1. Interplay of body mass index and metabolic syndrome : association with physiological age from midlife to late-life
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Ler, Peggy, Ploner, Alexander, Finkel, Deborah, Reynolds, Chandra A., Zhan, Yiqiang, Jylhävä, Juulia, Dahl Aslan, Anna K., Karlsson, Ida K., Ler, Peggy, Ploner, Alexander, Finkel, Deborah, Reynolds, Chandra A., Zhan, Yiqiang, Jylhävä, Juulia, Dahl Aslan, Anna K., and Karlsson, Ida K.
- Abstract
Obesity and metabolic syndrome (MetS) share common pathophysiological characteristics with aging. To better understand their interplay, we examined how body mass index (BMI) and MetS jointly associate with physiological age, and if the associations changed from midlife to late-life. We used longitudinal data from 1,825 Swedish twins. Physiological age was measured as frailty index (FI) and functional aging index (FAI) and modeled independently in linear mixed-effects models adjusted for chronological age, sex, education, and smoking. We assessed curvilinear associations of BMI and chronological age with physiological age, and interactions between BMI, MetS, and chronological age. We found a significant three-way interaction between BMI, MetS, and chronological age on FI (p-interaction = 0·006), not FAI. Consequently, we stratified FI analyses by age: < 65, 65–85, and ≥ 85 years, and modeled FAI across ages. Except for FI at ages ≥ 85, BMI had U-shaped associations with FI and FAI, where BMI around 26-28 kg/m2 was associated with the lowest physiological age. MetS was associated with higher FI and FAI, except for FI at ages < 65, and modified the BMI-FI association at ages 65–85 (p-interaction = 0·02), whereby the association between higher BMI levels and FI was stronger in individuals with MetS. Age modified the MetS-FI association in ages ≥ 85, such that it was stronger at higher ages (p-interaction = 0·01). Low BMI, high BMI, and metabolic syndrome were associated with higher physiological age, contributing to overall health status among older individuals and potentially accelerating aging., CC BY 4.0 DEED© 2023, The Author(s)Published: 16 December 2023Correspondence Address: P. Ler; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Nobels väg 12A, Solna, 171 65, Sweden; email: peggy.ler@ki.seOpen access funding provided by Karolinska Institute. This work was supported by the Swedish Research Council for Health, Working Life and Welfare (Forte; 2022-00672); the Strategic Research Program in Epidemiology (SFOepi) at Karolinska Institutet, Karolinska Institutet’s Research Foundation (2022-01718); Loo and Hans Osterman’s Foundation (2022-01222, 2023-01855); the Foundation for Geriatric Diseases at Karolinska Institutet (2022-01296); the National Institutes of Health (NIH; R01 AG060470, AG059329), and the Swedish Research Council (Vetenskaprådet; 2016–03081). SATSA was supported by 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, 2009-0795), and the Swedish Research Council (825-2007-7460 and 825-2009-6141). OCTO-Twin was supported by the NIH (R01AG08861). GENDER was supported by the MacArthur Foundation Research Network on Successful Aging, The Axel and Margaret Ax:son Johnson’s Foundation, The Swedish Council for Social Research, and the Swedish Foundation for Health Care Sciences and Allergy Research. The funders had no role in the study design, data collection, data analysis, interpretation, or writing of the manuscript.
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- 2024
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