# Sedentary behavior accelerates biological aging mediated by body mass index in adults

**Authors:** Jinhang Che, Jie Huai, Lihong Luo, Yunxiang Tang, Tao Zeng

PMC · DOI: 10.1038/s41598-025-06325-x · Scientific Reports · 2025-07-01

## TL;DR

Sitting too much is linked to faster biological aging, partly because it increases body mass index, according to a study of over 12,000 adults.

## Contribution

The study identifies a linear, dose-response relationship between sitting time and biological aging, partially mediated by BMI.

## Key findings

- Longer sitting time is associated with higher risk of biological aging acceleration.
- BMI partially mediates the relationship between sitting time and phenotypic age acceleration.
- The association remains significant after adjusting for multiple covariates.

## Abstract

Sedentary behavior is widely recognized as a detriment to health. Limited conclusions have been drawn about the relationship between sitting time and biomarkers-measured aging. 12,504 eligible adults were included from the National Health and Nutrition Examination Survey (NHANES) 2007 to 2016. Weighted logistic regression, subgroup analysis, and restricted cubic spline regression were conducted to investigate the association and dose-response relationship between sitting time and phenotypic age acceleration (PhenoAgeAccel). The mediating effect of body mass index (BMI) on this correlation was revealed by mediation analysis. After adjusting for multiple covariates, longer sitting time (4–6 h: OR 1.30, 95%CI 1.06–1.58, p = 0.013; 6–8 h: OR 1.25, 95%CI 1.01–1.55, p = 0.038; ≥8 h: OR 1.58, 95%CI 1.33–1.88, p < 0.001) significantly had higher risk of aging comparing to the reference (< 4 h). The dose-response relationship exhibited an approximately linear dependence. Additionally, BMI partially mediated the association between sitting time and PhenoAgeAccel by a 21.0% proportion. Our study revealed a strong, significant, independent, linear relationship between sitting time and phenotypic age. BMI served as a mediator of the correlation between sitting time and PhenoAgeAccel.

## Full-text entities

- **Genes:** GH1 (growth hormone 1) [NCBI Gene 2688] {aka GH, GH-N, GHB5, GHN, IGHD1A, IGHD1B}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, MTOR (mechanistic target of rapamycin kinase) [NCBI Gene 2475] {aka FRAP, FRAP1, FRAP2, RAFT1, RAPT1, SKS}, GGH (gamma-glutamyl hydrolase) [NCBI Gene 8836] {aka GATD10, GH}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, IGF1 (insulin like growth factor 1) [NCBI Gene 3479] {aka IGF, IGF-I, IGFI, MGF}
- **Diseases:** insulin resistance (MESH:D007333), stroke (MESH:D020521), CHD (MESH:D003327), Parkinson's disease (MESH:D010300), metabolic syndrome (MESH:D024821), inflammatory (MESH:D007249), tumor (MESH:D009369), NCHS (OMIM:603663), death (MESH:D003643), cardiovascular disease (MESH:D002318), diabetes (MESH:D003920), age-related diseases (MESH:D010024), CHF (MESH:D006333), mitochondrial dysfunction (MESH:D028361), obesity (MESH:D009765), HTN (MESH:D006973)
- **Chemicals:** testosterone (MESH:D013739), reactive oxygen species (MESH:D017382), glucose (MESH:D005947), creatinine (MESH:D003404), PIR (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12219758/full.md

## References

11 references — full list in the complete paper: https://tomesphere.com/paper/PMC12219758/full.md

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Source: https://tomesphere.com/paper/PMC12219758