Table_1_A diet-wide Mendelian randomization analysis: causal effects of dietary habits on type 2 diabetes.docx

BackgroundTraditional clinical studies have indicated a link between certain food intakes and type 2 diabetes (T2D), but the causal relationships between different dietary habits and T2D remain unknown. Using Mendelian randomization (MR) approaches, we investigated the potential causal association between dietary habits and T2D risk.
MethodsWe collected publicly available genome-wide association studies’ summary statistics for 18 dietary habits from the UK Biobank and T2D data from the DIAbetes Genetics Replication And Meta-analysis (DIAGRAM) consortium. We applied the inverse variance weighted (IVW) method, supplemented with the MR-Egger method, weighted median method (WMM), simple method, weighted mode, MR-Egger regression, and the MR pleiotropy residual sum and outlier test to determine whether a particular diet was causal for T2D.
ResultsReliable and robust MR estimates demonstrated that poultry intake has a causal effect on a higher risk of T2D (IVW: OR 6.30, 95% CI 3.573–11.11, p = 2.02e − 10; WMM: OR 5.479, 95% CI 0.2758–10.88, p = 1.19e − 06). Conversely, dried fruit intake (IVW: OR 0.380, 95% CI 0.237–0.608, p = 5.57e − 05; WMM: OR 0.450, 95% CI 0.321–0.630, p = 3.33e − 06) and cereal intake (IVW: OR 0.455, 95% CI 0.317–0.653, p = 1.924e − 05; WMM: OR 0.513, 95% CI 0.379–0.694, p = 1.514e − 05) were causally associated with T2D as protective factors. Sensitivity analyses confirmed the reliability and robustness of these findings.
DiscussionOur study established the causal effects of poultry intake, dried fruit intake, and cereal intake on T2D, identifying poultry intake as a risk factor and the other two as protective factors. Further research into potential mechanisms is required to validate these novel findings.

背景
传统临床研究已表明特定食物摄入与2型糖尿病（type 2 diabetes, T2D）存在关联，但不同饮食习惯与T2D之间的因果关系仍未明确。本研究采用孟德尔随机化（Mendelian randomization, MR）方法，探究饮食习惯与T2D发病风险之间的潜在因果关联。
方法
我们从英国生物库（UK Biobank）获取了18种饮食习惯的全基因组关联研究（genome-wide association studies, GWAS）公开汇总统计数据，并从糖尿病遗传学复制与荟萃分析（DIAbetes Genetics Replication And Meta-analysis, DIAGRAM）联盟获取T2D相关数据。我们采用逆方差加权（inverse variance weighted, IVW）法，并辅以MR-Egger法、加权中位数法（weighted median method, WMM）、简单法、加权众数法、MR-Egger回归以及孟德尔随机化多效性残差和离群值检验，以判定特定饮食是否对T2D存在因果影响。
结果
可靠且稳健的孟德尔随机化估算结果显示，禽类肉摄入会升高T2D发病风险（IVW：OR 6.30，95% CI 3.573–11.11，p=2.02×10^−10；WMM：OR 5.479，95% CI 0.2758–10.88，p=1.19×10^−06）。相反，干果摄入（IVW：OR 0.380，95% CI 0.237–0.608，p=5.57×10^−05；WMM：OR 0.450，95% CI 0.321–0.630，p=3.33×10^−06）与谷类摄入（IVW：OR 0.455，95% CI 0.317–0.653，p=1.924×10^−05；WMM：OR 0.513，95% CI 0.379–0.694，p=1.514×10^−05）对T2D具有保护性因果关联。敏感性分析证实了上述研究结果的可靠性与稳健性。
讨论
本研究明确了禽类肉摄入、干果摄入及谷类摄入对T2D的因果效应，其中禽类肉摄入为T2D的风险因素，其余二者为保护因素。未来需开展进一步研究以阐明其潜在作用机制，验证这些全新研究发现。