Luo Pei, Huang Can
Department of Thoracic Surgery, Tangdu Hospital, Air Force Medical University, Xi'an, Shaanxi, China.
Department of Cardiovascular Surgery, Peking University Shenzhen Hospital, Shenzhen, China.
Front Nutr. 2024 Oct 2;11:1375179. doi: 10.3389/fnut.2024.1375179. eCollection 2024.
Previous research has established a connection between Type 2 Diabetes Mellitus (T2DM), glycemic traits, dietary habits, and the risk of Pressure Ulcers (PUs). The aim of our study is to disentangle any potential causal relationship between T2DM, glycemic traits, and dietary factors, and the risk of PUs.
The exposure and outcome datasets were sourced from the IEU Open GWAS project, the Meta-Analyses of Glucose and Insulin-related traits Consortium (MAGIC), and the FinnGen biobank, respectively. The primary MR analysis method employed was the inverse variance-weighted method. Furthermore, we employed multivariable MR (MVMR) adjusting for BMI. Then, we investigated the possibility of a reverse association between glycemic traits and PUs through bidirectional MR. Finally, Heterogeneity and pleiotropic analysis were conducted to ensure the accuracy and robustness of the results.
The findings revealed that T2DM (OR = 1.282, 95% CI: 1.138-1.445, < 0.001) and Fasting Glucose (FG; OR = 2.111, 95% CI: 1.080-4.129, = 0.029) were associated with an increased risk of PUs, while salad/raw vegetable intake (OR: 0.014; 95% CI: 0.001-0.278; = 0.005) was identified as a protective element. However, no other dietary elements demonstrated a statistically significant causality with PUs. In addition, in the reverse direction, there were positive correlation between genetic susceptibility to PUs and an increase in FG (OR: 1.007, 95% CI: 1.000-1.013, = 0.048) and Fasting Insulin (FI; OR: 1.012, 95% CI: 1.003-1.022, = 0.011). MVMR results indicated that the causal effect of T2DM on PUs was independent of BMI (OR: 1.260, 95% CI: 1.112-1.427, < 0.001). These results remained robust when considering weak instrument bias, pleiotropy, and heterogeneity.
This study establishes a causal link between genetically predicted T2DM, FG and an increased risk of PUs. Conversely, Salad/raw vegetable intake is significantly inversely associated with PUs. Simultaneously, we identified two downstream effector factor (FG and FI) that were associated with PUs. These findings may have clinical implications for both prevention and treatment.
先前的研究已经建立了2型糖尿病（T2DM）、血糖特征、饮食习惯与压疮（PU）风险之间的联系。我们研究的目的是理清T2DM、血糖特征和饮食因素与PU风险之间任何潜在的因果关系。
暴露和结果数据集分别来自IEU开放全基因组关联研究项目、葡萄糖和胰岛素相关特征联盟的荟萃分析（MAGIC）以及芬兰生物银行。采用的主要孟德尔随机化（MR）分析方法是逆方差加权法。此外，我们采用多变量MR（MVMR）并对体重指数（BMI）进行了调整。然后，我们通过双向MR研究了血糖特征与PU之间反向关联的可能性。最后，进行了异质性和多效性分析，以确保结果的准确性和稳健性。
研究结果显示，T2DM（优势比[OR]=1.282，95%置信区间[CI]：1.138 - 1.445，P<0.001）和空腹血糖（FG；OR = 2.111，95% CI：1.080 - 4.129，P = 0.029）与PU风险增加相关，而沙拉/生蔬菜摄入量（OR：0.014；95% CI：0.001 - 0.278；P = 0.005）被确定为一个保护因素。然而，没有其他饮食因素显示与PU存在统计学上显著的因果关系。此外，在反向分析中，PU的遗传易感性与FG升高（OR：1.007，95% CI：1.000 - 1.013，P = 0.048）和空腹胰岛素（FI；OR：1.012，95% CI：1.003 - 1.022，P = 0.011）之间存在正相关。MVMR结果表明，T2DM对PU的因果效应独立于BMI（OR：1.260，95% CI：1.112 - 1.427，P<0.001）。在考虑弱工具变量偏差、多效性和异质性时，这些结果仍然稳健。
本研究建立了基因预测的T2DM、FG与PU风险增加之间的因果联系。相反，沙拉/生蔬菜摄入量与PU显著负相关。同时，我们确定了两个与PU相关的下游效应因子（FG和FI）。这些发现可能对预防和治疗都具有临床意义。
