Almanza-Aguilera Enrique, Guiñón-Fort Daniel, Perez-Cornago Aurora, Martínez-Huélamo Miriam, Andrés-Lacueva Cristina, Tjønneland Anne, Eriksen Anne Kirstine, Katzke Verena, Bajracharya Rashmita, Schulze Matthias B, Masala Giovanna, Oliverio Andreina, Tumino Rosario, Manfredi Luca, Lasheras Cristina, Crous-Bou Marta, Sánchez Maria-José, Amiano Pilar, Colorado-Yohar Sandra M, Guevara Marcela, Sonestedt Emily, Bjartell Anders, Thysell Elin, Weiderpass Elisabete, Aune Dagfinn, Aglago Elom K, Travis Ruth C, Zamora-Ros Raul
Unit of Nutrition and Cancer, Cancer Epidemiology Research Program, Catalan Institute of Oncology (ICO), Bellvitge Biomedical Research Institute (IDIBELL), 08908 Barcelona, Spain.
Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford OX3 7LF, UK.
Cancers (Basel). 2023 Aug 11;15(16):4067. doi: 10.3390/cancers15164067.
Existing epidemiological evidence regarding the potential role of (poly)phenol intake in prostate cancer (PCa) risk is scarce and, in the case of flavonoids, it has been suggested that their intake may increase PCa risk. We investigated the associations between the intake of the total and individual classes and subclasses of (poly)phenols and the risk of PCa, including clinically relevant subtypes. The European Prospective Investigation into Cancer and Nutrition (EPIC) cohort included 131,425 adult men from seven European countries. (Poly)phenol intake at baseline was assessed by combining validated center/country-specific dietary questionnaires and the Phenol-Explorer database. Multivariable-adjusted Cox proportional hazards models were used to estimate the hazard ratios (HR) and 95% confidence intervals (CI). In total, 6939 incident PCa cases (including 3501 low-grade and 710 high-grade, 2446 localized and 1268 advanced, and 914 fatal Pca cases) were identified during a mean follow-up of 14 years. No associations were observed between the total intake of (poly)phenols and the risk of PCa, either overall (HR = 0.99, 95% CI 0.94-1.04) or according to PCa subtype. Null associations were also found between all classes (phenolic acids, flavonoids, lignans, and stilbenes) and subclasses of (poly)phenol intake and the risk of PCa, overall and according to PCa subtype. The results of the current large prospective cohort study do not support any association between (poly)phenol intake and PCa incidence.
关于（多）酚类物质摄入在前列腺癌（PCa）风险中潜在作用的现有流行病学证据很少，就黄酮类化合物而言，有人认为其摄入可能会增加PCa风险。我们研究了（多）酚类物质的总摄入量以及各个类别和亚类的摄入量与PCa风险之间的关联，包括临床相关亚型。欧洲癌症与营养前瞻性调查（EPIC）队列包括来自七个欧洲国家的131425名成年男性。通过结合经过验证的中心/国家特定饮食问卷和酚类物质探索者数据库来评估基线时的（多）酚类物质摄入量。使用多变量调整的Cox比例风险模型来估计风险比（HR）和95%置信区间（CI）。在平均14年的随访期间，共确定了6939例PCa新发病例（包括3501例低级别和710例高级别、2446例局限性和1268例晚期以及914例致命性PCa病例）。无论是总体上（HR = 0.99，95% CI 0.94 - 1.04）还是根据PCa亚型，均未观察到（多）酚类物质总摄入量与PCa风险之间存在关联。在（多）酚类物质摄入量的所有类别（酚酸、黄酮类化合物、木脂素和芪类化合物）和亚类与PCa风险之间，总体上以及根据PCa亚型，也均未发现关联。当前这项大型前瞻性队列研究的结果不支持（多）酚类物质摄入量与PCa发病率之间存在任何关联。
