Department of Cardiology, Second Affiliated Hospital of Harbin Medical University, Harbin, China; The Key Laboratory of Myocardial Ischemia, Chinese Ministry of Education, China; State Key Laboratory of Frigid Zone Cardiovascular Diseases (SKLFZCD), Harbin, China; Department of Epidemiology and Biostatistics, School of Public Health, Jiamusi University, Jiamusi, China.
Department of Cardiology, Second Affiliated Hospital of Harbin Medical University, Harbin, China; The Key Laboratory of Myocardial Ischemia, Chinese Ministry of Education, China; State Key Laboratory of Frigid Zone Cardiovascular Diseases (SKLFZCD), Harbin, China.
Diabetes Metab Syndr. 2024 Jun;18(6):103050. doi: 10.1016/j.dsx.2024.103050. Epub 2024 May 31.
We aimed to investigate the associations of diabetes mellitus (DM) and C-reactive protein (CRP) with biological ageing acceleration and mortality risk.
We analyzed data from 41,634 adults with CRP and DM at baseline. Subjects were categorized into high CRP (>3 mg/L) and low CRP (≤3 mg/L) groups. The cross-sectional endpoints of the study were biological ageing indicators Klemera-Doubal method BioAge acceleration (KDMAccel) and Phenotypic age acceleration (PhenoAgeAccel), and the follow-up endpoints were all-cause mortality and cardiovascular mortality.
In adults with high CRP, compared with those without DM, PhenoAgeAccel increased by 1.66 years (95 % CI: 1.38-1.93), and 8.74 years (95 % CI: 8.25-9.22) in adults with prediabetes and DM, respectively (p for interaction <0.001). Using the CRP/non-DM group as a reference, adults in the CRP/non-DM, CRP/DM, and CRP/DM groups had significantly advanced biological ageing. Compared to adults without DM, low CRP, and no ageing acceleration, the multivariable-adjusted HRs (95%CIs) of all-cause and cardiovascular mortality in those with DM, CRP, and ageing acceleration were 3.22 (2.79-3.72), and 3.57 (2.81-4.54), respectively.
These findings suggest that the joint presence of low-grade inflammation and DM might be associated with higher odds of biological ageing acceleration and premature mortality.
本研究旨在探讨糖尿病（DM）和 C 反应蛋白（CRP）与生物年龄加速和死亡风险的相关性。
我们分析了基线时 CRP 和 DM 并存的 41634 名成年人的数据。受试者分为高 CRP（>3mg/L）和低 CRP（≤3mg/L）组。研究的横断面终点为生物年龄加速的 Klemera-Doubal 方法生物年龄加速（KDMAccel）和表型年龄加速（PhenoAgeAccel），随访终点为全因死亡率和心血管死亡率。
在高 CRP 的成年人中，与无 DM 者相比，糖尿病前期和 DM 者的 PhenoAgeAccel 分别增加了 1.66 岁（95%CI：1.38-1.93）和 8.74 岁（95%CI：8.25-9.22）（交互作用 p<0.001）。以 CRP/非 DM 组为参照，CRP/非 DM、CRP/DM 和 CRP/DM 组的成年人生物年龄明显提前。与无 DM、低 CRP 和无年龄加速的成年人相比，DM、CRP 和年龄加速的成年人全因和心血管死亡率的多变量调整 HR（95%CI）分别为 3.22（2.79-3.72）和 3.57（2.81-4.54）。
这些发现表明，低度炎症和 DM 的共同存在可能与更高的生物年龄加速和过早死亡风险相关。
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