Cancers attributable to consumption of alcohol in the UK in 2010
Cancers attributable to consumption of alcohol in the UK in 2010
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DOI：
10.1038/bjc.2011.476
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发表时间：
2011-12-06
影响因子：
8.8
通讯作者：
Parkin, D. M.
中科院分区：
文献类型：
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作者：
Parkin, D. M.
表 1 显示了与每天饮酒 1 克酒精相关的风险增加。这些研究中的估计值已针对主要混杂因素（尤其是吸烟）进行了调整。关于乳腺癌，该估计值来自乳腺癌激素因素合作小组（Hamajima 等，2002）对 53 项研究进行的荟萃分析，该分析发现，每日饮酒量每 10 克，患乳腺癌的风险就会增加 7.1%。后续研究中观察到的值并无显着差异。对包含酒精和饮食因素数据的六项队列研究进行的汇总分析发现，随着酒精摄入量的增加，患乳腺癌的风险单调增加；每天增加 10 克酒精的多变量相对风险 (RR) 为 1.09（95% CI 1/4 1.04–1.13；Smith-Warner 等，1998）。 EPIC 研究（Tjønneland 等人，2007 年）发现，近期每天摄入 10 克酒精的风险为 1.03（95% CI 1/4 1.01–1.05），而在百万女性研究中，每天摄入 10 克酒精的风险增加为 12%（Allen 等人，2009 年）。关于结直肠癌，八项队列研究的汇总分析报告显示，每天饮酒 30-45 克酒精的人，风险增加了 16%，具有统计学显着性；每天饮酒 45 克的人，风险显着增加了 41%（Cho 等人，2004 年）。最近的一项队列研究荟萃分析发现，每周饮酒量增加 100 克，患结肠癌或直肠癌的风险会增加 15%（Moskal 等人，2007 年），男性和女性之间没有差异。在 EPIC 研究中（Ferrari 等人，2007 年），效果稍弱一些，研究基线时每摄入 15 克酒精，结直肠癌风险就会增加 9%，直肠癌的风险高于远端结肠癌，而远端结肠癌的风险又高于近端结肠癌的风险。在 WCRF (2007) 报告中，对 8 项结肠癌研究的荟萃分析得出的综合 RR 为每 10 克每天摄入量 1.09 (1.03–1.14)，对 9 项直肠癌研究的荟萃分析得出的 RR 为每 10 克每天摄入量 1.06 (1.01–1.12)。 Cho 等人 (2004) 荟萃分析中的平均值， Moskal 等人 (2007)、EPIC 研究 (Ferrari 等人，2007) 和 WCRF (2007) 对于结肠癌每天每克酒精含量为 0.75%，对于直肠癌每天每克酒精含量为 0.85%。由于这些估计值相似，因此对整个结直肠癌使用每克 0.8% 的全球数字（每天每克增加 0.008%）（表 1）。对于其余癌症，Corrao 等人 (2004) 的荟萃分析用于估计 RR。他们提出了与每天平均摄入 0、25、50 和 100 克酒精相关的相对比。每克酒精摄入量的 RR 是通过假设暴露与风险之间的对数线性关系来估计的，因此：
Table 1 shows the increase in risk associated with consumption of 1g per day of alcohol. The estimates in these studies had been adjusted for major confounders, notably smoking. With respect to breast cancer, the estimate was derived from a meta-analysis of 53 studies, conducted by the Collaborative Group on Hormonal Factors in Breast Cancer (Hamajima et al, 2002), which found that the risk was increased by 7.1% for every 10 g of daily alcoholintake. The values observed in subsequent studies are not substantially different. A pooled analysis of six cohort studies with data on alcohol and dietary factors found that the risk of breast cancer increased monotonically with increasing intake of alcohol; the multivariate relative risk (RR) for a 10-g per day increase in alcohol was 1.09 (95% CI ¼ 1.04–1.13; Smith-Warner et al, 1998). The EPIC study (Tjønneland et al, 2007) found that the risk was 1.03 (95% CI ¼ 1.01–1.05) per 10-g per day recent alcohol intake, whereas in the Million Women Study the increase in risk associated with 10 g per day intake was 12%(Allen et al, 2009). With respect to cancers of the colorectum, a pooled analysis of eight cohort studies reported a borderline statistically significant 16% risk increase for people drinking 30–45g per day of alcohol and a significant 41% risk increase for people drinking X45 g per day (Cho et al, 2004). A more recent meta-analysis of cohort studies found a 15% increase in the risk of colon or rectal cancer for an increase of 100g alcohol intake per week (Moskal et al, 2007), with no difference between men and women. In the EPIC study (Ferrari et al, 2007), the effect was a bit weaker, with alcohol intake at study baseline increasing colorectal cancer risk by 9% per 15 g per day, a risk greater for rectal cancer than for cancer of the distal colon, which in turn was greater than the risk for cancer of the proximal colon. In the WCRF (2007) report, a meta-analysis of eight studies of colon cancer yielded a combined RR of 1.09 (1.03–1.14) per 10g intake per day, and a meta-analysis of nine studies of rectal cancer yielded an RR of 1.06 (1.01–1.12) per 10 g intake per day.The means in the meta-analyses of Cho et al(2004), Moskal et al (2007), the EPIC study (Ferrari et al, 2007) and WCRF (2007) are 0.75% per gram alcohol per day for colon cancer and 0.85% per gram per day for rectal cancer. As these estimates are similar, the global figure of 0.8% per gram (increase of 0.008 per gram per day) was used for colorectal cancer as a whole (Table 1). For the remaining cancers, the meta-analysis of Corrao et al (2004) was used to estimate the RRs. They present RRs associated with a mean intake of 0, 25, 50 and 100 g of alcohol per day. The RR per gram of alcohol intake was estimated by assuming a log–linear relationship between exposure and risk, so that: