ArticleBMC public health2025
Sarcopenic obesity, physical activity, and their combined impact on biological aging in US adults.
Article in BMC public health, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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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.
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Who cites it
2 citing papers in PubMed.
- Article
- Phenotypic Age Acceleration and Risk of All-Cause and Cardiovascular Mortality in US Adults With Asthma: A Retrospective Cohort Study.Dose-response : a publication of International Hormesis SocietyArticle
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Authors and funding
6 authors.
Funding
Abstract
objectiveOur study aimed to examine the independent and combined associations of sarcopenia, sarcopenic obesity (SO) and physical activity (PA) status with phenotypic age acceleration (PhenoAgeAccel) in US adults.
methodThe analyses included 9661 participants from the National Health and Nutrition Examination Survey (NHANES) 2005-2010 & 2015-2018. PhenoAgeAccel was calculated as the residuals from regressing phenotypic age (PhenoAge) on chronological age. Sarcopenia and SO were identified using the FNIH definition. Weighted multivariable logistic regression models, along with stratified and sensitivity analyses, were employed to evaluate the associations between sarcopenia, SO, and PhenoAgeAccel. Additionally, the population attributable fraction (PAF) was calculated to estimate the percentage of PhenoAgeAccel cases that could potentially be prevented by eliminating SO or PA deficiency.
resultsA total of 9661 US adults were included in analysis. The weighted mean (SD) age was 32.78 (15.81) years, and 50.21% were males. Sarcopenia was not associated with PhenoAgeAccel in US adults in any subgroup or model. The multivariate-adjusted OR (95%CI) for PhenoAgeAccel with SO were 2.68 (2.13, 3.37) (p < 0.0001) for all, and 2.65 (2.10, 3.36) (p < 0.0001) for participants whose age ≤ 65 years old. Furthermore, compared to the combination of nonsarcopenia and adequate PA, combining SO and PA deficiency exhibited the highest risk of PhenoAgeAccel (OR 3.87; 95% CI 2.75, 5.46; p < 0.0001). SO increased the risk of PhenoAgeAccel by 29.3%, and adequate PA reduced the risk of PhenoAgeAccel by 9.1%, respectively. Notably, 18.5% increase was attributable to both SO and adequate PA concurrently.
conclusionSO was significantly associated with higher risk of biological aging, especially in middle or young adults. Combining SO and PA deficiency enhanced the risk of accelerated aging. These findings underscore the importance of addressing SO through comprehensive lifestyle interventions to promote healthy aging and enhance health span.
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