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2025 (English)In: Journal of Cachexia, Sarcopenia and Muscle, ISSN 2190-5991, E-ISSN 2190-6009, Vol. 16, no 3, article id e13824Article in journal (Refereed) Published
Abstract [en]
Background: Obesity and aging share biological processes, but their relationship remains unclear, especially in late life. Understanding how body mass index (BMI) and biological aging influence each other can guide strategies to reduce age- and obesity-related health risks. We examined the bidirectional, longitudinal association between changes in BMI and biological aging, measured by frailty index (FI) and functional aging index (FAI), across late life.
Methods: This longitudinal cohort study used data from the Swedish Twin Registry substudies, GENDER, OCTO-Twin and SATSA, collected via in-person assessments from 1986 to 2014 at 2- to 4-year intervals. We analysed 6216–6512 evaluations from 1902 to 1976 Swedish twins. Dual change score models were applied to assess the bidirectional, longitudinal association between BMI and FI or FAI from ages 60.0–91.9. FI measured physiological aging, while FAI assessed functional aging through a composite score of functional abilities.
Results: At first measurement, mean age was 74 ± 8, and 41% were males. BMI–FI relationship was bidirectional (p value ≤ 0.001): Higher BMI predicted a greater increase in FI over time (coupling effect [γ] = 0.86, 95% confidence interval [CI] = 0.65–1.06, p value ≤ 0.001), and higher FI predicted steeper decline in BMI (γ = −0.04, 95% CI = −0.05 to −0.03, p value ≤ 0.001). When including coupling from FI, BMI showed a nonlinear trajectory with a mean intercept of 26.32 kg/m2 (95% CI = 25.76–26.88), declining more rapidly after age 75. When including BMI coupling, FI increased from a mean intercept of 7.91% (95% CI = 6.41–9.42), with steeper growth from ages 60–75. BMI–FAI relationship was unidirectional (p value ≤ 0.001): Higher FAI predicted a steeper BMI decline (γ = −0.02, 95% CI = −0.02 to −0.01, p value ≤ 0.001). By including FAI coupling, BMI had a mean intercept of 26.10 kg/m2 (95% CI = 25.47–26.74), declining rapidly after age 75. FAI increased exponentially from a mean intercept of 36.49 (95% CI = 34.54–38.43).
Conclusions: Higher BMI predicted a steeper increase in FI, substantiating the hypothesis that obesity accelerates biological aging. Higher biological aging, measured as FI and FAI, drove a steeper BMI decline in late life, signalling that late-life weight loss may result from accelerated aging. Higher BMI may accelerate aspects of the aging process, and the aging process, in turn, accelerates late-life BMI decline, necessitating an integrated approach to manage both obesity and unintentional weight loss among older adults.
Place, publisher, year, edition, pages
John Wiley & Sons, 2025
Keywords
biological aging, body mass index, dual change score, frailty index, obesity, trajectory
National Category
Gerontology, specialising in Medical and Health Sciences Geriatrics Public Health, Global Health and Social Medicine
Research subject
Wellbeing in long-term health problems (WeLHP)
Identifiers
urn:nbn:se:his:diva-25159 (URN)10.1002/jcsm.13824 (DOI)001522046100020 ()40342213 (PubMedID)2-s2.0-105004687533 (Scopus ID)
Funder
Forte, Swedish Research Council for Health, Working Life and Welfare, 2022-00672Karolinska InstituteLoo och Hans Ostermans Stiftelse för medicinsk forskning, 2022-01222Loo och Hans Ostermans Stiftelse för medicinsk forskning, 2023-01855Loo och Hans Ostermans Stiftelse för medicinsk forskning, 2024-02197Foundation for Geriatric Diseases at Karolinska Institutet, 2022-01296Foundation for Geriatric Diseases at Karolinska Institutet, 2023-01854Foundation for Geriatric Diseases at Karolinska Institutet, 2024-02116NIH (National Institutes of Health), R01AG060470NIH (National Institutes of Health), AG059329NIH (National Institutes of Health), R01AG037985NIH (National Institutes of Health), R01AG081248NIH (National Institutes of Health), R01AG089666Swedish Research Council, 2016–03081Swedish Research CouncilEdith och Erik Fernströms Stiftelse för medicinsk forskningNIH (National Institutes of Health), AG04563NIH (National Institutes of Health), AG10175Forte, Swedish Research Council for Health, Working Life and Welfare, 97:0147:1BForte, Swedish Research Council for Health, Working Life and Welfare, 2009-0795Swedish Research Council, 825-2007-7460Swedish Research Council, 825-2009-6141NIH (National Institutes of Health), R01AG08861Axel and Margaret Ax:son Johnson FoundationVårdal FoundationThe Karolinska Institutet's Research Foundation, 2022-01718
Note
CC BY 4.0
© 2025 The Author(s). Journal of Cachexia, Sarcopenia and Muscle published by Wiley Periodicals LLC.
Correspondence Address: P. Ler; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden; email: peggy.ler@ki.se; I. Karlsson; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden; email: ida.karlsson@ki.se
This research was funded by the Swedish Research Council for Health, Working Life and Welfare (Forte; 2022-00672), the Strategic Research Program in Epidemiology (SFOepi) at Karolinska Institutet, Loo and Hans Osterman's Foundation (2022-01222, 2023-01855 and 2024-02197), the Foundation for Geriatric Diseases at Karolinska Institutet (2022-01296, 2023-01854 and 2024-02116), the National Institutes of Health (R01AG060470 and AG059329), the National Institute on Aging (R01AG037985, R01AG081248 and R01AG089666), the Swedish Research Council (Vetenskaprådet; 2016–03081), Erik och Edith Fernströms stiftelse för medicinsk forskning and Swedish National Research School of Aging and Health (SWEAH). The SATSA project received support from the NIH (Grants AG04563 and AG10175), the MacArthur Foundation Research Network on Successful Aging, the Swedish Research Council for Working Life and Social Research (97:0147:1B and 2009-0795) and the Swedish Research Council (825-2007-7460 and 825-2009-6141). Funding for the OCTO-Twin was provided by the NIH (R01AG08861). GENDER was funded by the MacArthur Foundation Research Network on Successful Aging, the Axel and Margaret Ax:son Johnson's Foundation, the Swedish Council for Social Research, the Swedish Foundation for Health Care Sciences and Allergy Research and the Karolinska Institutet's Research Foundation (2022-01718). The research funders did not contribute to the development of study design, analysis, interpretation of results and manuscript writing.
2025-05-222025-05-222025-09-29Bibliographically approved