Obesity in early adulthood and physical functioning in mid-life: Investigating the mediating role of c-reactive protein.
Obesity in early adulthood and physical functioning in mid-life: Investigating the mediating role of c-reactive protein.
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DOI：
10.1016/j.bbi.2022.03.008
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发表时间：
2022-05
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影响因子：
--
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33岁时肥胖导致50岁时身体机能不良的几率增加一倍以上。因果调节模型评估了c反应蛋白在这种关系中的作用。23%的肥胖对PF的影响是通过对CRP的下游影响来实现的。成年期肥胖与老年时身体功能（PF）下降有关。然而，这种关联的机制尚不清楚。我们调查了C-反应蛋白（CRP）是否以及在多大程度上介导了早期成人肥胖和中年PF之间的关联。我们使用了1958年英国出生队列研究中8495名参与者的数据。分别在33岁、45岁和50岁时测量体重指数（BMI）、CRP和PF。PF差定义为简表36身体功能子量表中最低（性别特异性）10%。我们解释了早期生活中前瞻性测量的混杂因素（例如，出生时的社会阶级）和成年中期（例如，42岁合并症）。我们通过采用基于参数g计算的中介分析，将早期成人肥胖对中年PF的总影响分解为直接和间接（通过CRP）影响。33岁时肥胖对50岁时PF较差的估计总效应（以比值比（OR）表示）为2.41（95%CI：1.89，3.08）。肥胖对PF不良的直接影响（即，未通过CRP进行操作），为1.97（95% CI：1.51，2.56），间接影响为1.23（95% CI：1.10，1.37）。因此，45岁时肥胖对CRP的影响介导的总效应比例为23.27%（95% CI：8.64%，37.90%）。成年早期的肥胖与中年PF不良几率的两倍以上相关，约23%的肥胖效应通过对CRP的下游效应起作用。由于目前的年轻一代可能会在老年和肥胖中度过更大比例的生命历程，这两者都与PF不足有关，因此迫切需要确定将肥胖与PF不足联系起来的机制，从而确定潜在的可改变的中介。
Obesity at 33y resulted in more than twice the odds of poor physical functioning at 50y. Causal mediation models assessed the role of c-reactive protein on this relationship. 23% of the obesity effect on PF operated via a downstream effect on CRP. Obesity in adulthood is associated with reduced physical functioning (PF) at older ages. However, mechanisms underpinning this association are not well understood. We investigated whether and the extent to which C-reactive protein (CRP) mediates the association between early-adult obesity and mid-life PF. We used data from 8495 participants in the 1958 British birth cohort study. Body mass index (BMI), CRP and PF were measured at 33, 45 and 50y, respectively. Poor PF was defined as the lowest (sex-specific) 10% on the Short-form 36 Physical Functioning subscale. We accounted for prospectively measured confounders in early-life (e.g., social class at birth) and in mid-adulthood (e.g., 42y comorbidities). We decomposed the total effect of early-adult obesity on mid-life PF into direct and indirect (via CRP) effects, by employing a mediation analysis based on parametric g-computation. The estimated total effect of obesity at 33y on poor PF at 50y, expressed as an odds ratio (OR), was 2.41 (95% CI: 1.89, 3.08). The direct effect of obesity on poor PF (i.e., not operating via CRP), was 1.97 (95% CI: 1.51, 2.56), with an indirect effect of 1.23 (95% CI: 1.10, 1.37). As such, the proportion of the total effect which was mediated by the effect of obesity on CRP at 45y, was 23.27% (95% CI: 8.64%, 37.90%). Obesity in early-adulthood was associated with over twice the odds of poor PF in mid-life, with approximately 23% of the obesity effect operating via a downstream effect on CRP. As current younger generations are likely to spend greater proportions of their life course in older age and with obesity, both of which are associated with poor PF, there is an urgent need to identify mechanisms, and thus potential modifiable intermediaries, linking obesity to poor PF.
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影响因子：
5.8
作者：
Bochud, Murielle;Marquant, Fabienne;Rousson, Valentin
通讯作者：
Rousson, Valentin
影响因子：
5.5
作者：
FRIED, LP;BUSH, TL
通讯作者：
BUSH, TL
DOI：
10.1093/gerona/gln038
发表时间：
2009-04-01
影响因子：
5.1
作者：
Brinkley, Tina E.;Leng, Xiaoyan;Nicklas, Barbara J.
通讯作者：
Nicklas, Barbara J.
DOI：
10.1111/j.1532-5415.1997.tb00986.x
发表时间：
1997-01-01
影响因子：
6.3
作者：
Fried, LP;Guralnik, JM
通讯作者：
Guralnik, JM
影响因子：
4.9
作者：
Aronson, D;Bartha, P;Levy, Y
通讯作者：
Levy, Y