孟德尔随机化
结直肠癌
肿瘤科
癌症
医学
内科学
因果关系(物理学)
生理学
生物
遗传学
基因
基因型
遗传变异
量子力学
物理
作者
Tian Xie,Juntao Ni,Tao Lin,Tian Xie
出处
期刊:PLOS ONE
[Public Library of Science]
日期:2022-08-22
卷期号:17 (8): e0273452-e0273452
被引量:5
标识
DOI:10.1371/journal.pone.0273452
摘要
Purpose We conducted a bidirectional two-sample Mendelian randomization (MR) study to determine whether genetically predicted basal metabolic rate (BMR) was a causal risk factor for colorectal cancer (CRC) or whether a genetically predicted CRC risk can influence the BMR level (i.e., reverse causation). Methods We employed 1,040 genetic variants as proxies for BMR to obtain effect estimates on CRC risk. Another 58 CRC-associated variants were used to estimate effects on BMR levels. Stratified analysis by tumor site was used to examine the causal associations between BMR and colon/rectal cancer risk. Results The inverse variance weighted (IVW) method indicated a significant causal effect of genetically determined BMR on CRC risk (OR SD = 1.27, 95% CI = 1.07–1.51). No significant reverse causal association was identified between genetically increased CRC risk and BMR levels [IVW ( β = 0, 95% CI = -0.01 to 0)]. The results of MR-Egger and the weighted median method were consistent with the IVW method. Stratified analysis by CRC sites identified significant causal associations between BMR and colon cancer [IVW (OR SD = 1.45, 95% CI = 1.16-1-80)], and null evidence of a causal association between BMR and rectal cancer risk was found ( p > 0.05). Conclusion Our findings add to the current literature by validating a positive relationship between high BMR levels and CRC risk instead of reverse causality. The genetically predicted BMR level was causally associated with colon cancer risk but not rectal cancer risk.
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