BMI与癌症的风险性相关,具有大规模人群水平的效应。各种癌症之间效应的异质性提示不同的机制与不同的肿瘤部位和不同人群亚组有关。

—2014年8月30日《柳叶刀》


中文翻译


 

题目】身体质量指数与罹患22种癌症的风险:一项基于524万英国成年人人群的队列研究

译文

背景:身体质量指数 (BMI)数值高的人易患多种特定部位的癌症,但是在所有常见癌症中,尚无对多种可能混杂因素进行调整后,得出大规模系统而详细的风险模式特征。我们的目的是研究BMI和绝大多数特定部位的癌症之间的关联。

方法:我们从临床实践研究数据链BMI数据中获取个人的原始健康数据,拟合Cox模型并调整可能的混杂因素,以研究BMI22种最常见的癌症之间的关联。我们先拟合线性模型,之后又拟合了非线性模型,观察了性别、绝经情况、吸烟史和年龄的修饰效应,并估算了群体效应。

结果:研究纳入524万人,其中166 955人发生所研究的癌症。BMI22种癌症中的17种有关,但是根据发生癌症的部位不同,其效应明显不同。粗略的线性相关分析显示,BMI每增加5 kg/m2与子宫 (危险比 [HR] 1·62, 99% CI 1·56—1·69; p<0·0001),胆囊(1·31, 1·12—1·52; p<0·0001), 肾 (1·25, 1·17—1·33; p<0·0001),宫颈 (1·10, 1·03—1·17; p=0·00035),甲状腺 (1·09, 1·00—1·19; p=0·0088)发生癌症以及白血病 (1·09, 1·05—1·13; p≤0·0001)的风险均相关。在总人群中,BMI与肝癌(1·19, 1·12—1·27), 结肠癌 (1·10, 1·07—1·13), 卵巢癌 (1·09, 1.04—1.14)和绝经后发生乳腺癌(1·05, 1·03—1·07)呈正相关(全部p<0·0001),但是这些效应随基础BMI值和个体水平的特点而存在差异。我们发现在总人群和从无吸烟史的人群中,BMI与前列腺癌和绝经后乳腺癌风险均呈负相关(总人群:前列腺癌 0·98, 0·95—1·00;绝经后乳腺癌0·89, 0·86—0·92;无吸烟史人群:前列腺癌 0·96, 0·93—0·99;绝经后乳腺癌 0·89, 0·85—0·94)。相比之下,在从无吸烟史的人群中,我们没有发现肺癌和口腔癌与BMI之间有相关性。这种总体相反的相关性是由正在吸烟的人和已戒烟的人所致,可能是因为存在吸烟量所致的混杂因素。41%的子宫癌,大于10%的胆囊癌、肾癌、肝癌和结肠癌可归因为超重。我们发现人群中BMI每增加1 kg/m2,可导致英国每年新增3790个癌症病人,这些病人会罹患与BMI呈正相关的10种癌症中的1种。

说明:BMI与癌症的风险性相关,具有大规模人群水平的效应。各种癌症之间效应的异质性提示不同的机制与不同的肿瘤部位和不同人群亚组有关。

 

英文原稿


 

[Title]

Body-mass index and risk of 22 specific cancers: a population-based cohort study of 5·24 million UK adults.

[Authors]

Bhaskaran K, Douglas I, Forbes H, Dos-Santos-Silva I, Leon DA, Smeeth L.

[Abstract]

Background: High body-mass index (BMI) predisposes to several site-specific cancers, but a large-scale
systematic and detailed characterisation of patterns of risk across all common cancers adjusted
for potential confounders has not previously been undertaken. We aimed to investigate the links
between BMI and the most common site-specific cancers.

Methods: With primary care data from individuals in the Clinical Practice Research Datalink with BMI data,
we fitted Cox models to investigate associations between BMI and 22 of the most common cancers,
adjusting for potential confounders. We fitted linear then non-linear (spline) models; investigated effect
modification by sex, menopausal status, smoking, and age; and calculated population effects.

Findings: 5·24 million individuals were included; 166 955 developed cancers of interest. BMI was associated
with 17 of 22 cancers, but effects varied substantially by site. Each 5 kg/m2 increase in BMI was roughly
linearly associated with cancers of the uterus (hazard ratio [HR] 1·62, 99% CI 1·56—1·69; p<0·0001),
gallbladder (1·31, 1·12—1·52; p<0·0001), kidney (1·25, 1·17—1·33; p<0·0001), cervix
(1·10, 1·03—1·17; p=0·00035), thyroid (1·09, 1·00—1·19; p=0·0088), and leukaemia (1·09, 1·05—
1·13; p≤0·0001). BMI was positively associated with liver (1·19, 1·12—1·27), colon (1·10, 1·07—1·13),
ovarian (1·09, 1.04—1.14), and postmenopausal breast cancers (1·05, 1·03—1·07) overall (all p<0·0001),
but these effects varied by underlying BMI or individual-level characteristics. We estimated inverse associations
with prostate and premenopausal breast cancer risk, both overall (prostate 0·98, 0·95—1·00; premenopausal
breast cancer 0·89, 0·86—0·92) and in never-smokers (prostate 0·96, 0·93—0·99; premenopausal breast
cancer 0·89, 0·85—0·94). By contrast, for lung and oral cavity cancer, we observed no association in never
smokers (lung 0·99, 0·93—1·05; oral cavity 1·07, 0·91—1·26): inverse associations overall were driven by
current smokers and ex-smokers, probably because of residual confounding by smoking amount. Assuming
causality, 41% of uterine and 10% or more of gallbladder, kidney, liver, and colon cancers could be attributable
to excess weight. We estimated that a 1 kg/m2 population-wide increase in BMI would result in 3790 additional annual
UK patients developing one of the ten cancers positively associated with BMI.

Interpretation

BMI is associated with cancer risk, with substantial population-level effects. The heterogeneity in the effects suggests that different
mechanisms are associated with different cancer sites and different patient subgroups.

原文地址

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(14)60892-8/abstract

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