BMI and all cause mortality: systematic review and non-linear dose-response meta-analysis of 230 cohort studies with 3.74 million deaths among 30.3 million participants.
BMI and all cause mortality: systematic review and non-linear dose-response meta-analysis of 230 cohort studies with 3.74 million deaths among 30.3 million participants.
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DOI：
10.1136/bmj.i2156
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发表时间：
2016-05-04
期刊：
影响因子：
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通讯作者：
Vatten LJ
中科院分区：
文献类型：
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作者：
Aune D;Sen A;Prasad M;Norat T;Janszky I;Tonstad S;Romundstad P;Vatten LJ
目的对体质指数（BMI）与全因死亡风险的队列研究进行系统回顾和荟萃分析，阐明剂量-反应曲线的形状和最低点，以及吸烟、疾病相关体重减轻和临床前疾病等混杂因素对结果的影响。数据来源PubMed和Embase数据库检索截止到2015年9月23日。研究选择：报告了至少三类BMI与全因死亡率相关的调整风险估计的队列研究。采用随机效应模型计算总结相对风险。用分数阶多项式模型探讨非线性关联。结果纳入230项队列研究（207篇出版物）。对从不吸烟者的分析包括53项队列研究（44项风险估计），其中有1738144例死亡和997677例参与者。对所有参与者的分析包括228项队列研究（198项风险估计），30233329名参与者中有303744722人死亡。BMI增加5个单位的总相对危险度在从不吸烟者中为1.18(95%可信区间1.15 ~ 1.21;I2=95%, n=44)，在健康从不吸烟者中为1.21 (1.18 ~ 1.25;I2=93%, n=25)，在排除早期随访的健康从不吸烟者中为1.27 (1.21 ~ 1.33;I2=89%, n=11)，在所有参与者中为1.05 （1.04 ~ 1.07;I2=97%, n=198）。不吸烟者呈J型剂量-反应关系（p非线性<0.001），不吸烟者BMI为23-24时风险最低，健康不吸烟者为22-23，不吸烟者随访≥20年为20-22时风险最低。相比之下，在具有较大偏倚可能性的分析中（包括所有参与者，当前吸烟者、曾经吸烟者或曾经吸烟者），以及在随访时间较短（<5年或<10年）或研究质量评分中等的研究中，BMI和死亡率之间呈U形关联。结论超重和肥胖与全因死亡风险增加有关，不吸烟者BMI指数在23-24处，健康不吸烟者BMI指数在22-23处，随访时间较长的BMI指数在20-22处出现曲线最低点。在体重过轻的人群中观察到的死亡风险增加至少部分可能是由诊断前疾病的残留混淆引起的。缺乏对曾经吸烟者、患有流行疾病和临床前疾病的人以及早期随访的排除，可能使结果更偏向于U形关联。
Objective To conduct a systematic review and meta-analysis of cohort studies of body mass index (BMI) and the risk of all cause mortality, and to clarify the shape and the nadir of the dose-response curve, and the influence on the results of confounding from smoking, weight loss associated with disease, and preclinical disease. Data sources PubMed and Embase databases searched up to 23 September 2015. Study selection Cohort studies that reported adjusted risk estimates for at least three categories of BMI in relation to all cause mortality. Data synthesis Summary relative risks were calculated with random effects models. Non-linear associations were explored with fractional polynomial models. Results 230 cohort studies (207 publications) were included. The analysis of never smokers included 53 cohort studies (44 risk estimates) with >738 144 deaths and >9 976 077 participants. The analysis of all participants included 228 cohort studies (198 risk estimates) with >3 744 722 deaths among 30 233 329 participants. The summary relative risk for a 5 unit increment in BMI was 1.18 (95% confidence interval 1.15 to 1.21; I2=95%, n=44) among never smokers, 1.21 (1.18 to 1.25; I2=93%, n=25) among healthy never smokers, 1.27 (1.21 to 1.33; I2=89%, n=11) among healthy never smokers with exclusion of early follow-up, and 1.05 (1.04 to 1.07; I2=97%, n=198) among all participants. There was a J shaped dose-response relation in never smokers (Pnon-linearity <0.001), and the lowest risk was observed at BMI 23-24 in never smokers, 22-23 in healthy never smokers, and 20-22 in studies of never smokers with ≥20 years’ follow-up. In contrast there was a U shaped association between BMI and mortality in analyses with a greater potential for bias including all participants, current, former, or ever smokers, and in studies with a short duration of follow-up (<5 years or <10 years), or with moderate study quality scores. Conclusion Overweight and obesity is associated with increased risk of all cause mortality and the nadir of the curve was observed at BMI 23-24 among never smokers, 22-23 among healthy never smokers, and 20-22 with longer durations of follow-up. The increased risk of mortality observed in underweight people could at least partly be caused by residual confounding from prediagnostic disease. Lack of exclusion of ever smokers, people with prevalent and preclinical disease, and early follow-up could bias the results towards a more U shaped association.