Ler Peggy, Mak Jonathan K L, Reynolds Chandra A, Ploner Alexander, Pedersen Nancy L, Jylhävä Juulia, Dahl Aslan Anna K, Finkel Deborah, Karlsson Ida K
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden.
Department of Pharmacology and Pharmacy Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.
J Cachexia Sarcopenia Muscle. 2025 Jun;16(3):e13824. doi: 10.1002/jcsm.13824.
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.
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.
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/m (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/m (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).
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.
肥胖与衰老存在共同的生物学过程,但其关系仍不明确,尤其是在老年阶段。了解体重指数(BMI)与生物学衰老如何相互影响,可为降低与年龄和肥胖相关的健康风险的策略提供指导。我们研究了BMI变化与生物学衰老之间的双向纵向关联,生物学衰老通过衰弱指数(FI)和功能衰老指数(FAI)来衡量,研究对象为老年人。
这项纵向队列研究使用了瑞典双胞胎登记处子研究GENDER、OCTO-Twin和SATSA的数据,这些数据通过1986年至2014年期间每2至4年进行一次的现场评估收集。我们分析了1902至1976对瑞典双胞胎的6216 - 6512次评估。采用双变化评分模型评估60.0至91.9岁之间BMI与FI或FAI之间的双向纵向关联。FI衡量生理衰老,而FAI通过功能能力综合评分评估功能衰老。
首次测量时,平均年龄为74±8岁,男性占41%。BMI与FI的关系是双向的(p值≤0.001):较高的BMI预测FI随时间的增加幅度更大(耦合效应[γ]=0.86,95%置信区间[CI]=0.65 - 1.06,p值≤0.001),而较高的FI预测BMI下降更陡峭(γ=-0.04,95%CI=-0.05至-0.03,p值≤0.001)。当纳入来自FI的耦合时,BMI呈现非线性轨迹,平均截距为26.32kg/m(95%CI=25.76 - 26.88),在75岁后下降更快。当纳入BMI耦合时,FI从平均截距7.91%(95%CI=6.41 - 9.42)开始增加,在60至75岁时增长更陡峭。BMI与FAI的关系是单向的(p值≤0.001):较高的FAI预测BMI下降更陡峭(γ=-0.02,95%CI=-0.02至-0.01,p值≤0.001)。通过纳入FAI耦合,BMI的平均截距为26.10kg/m(95%CI=25.47 - 26.74),在75岁后迅速下降。FAI从平均截距36.49(95%CI=34.54 - 38.43)开始呈指数增长。
较高的BMI预测FI上升更陡峭,证实了肥胖加速生物学衰老的假设。以FI和FAI衡量的较高生物学衰老导致老年期BMI下降更陡峭,这表明老年期体重减轻可能是衰老加速的结果。较高的BMI可能加速衰老过程的某些方面,而衰老过程反过来又加速老年期BMI下降,因此需要一种综合方法来管理老年人的肥胖和非自愿体重减轻问题。