PDF(Pubmed)
Abstract：
UNASSIGNED: The causality between frailty and gestational diabetes mellitus (GDM) has not yet been fully explored. A potential bidirectional causality was also needed to be confirmed.
UNASSIGNED: A bidirectional two-sample Mendelian randomization (MR) was conducted, with frailty-related data was collected from UK Biobank and TwinGen and GDM-related data was collected from the FinnGen consortium. We performed univariable and multivariable-adjusted MR with adjustments for body mass index (BMI). Several methodologies of MR were conducted to confirm the robustness of results.
UNASSIGNED: Frailty was significantly associated with elevated risks of GDM (OR, 3.563; 95% CI, 1.737 to 7.309; P< 0.001) and GDM was also significantly associated with elevated risks of frailty ( β , 0.087; 95% CI, 0.040 to 0.133; P< 0.001). There is no evidence demonstrating the existence of horizontal pleiotropy and heterogeneity. This association was robust after adjustments for BMI. The sensitivity analyses with Weighted median, Maximum likelihood, Penalised weighted median, MR Egger and MR PRESSO methods indicated consistent results.
UNASSIGNED: Our study provides evidence of the bidirectional causal association between frailty and GDM from genetic perspectives, signaling that the identification and assessment of frailty should become a standard strategy during the early stages and care of gestational diabetes.
UNASSIGNED: A bidirectional two-sample Mendelian randomization (MR) was conducted, with frailty-related data was collected from UK Biobank and TwinGen and GDM-related data was collected from the FinnGen consortium. We performed univariable and multivariable-adjusted MR with adjustments for body mass index (BMI). Several methodologies of MR were conducted to confirm the robustness of results.
UNASSIGNED: Frailty was significantly associated with elevated risks of GDM (OR, 3.563; 95% CI, 1.737 to 7.309; P< 0.001) and GDM was also significantly associated with elevated risks of frailty ( β , 0.087; 95% CI, 0.040 to 0.133; P< 0.001). There is no evidence demonstrating the existence of horizontal pleiotropy and heterogeneity. This association was robust after adjustments for BMI. The sensitivity analyses with Weighted median, Maximum likelihood, Penalised weighted median, MR Egger and MR PRESSO methods indicated consistent results.
UNASSIGNED: Our study provides evidence of the bidirectional causal association between frailty and GDM from genetic perspectives, signaling that the identification and assessment of frailty should become a standard strategy during the early stages and care of gestational diabetes.
摘要：
■虚弱与妊娠期糖尿病（GDM）之间的因果关系尚未得到充分探讨。还需要确认潜在的双向因果关系。
■进行了双向双样本孟德尔随机化（MR），与虚弱相关的数据是从英国生物银行和TwinGen收集的，与GDM相关的数据是从FinnGen联盟收集的。我们进行了单变量和多变量调整MR，并调整了体重指数（BMI）。进行了几种MR方法以确认结果的稳健性。
■虚弱与GDM风险升高显著相关(OR，3.563；95%CI，1.737至7.309；P<0.001），GDM也与虚弱风险升高显著相关（β，0.087；95%CI，0.040~0.133；P<0.001）。没有证据表明存在水平多效性和异质性。在调整BMI后，这种关联是稳健的。用加权中位数进行敏感性分析，最大似然,惩罚加权中位数，MREgger和MRPRESSO方法显示出一致的结果。
■我们的研究从遗传角度提供了虚弱与GDM之间双向因果关联的证据。信号表明，在妊娠糖尿病的早期阶段和护理中，对虚弱的识别和评估应成为标准策略。
■进行了双向双样本孟德尔随机化（MR），与虚弱相关的数据是从英国生物银行和TwinGen收集的，与GDM相关的数据是从FinnGen联盟收集的。我们进行了单变量和多变量调整MR，并调整了体重指数（BMI）。进行了几种MR方法以确认结果的稳健性。
■虚弱与GDM风险升高显著相关(OR，3.563；95%CI，1.737至7.309；P<0.001），GDM也与虚弱风险升高显著相关（β，0.087；95%CI，0.040~0.133；P<0.001）。没有证据表明存在水平多效性和异质性。在调整BMI后，这种关联是稳健的。用加权中位数进行敏感性分析，最大似然,惩罚加权中位数，MREgger和MRPRESSO方法显示出一致的结果。
■我们的研究从遗传角度提供了虚弱与GDM之间双向因果关联的证据。信号表明，在妊娠糖尿病的早期阶段和护理中，对虚弱的识别和评估应成为标准策略。
