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加快的生物衰老和炎症性肠病风险:对401013名参与者的前性研究
Baolong Cao1, Xiaoke Zhao1, Zhixi Lu2
1Department of Rehabilitation, Children's Hospital of Nanjing Medical University, Guangzhou Road #72, Nanjing 210008, China.
The journal of nutrition, health & aging
|February 14, 2025
概括
通过PhenoAge测量的加速生物衰老显著增加了炎症性肠病 (IBD) 的风险,特别是当与高遗传倾向相结合时. 识别加速衰老的个体可以帮助降低IBD风险.
科学领域:
- 老年学是一门学科.
- 胃肠病学 胃肠病学
- 遗传学 遗传学 是一个
背景情况:
- 生物衰老与炎症性肠病 (IBD) 之间的关系尚不清楚.
- IBD包括克罗恩病 (CD) 和性结肠炎 (UC),以及消化道的慢性炎症状况.
研究的目的:
- 研究生物年龄和遗传倾向与IBD风险之间的关联.
- 评估生物年龄和IBD发展遗传风险的预测能力.
主要方法:
- 使用PhenoAge评估生物年龄,并通过多基因风险评分 (PRS) 量化遗传倾向.
- 考克斯比例危险模型用于计算IBD,UC和CD的危险比率 (HR) 和95%置信区间 (CI).
- 研究了添加性相互作用,以评估PhenoAge和PRS的联合作用.
主要成果:
- PhenoAge的加速与IBD,UC和CD的风险增加显著相关.
- 每一个标准偏差加快PhenoAge的增加都与38%的IBD风险增加有关.
- 高PRS和加速PhenoAge的个体表现出UC和CD的最高风险,HR分别为9.16和7.72.
- 结合PhenoAge和PRS提高了IBD预测的准确性,C统计达到UC的0.71和CD的0.72.
结论:
- 加快的生物衰老是发展IBD的一个重要风险因素.
- 加速衰老和高遗传倾向的综合效应大大提高了IBD风险.
- 识别加速生物衰老的个体对于有针对性的IBD风险降低策略至关重要.
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