DataSheet_2_The causal relationship between sarcopenic obesity factors and benign prostate hyperplasia.pdf

BackgroundBoth benign prostatic hyperplasia (BPH) and sarcopenic obesity (SO) are common conditions among older adult/adults males. The prevalent lifestyle associated with SO is a significant risk factor for the development of BPH. Therefore, we investigated the causal relationship between SO factors and BPH.
MethodThe instrumental variables for SO factors were selected using the inverse variance-weighted method, which served as the primary approach for Mendelian randomization analysis to assess the causal effect based on summary data derived from genome-wide association studies of BPH.
ResultThe increase in BMR (OR = 1.248; 95% CI = (1.087, 1.432); P = 0.002) and ALM (OR = 1.126; 95% CI = (1.032, 1.228); P = 0.008) was found to be associated with an elevated risk of BPH. However, no genetic causality between fat-free mass distribution, muscle mass distribution, and BPH was observed.
ConclusionOur findings indicate that a genetic causal association between BMR, ALM and BPH. BMR and ALM are risk factors for BPH. The decrease in BMR and ALM signified the onset and progression of SO, thus SO is a protective factor for BPH.

背景 良性前列腺增生（benign prostatic hyperplasia, BPH）与肌少症性肥胖（sarcopenic obesity, SO）均为老年男性群体中的常见疾病。与肌少症性肥胖相关的普遍生活方式是良性前列腺增生发病的重要危险因素。因此，本研究探讨了肌少症性肥胖相关因素与良性前列腺增生之间的因果关联。
方法 本研究采用逆方差加权法筛选肌少症性肥胖相关因素的工具变量，以此作为孟德尔随机化（Mendelian randomization）分析的核心方法，基于良性前列腺增生全基因组关联研究的汇总数据评估其因果效应。
结果 基础代谢率（basal metabolic rate, BMR）升高（比值比OR=1.248；95%置信区间CI=(1.087, 1.432)；P=0.002）与四肢肌肉量（appendicular lean mass, ALM）增加（OR=1.126；95%CI=(1.032, 1.228)；P=0.008）均与良性前列腺增生的发病风险升高显著相关。但未观察到去脂体重分布、肌肉量分布与良性前列腺增生之间存在遗传因果关联。
结论 本研究结果显示，基础代谢率、四肢肌肉量与良性前列腺增生之间存在遗传因果关联。基础代谢率与四肢肌肉量均为良性前列腺增生的危险因素。而基础代谢率与四肢肌肉量的降低提示肌少症性肥胖的发生与进展，因此肌少症性肥胖是良性前列腺增生的保护因素。