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Updated: May 28, 2025

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植物性饮食模式,遗传风险,蛋白质组和肺癌风险:一项大型前性队列研究
Wenmin Zhu1,2, Ziwei Shi1,2, Xiaolong Yan1,2
1School of Public Health and Emergency Management, Southern University of Science and Technology, Shenzhen, 518055, Guangdong, China.
European journal of nutrition
|February 11, 2025
概括
较高的植物性饮食 (PDI) 与较低的肺癌风险有关,而不健康的植物性饮食 (uPDI) 增加了风险. 遗传倾向与不良的植物性饮食相结合,显著提高了肺癌的风险.
科学领域:
- 营养流行病学 营养流行病学
- 在瘤学瘤学.
- 遗传学 遗传学 是一个
背景情况:
- 肺癌仍然是全球癌症相关死亡的主要原因.
- 饮食模式,特别是植物性饮食 (PDI),越来越多地被认为对预防癌症的潜在作用.
- 通过多基因风险评分 (PRS) 评估的遗传倾向是包括肺癌在内的各种癌症的已知风险因素.
研究的目的:
- 研究植物性饮食模式 (总体PDI,健康的hPDI和不健康的UPDI) 与肺癌风险之间的关联.
- 检查植物性饮食模式和遗传风险 (PRS) 对肺癌发病率的综合影响.
- 为了确定特定的蛋白质,调解植物性饮食和肺癌风险之间的关系.
主要方法:
- 分析了来自英国生物银行189541名参与者的数据.
- 利用考克斯的比例危险模型和受限制的立方线来评估饮食与肺癌的关联.
- 构建了一个多基因风险评分 (PRS) 并使用调解分析来探索蛋白质参与.
主要成果:
- 总体较高的PDI与肺癌风险降低有关 (HR:每SD0.90).
- 升高的不健康的PDI (uPDI) 与增加的肺癌风险显著相关 (HR:每SD1.08).
- 高PRS和低PDI或高UPDI的组合显著增加了肺癌风险 (HR:分别为2.09和1.86).
- 42种蛋白质调解了PDI-肺癌关联,而117种蛋白质调解了UPDI-肺癌关联,其中细胞因子-细胞因子受体相互作用是显著的途径.
结论:
- 植物性饮食模式显示了与肺癌风险的剂量反应关系,较高的整体PDI是保护性的,较高的UPDI是有害的.
- 具有高遗传风险和低于最佳的植物性饮食的人面临肺癌的风险大幅增加.
- 参与细胞因子-细胞因子受体相互作用的蛋白质可能在调解植物性饮食和肺癌之间的联系方面发挥关键作用.
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