Accelerated aging: A marker for social factors resulting in cardiovascular events?

Accelerated aging: A marker for social factors resulting in cardiovascular events?
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加速老化:社会因素导致心血管事件的标志?

DOI:
10.1016/j.ssmph.2021.100733
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发表时间:
2021-03
期刊:
SSM - population health
影响因子:
--
通讯作者:
Kiefe CI
Kiefe CI
中科院分区:
其他
文献类型:
--
作者:
Forrester SN;Zmora R;Schreiner PJ;Jacobs DR Jr;Roger VL;Thorpe RJ Jr;Kiefe CI

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医学和公共卫生正在从纯粹的“个人责任”心血管疾病(CVD)预防模式转向针对社会和环境条件以及这些条件如何导致疾病的社会观点。鉴于社会条件和CVD结果之间的强相关性,我们假设加速老化,通过生物标志物的组合测量与时间老化相关的早期健康下降,可能是社会条件和CVD之间的关联的标志物。我们使用的数据来自年轻人冠状动脉风险发展研究(CARDIA)。加速老化定义为生物学年龄和实际年龄之间的差异。生物学年龄由7种生物标志物(总胆固醇、HDL、葡萄糖、BMI、CRP、FEV 1/h2、MAP)的组合得出,代表通常与实足衰老相关的“磨损”的生理效应。我们研究了2005-06年测量的加速老化,作为2000-01年测量的社会因素与1)任何意外CVD事件; 2)中风; 3)2007年至2018年发生的全因死亡率之间关联的中介。在2978名中年参与者中,平均(SD)加速老化为3.6(11.6)年,即,CARDIA组平均比实际年龄大3岁。加速老化部分介导了社会因素与CVD(N=219)、卒中(N=36)和死亡率(N=59)之间的相关性。在调整协变量后,加速老化介导了种族歧视对中风总影响的41%。加速老化也介导了其他关系,但程度较低。我们提供了新的证据,表明基于易于测量的生物标志物的加速衰老可能是一个可行的标志物,可以部分解释社会因素如何导致心血管疾病和死亡。加速老化与心理社会压力和心血管疾病之间的中介一致。加速老化介导种族歧视和中风之间的关联。加速老化可能是研究健康差异的一个候选机制。
Medicine and public health are shifting away from a purely “personal responsibility” model of cardiovascular disease (CVD) prevention towards a societal view targeting social and environmental conditions and how these result in disease. Given the strong association between social conditions and CVD outcomes, we hypothesize that accelerated aging, measuring earlier health decline associated with chronological aging through a combination of biomarkers, may be a marker for the association between social conditions and CVD. We used data from the Coronary Artery Risk Development in Young Adults study (CARDIA). Accelerated aging was defined as the difference between biological and chronological age. Biological age was derived as a combination of 7 biomarkers (total cholesterol, HDL, glucose, BMI, CRP, FEV1/h2, MAP), representing the physiological effect of “wear and tear” usually associated with chronological aging. We studied accelerated aging measured in 2005-06 as a mediator of the association between social factors measured in 2000-01 and 1) any incident CVD event; 2) stroke; and 3) all-cause mortality occurring from 2007 through 18. Among 2978 middle-aged participants, mean (SD) accelerated aging was 3.6 (11.6) years, i.e., the CARDIA cohort appeared to be, on average, 3 years older than its chronological age. Accelerated aging partially mediated the association between social factors and CVD (N=219), stroke (N=36), and mortality (N=59). Accelerated aging mediated 41% of the total effects of racial discrimination on stroke after adjustment for covariates. Accelerated aging also mediated other relationships but to lesser degrees. We provide new evidence that accelerated aging based on easily measurable biomarkers may be a viable marker to partially explain how social factors can lead to cardiovascular outcomes and death. Accelerated aging is consistent with a mediator between psychosocial stress and CVD. Accelerated aging mediates the association between racial discrimination and stroke. Accelerated aging may be a candidate mechanism for studying health disparities.
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