Peggy Ler, Jonathan K. L. Mak, Chandra A. Reynolds, Alexander Ploner, Nancy L. Pedersen, Juulia Jylhävä, Anna K. Dahl Aslan, Deborah Finkel, Ida K. Karlsson
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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.</p>\n </section>\n \n <section>\n \n <h3> Methods</h3>\n \n <p>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.</p>\n </section>\n \n <section>\n \n <h3> Results</h3>\n \n <p>At first measurement, mean age was 74 ± 8, and 41% were males. BMI–FI relationship was bidirectional (<i>p</i> value ≤ 0.001): Higher BMI predicted a greater increase in FI over time (coupling effect [<i>γ</i>] = 0.86, 95% confidence interval [CI] = 0.65–1.06, <i>p</i> value ≤ 0.001), and higher FI predicted steeper decline in BMI (<i>γ</i> = −0.04, 95% CI = −0.05 to −0.03, <i>p</i> value ≤ 0.001). When including coupling from FI, BMI showed a nonlinear trajectory with a mean intercept of 26.32 kg/m<sup>2</sup> (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 (<i>p</i> value ≤ 0.001): Higher FAI predicted a steeper BMI decline (<i>γ</i> = −0.02, 95% CI = −0.02 to −0.01, <i>p</i> value ≤ 0.001). By including FAI coupling, BMI had a mean intercept of 26.10 kg/m<sup>2</sup> (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).</p>\n </section>\n \n <section>\n \n <h3> Conclusions</h3>\n \n <p>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.</p>\n </section>\n </div>","PeriodicalId":48911,"journal":{"name":"Journal of Cachexia Sarcopenia and Muscle","volume":"16 3","pages":""},"PeriodicalIF":9.4000,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcsm.13824","citationCount":"0","resultStr":"{\"title\":\"A Longitudinal Study of the Bidirectional Temporal Dynamics Between Body Mass Index and Biological Aging\",\"authors\":\"Peggy Ler, Jonathan K. L. Mak, Chandra A. Reynolds, Alexander Ploner, Nancy L. Pedersen, Juulia Jylhävä, Anna K. Dahl Aslan, Deborah Finkel, Ida K. 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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 (<i>p</i> value ≤ 0.001): Higher FAI predicted a steeper BMI decline (<i>γ</i> = −0.02, 95% CI = −0.02 to −0.01, <i>p</i> value ≤ 0.001). By including FAI coupling, BMI had a mean intercept of 26.10 kg/m<sup>2</sup> (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).</p>\\n </section>\\n \\n <section>\\n \\n <h3> Conclusions</h3>\\n \\n <p>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. 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引用次数: 0
摘要
肥胖和衰老有共同的生物学过程，但它们之间的关系尚不清楚，尤其是在晚年。了解身体质量指数（BMI）和生物衰老是如何相互影响的，可以指导降低年龄和肥胖相关健康风险的策略。我们通过脆弱性指数（FI）和功能性衰老指数（FAI）检测了BMI变化与生物衰老之间的双向纵向关联。方法：该纵向队列研究使用了瑞典双胞胎登记处亚研究、GENDER、OCTO-Twin和SATSA的数据，这些数据是通过1986年至2014年每隔2至4年的面对面评估收集的。我们分析了从1902年到1976年瑞典双胞胎的6216-6512项评价。采用双变化评分模型评估60.0-91.9岁BMI与FI或FAI之间的双向纵向关联。FI测量生理衰老，而FAI通过功能能力的综合评分来评估功能性衰老。结果首次测量时平均年龄为74±8岁，男性占41%。BMI - FI呈双向关系（p值≤0.001）：BMI越高预示着FI随时间的增加越大（耦合效应[γ] = 0.86, 95%可信区间[CI] = 0.65 ~ 1.06， p值≤0.001），FI越高预示着BMI下降越陡（γ = - 0.04, 95% CI = - 0.05 ~ - 0.03， p值≤0.001）。当包括来自FI的耦合时，BMI呈非线性轨迹，平均截距为26.32 kg/m2 (95% CI = 25.76-26.88)，在75岁后下降更快。当包括BMI耦合时，FI从平均截距7.91% （95% CI = 6.41-9.42）开始增加，从60-75岁开始增长更陡。BMI - FAI呈单向关系（p值≤0.001）：FAI越高，BMI下降越快（γ = - 0.02, 95% CI = - 0.02 ~ - 0.01， p值≤0.001）。通过纳入FAI耦合，BMI的平均截距为26.10 kg/m2 (95% CI = 25.47-26.74)，在75岁后迅速下降。平均截距为36.49，FAI呈指数增长（95% CI = 34.54-38.43）。高BMI预示着FI的急剧增加，证实了肥胖加速生物衰老的假设。以FI和FAI衡量的生物老化程度越高，晚年BMI下降越快，这表明晚年体重减轻可能是由加速衰老造成的。较高的体重指数可能会加速衰老过程的某些方面，而衰老过程反过来又会加速晚年体重指数的下降，因此需要一种综合的方法来管理老年人的肥胖和无意的体重减轻。
A Longitudinal Study of the Bidirectional Temporal Dynamics Between Body Mass Index and Biological Aging
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.
期刊介绍：
The Journal of Cachexia, Sarcopenia and Muscle is a peer-reviewed international journal dedicated to publishing materials related to cachexia and sarcopenia, as well as body composition and its physiological and pathophysiological changes across the lifespan and in response to various illnesses from all fields of life sciences. The journal aims to provide a reliable resource for professionals interested in related research or involved in the clinical care of affected patients, such as those suffering from AIDS, cancer, chronic heart failure, chronic lung disease, liver cirrhosis, chronic kidney failure, rheumatoid arthritis, or sepsis.
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