Zamora-Ros Raul, Barupal Dinesh K, Rothwell Joseph A, Jenab Mazda, Fedirko Veronika, Romieu Isabelle, Aleksandrova Krasimira, Overvad Kim, Kyrø Cecilie, Tjønneland Anne, Affret Aurélie, His Mathilde, Boutron-Ruault Marie-Christine, Katzke Verena, Kühn Tilman, Boeing Heiner, Trichopoulou Antonia, Naska Androniki, Kritikou Maria, Saieva Calogero, Agnoli Claudia, Santucci de Magistris Maria, Tumino Rosario, Fasanelli Francesca, Weiderpass Elisabete, Skeie Guri, Merino Susana, Jakszyn Paula, Sánchez Maria-José, Dorronsoro Miren, Navarro Carmen, Ardanaz Eva, Sonestedt Emily, Ericson Ulrika, Maria Nilsson Lena, Bodén Stina, Bueno-de-Mesquita H B As, Peeters Petra H, Perez-Cornago Aurora, Wareham Nicholas J, Khaw Kay-Thee, Freisling Heinz, Cross Amanda J, Riboli Elio, Scalbert Augustin
Section of Nutrition and Metabolism, International Agency for Research on Cancer (IARC-WHO), Lyon, France.
Unit of Nutrition and Cancer, Cancer Epidemiology Research Program, Catalan Institute of Oncology, Bellvitge Biomedical Research Institute (IDIBELL), Barcelona, Spain.
Int J Cancer. 2017 Apr 15;140(8):1836-1844. doi: 10.1002/ijc.30582. Epub 2017 Jan 19.
Flavonoids have been shown to inhibit colon cancer cell proliferation in vitro and protect against colorectal carcinogenesis in animal models. However, epidemiological evidence on the potential role of flavonoid intake in colorectal cancer (CRC) development remains sparse and inconsistent. We evaluated the association between dietary intakes of total flavonoids and their subclasses and risk of development of CRC, within the European Prospective Investigation into Cancer and Nutrition (EPIC) study. A cohort of 477,312 adult men and women were recruited in 10 European countries. At baseline, dietary intakes of total flavonoids and individual subclasses were estimated using centre-specific validated dietary questionnaires and composition data from the Phenol-Explorer database. During an average of 11 years of follow-up, 4,517 new cases of primary CRC were identified, of which 2,869 were colon (proximal = 1,298 and distal = 1,266) and 1,648 rectal tumours. No association was found between total flavonoid intake and the risk of overall CRC (HR for comparison of extreme quintiles 1.05, 95% CI 0.93-1.18; p-trend = 0.58) or any CRC subtype. No association was also observed with any intake of individual flavonoid subclasses. Similar results were observed for flavonoid intake expressed as glycosides or aglycone equivalents. Intake of total flavonoids and flavonoid subclasses, as estimated from dietary questionnaires, did not show any association with risk of CRC development.
黄酮类化合物已被证明在体外可抑制结肠癌细胞增殖，并在动物模型中预防结直肠癌的发生。然而，关于黄酮类化合物摄入量在结直肠癌（CRC）发生发展中潜在作用的流行病学证据仍然稀少且不一致。在欧洲癌症与营养前瞻性调查（EPIC）研究中，我们评估了总黄酮及其亚类的膳食摄入量与CRC发生风险之间的关联。在10个欧洲国家招募了477312名成年男性和女性队列。在基线时，使用特定中心验证的膳食问卷和来自酚类物质探索者数据库的成分数据估算总黄酮和各个亚类的膳食摄入量。在平均11年的随访期间，确定了4517例原发性CRC新病例，其中2869例为结肠癌（近端=1298例，远端=1266例），1648例为直肠癌。未发现总黄酮摄入量与总体CRC风险（极端五分位数比较的HR为1.05，95%CI为0.93-1.18；p趋势=0.58）或任何CRC亚型之间存在关联。对于任何单个黄酮类亚类的摄入量也未观察到关联。以糖苷或苷元当量表示的黄酮类化合物摄入量也观察到类似结果。根据膳食问卷估算的总黄酮和黄酮类亚类摄入量与CRC发生风险未显示出任何关联。
