关键词: Mendelian randomization biological aging causal relationship meat consumption processed meat red meat white meat

Mesh : Mendelian Randomization Analysis Humans Aging / genetics Meat DNA Methylation Animals DNA, Mitochondrial / genetics Phenotype Sheep Diet / adverse effects Causality Red Meat / adverse effects

来  源:   DOI:10.3390/nu16152433   PDF(Pubmed)

Abstract:
Existing research indicates that different types of meat have varying effects on health and aging, but the specific causal relationships remain unclear. This study aimed to explore the causal relationship between different types of meat intake and aging-related phenotypes. This study employed Mendelian randomization (MR) to select genetic variants associated with meat intake from large genomic databases, ensuring the independence and pleiotropy-free nature of these instrumental variables (IVs), and calculated the F-statistic to evaluate the strength of the IVs. The validity of causal estimates was assessed through sensitivity analyses and various MR methods (MR-Egger, weighted median, inverse-variance weighted (IVW), simple mode, and weighted mode), with the MR-Egger regression intercept used to test for pleiotropy bias and Cochran\'s Q test employed to evaluate the heterogeneity of the results. The findings reveal a positive causal relationship between meat consumers and DNA methylation PhenoAge acceleration, suggesting that increased meat intake may accelerate the biological aging process. Specifically, lamb intake is found to have a positive causal effect on mitochondrial DNA copy number, while processed meat consumption shows a negative causal effect on telomere length. No significant causal relationships were observed for other types of meat intake. This study highlights the significant impact that processing and cooking methods have on meat\'s role in health and aging, enhancing our understanding of how specific types of meat and their preparation affect the aging process, providing a theoretical basis for dietary strategies aimed at delaying aging and enhancing quality of life.
摘要:
现有研究表明,不同类型的肉类对健康和衰老有不同的影响,但具体的因果关系尚不清楚.本研究旨在探讨不同肉类摄入量与衰老相关表型之间的因果关系。本研究采用孟德尔随机化(MR)从大型基因组数据库中选择与肉类摄入相关的遗传变异,确保这些工具变量(IV)的独立性和多效性,并计算F统计量以评估IVs的强度。通过敏感性分析和各种MR方法(MR-Egger,加权中位数,逆方差加权(IVW),简单模式,和加权模式),MR-Egger回归截距用于测试多效性偏差,Cochran'sQ检验用于评估结果的异质性。研究结果揭示了肉类消费者与DNA甲基化PhenoAge加速之间的正因果关系,这表明增加肉类摄入量可能会加速生物衰老过程。具体来说,发现羔羊的摄入量对线粒体DNA拷贝数有积极的因果关系,而加工肉类消费对端粒长度有负面的因果关系。对于其他类型的肉类摄入量,没有观察到显着的因果关系。这项研究强调了加工和烹饪方法对肉类在健康和衰老中的作用的重大影响。加强我们对特定类型的肉类及其制备如何影响老化过程的理解,为旨在延缓衰老和提高生活质量的饮食策略提供理论依据。
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