体质指数（BMI）是一种容易获得的脂肪性指标。然而，即使BMI相同，不同个体的体成分和脂肪组织分布存在差异，关于与最低死亡风险相关的BMI存在争议。为了评估BMI、脂肪质量指数（FMI）和腰臀比（WHR）与死亡之间的关联性的强度和一致性。本队列研究使用了来自英国生物银行（UKB；2006-2022）的入院死亡数据，该数据包括英国22个临床评估中心的数据。UKB英国白人祖先的参与者（N = 387,672）被分为发现队列（n = 337,078）和验证队列（n = 50,594），后者包含25,297个死亡病例和25,297个对照病例。发现队列被用于计算基因决定脂肪性指标，而验证队列则用于分析。通过观察性和弥散性随机性分析分析了暴露 - 结果之间的关联。BMI、FMI和WHR。全因死亡和特定原因死亡（癌症，心血管疾病[CVD]，呼吸道疾病或其他原因）。观察性分析（平均[标准差]年龄，56.9 [8.0] 岁；177,340 [45.9%]男性，210,332 [54.2%]女性）和弥散性随机性分析（平均[标准差]年龄，61.6 [6.2] 岁；30,031 [59.3%]男性，20,563 [40.6%]女性）分别有387,672和50,594名参与者。测量的BMI和FMI与全因死亡之间存在J形关联，而WHR与全因死亡之间的关联使用风险比（HR）尺度为线性关系（WHR每SD增加HR，1.41 [95%CI，1.38-1.43]）。基因决定的WHR与全因死亡的关联性强于BMI（每SD增加WHR的OR，1.51 [95%CI，1.32-1.72]；每SD增加BMI的OR，1.29 [95%CI，1.20-1.38]；异质性P值=0.02）。这种关联在男性参与者中更强（OR，1.89 [95%CI，1.54-2.32]；异质性P值=0.01）。与BMI或FMI不同，无论观察到的BMI如何，基因决定的WHR与全因死亡的关联性都是一致的。在这个队列研究中，WHR与死亡之间的关联性最强且最一致，与BMI无关。临床建议应考虑将注意力集中在脂肪的分布而不是质量上。

Body mass index (BMI) is an easily obtained adiposity surrogate. However, there is variability in body composition and adipose tissue distribution between individuals with the same BMI, and there is controversy regarding the BMI associated with the lowest mortality risk.To evaluate which of BMI, fat mass index (FMI), and waist-to-hip (WHR) has the strongest and most consistent association with mortality.This cohort study used incident deaths from the UK Biobank (UKB; 2006-2022), which includes data from 22 clinical assessment centers across the United Kingdom. UKB British participants of British White ancestry (N = 387 672) were partitioned into a discovery cohort (n = 337 078) and validation cohort (n = 50 594), with the latter consisting of 25 297 deaths and 25 297 controls. The discovery cohort was used to derive genetically determined adiposity measures while the validation cohort was used for analyses. Exposure-outcome associations were analyzed through observational and mendelian randomization (MR) analyses.BMI, FMI, and WHR.All-cause and cause-specific (cancer, cardiovascular disease [CVD], respiratory disease, or other causes) mortality.There were 387 672 and 50 594 participants in our observational (mean [SD] age, 56.9 [8.0] years; 177 340 [45.9%] male, 210 332 [54.2%], female), and MR (mean [SD] age, 61.6 [6.2] years; 30 031 [59.3%] male, 20 563 [40.6%], female) analyses, respectively. Associations between measured BMI and FMI with all-cause mortality were J-shaped, whereas the association of WHR with all-cause mortality was linear using the hazard ratio (HR) scale (HR per SD increase of WHR, 1.41 [95% CI, 1.38-1.43]). Genetically determined WHR had a stronger association with all-cause mortality than BMI (odds ratio [OR] per SD increase of WHR, 1.51 [95% CI, 1.32-1.72]; OR per SD increase of BMI, 1.29 [95% CI, 1.20-1.38]; P for heterogeneity = .02). This association was stronger in male than female participants (OR, 1.89 [95% CI, 1.54-2.32]; P for heterogeneity = .01). Unlike BMI or FMI, the genetically determined WHR-all-cause mortality association was consistent irrespective of observed BMI.In this cohort study, WHR had the strongest and most consistent association with mortality irrespective of BMI. Clinical recommendations should consider focusing on adiposity distribution compared with mass.