK Biobank. Biological age was estimated using phenotypic age (PhenoAge), Klemera-Doubal methods (KDM-BA), and telomere length. We calculated KDM-BA acceleration and PhenoAge acceleration after subtracting the effect of chronological age by regression residual. The metabolic heterogeneity of obesity can be evaluated by four BMI metabolic phenotypes, namely metabolically unhealthy normal weight (MUNW), metabolically healthy normal weight (MHNW), metabolically unhealthy overweight/obesity (MUOO), and metabolically healthy overweight/obesity (MHOO). Cox models were employed to estimate the associations between biological aging, metabolic heterogeneity of obesity, and RA risk.
resultsA total of 2842 patients experienced RA during a mean follow-up time of 12.21 years. A standard deviation (SD) increase in KDM-BA acceleration and PhenoAge acceleration was associated with an increased risk of RA by 13% (hazard ratio = 1.13; 95% CI, 1.09-1.17) and 39% (HR = 1.39; 95% CI, 1.34-1.44), respectively. A SD increase in telomere length was associated with a reduced risk of RA by 5% (HR = 0.95; 95% CI, 0.91-0.98). Compared to the MHNW group, the MUOO group was associated with a 51% increase in the risk of incident RA. In the joint effect analysis, compared to the MHNW + KDM-BA younger subgroup, the HR (95% CI) for RA was 1.68 (1.48, 1.90) in the MUOO + KDM-BA older subgroup.
conclusionAccelerated biological aging may heighten the susceptibility to RA, particularly in individuals with obesity or metabolic dysfunction. Key Points •Accelerated biological aging increases the risk of developing RA. •Overweight/obese people with a healthy metabolism have a higher risk of RA than those with normal weight and healthy metabolism. •The BMI metabolic phenotype has a strong modifying effect on the association between KDM-BA/PhenoAge and RA risk.
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