ArticleClinical rheumatology2026
Association between Modified Cardiometabolic Index and rheumatoid arthritis: the mediating role of phenotypic age acceleration.
Article in Clinical rheumatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
backgroundModified Cardiometabolic Index (MCMI) is a novel metabolic assessment metric integrating waist-to-height ratio (WHtR), lipid, and fasting plasma glucose (FPG). Rheumatoid arthritis (RA), as an autoimmune disease, is closely linked to metabolic status, yet the relation of MCMI to RA remains unclear. Phenotypic age acceleration (PAA), reflecting biological aging, possibly mediates the relation of MCMI to RA. Our study aimed to elucidate the relation of MCMI to RA and assess the mediating effect of PAA.
methods1999-2010 and 2015-2020 National Health and Nutrition Examination Survey (NHANES) data on 10,564 adults were analyzed. RA status was determined via questionnaire. MCMI was calculated based on WHtR, triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), and FPG. PAA was derived as the residual of phenotypic age (PA) regressed on chronological age. The association of MCMI with RA was examined via weighted logistic regression (WLR), restricted cubic splines (RCS) assessed potential nonlinearity, and mediation analysis examined the effect of PAA.
resultsIn multivariable-adjusted models, every one-unit rise in MCMI was related to a 45.1% higher RA prevalence (OR = 1.451, 95% CI: 1.250-1.685). MCMI was split into tertiles. The highest tertile (T3) displayed a significantly higher RA prevalence than the lowest tertile (T1) (OR = 1.879, 95% CI: 1.379-2.559). RCS analysis indicated a linear relation of MCMI to RA (P for nonlinear = 0.331). PAA accounted for 17.446% of the relation of MCMI to RA in mediation analysis (P < 0.001).
conclusionMCMI is positively associated with RA risk, with PAA partially mediating this relationship. These findings suggest that metabolic dysregulation may influence RA development through accelerated biological aging, providing a novel perspective for early prevention and metabolic interventions in RA. Key Points • These findings suggest that poorer metabolic health may be associated with RA, partly through accelerated biological aging. • In practice, metabolic assessment may help identify people at higher risk of RA and support earlier lifestyle or clinical interventions. • The results also highlight biological aging as a possible pathway linking metabolism and RA.
Indexed as
Identifiers
42406254What 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.