1Department of Epidemiology and Biostatistics, Imperial College London, London, United Kingdom; 2Program in Public Health, College of Health Sciences, University of California, Irvine, California; 3Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden; 4Biomarker Group, Nutrition and Metabolism Section, International Agency for Research on Cancer (IARC), Lyon, France; 5Unit of Nutrition and Cancer, Cancer Epidemiology Research Programme, Catalan Institute of Oncology, Bellvitge Biomedical Research Institute (IDIBELL), Barcelona, Spain; 6Department of Medicine, Norwich Medical School, University of East Anglia, Norwich, United Kingdom; 7Norfolk and Norwich University Hospital NHS Trust, Norwich, United Kingdom; 8Strangeways Research Laboratory, Institute of Public Health, University of Cambridge, Cambridge, United Kingdom; 9Department of Gastroenterology and Hepatology, University Medical Center Utrecht, Utrecht, the Netherlands; 10Department of Public Health and Clinical Medicine, Nutritional Research, Umeå University, Umeå, Sweden; 11Department of Public Health and Clinical Medicine, GI Unit, Umeå University, Umeå, Sweden; 12Department of Clinical Sciences, University Hospital, Malmö, Sweden; 13Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom; 14Department of Epidemiology, German Institute of Human Nutrition, Potsdam, Germany; 15Department of Public Health, Section for Epidemiology, Aarhus University, Aarhus, Denmark; 16Molecular and Nutritional Epidemiology Unit, Cancer Research and Prevention Centre, Florence, Italy; 17INSERM, Centre for Research in Epidemiology and Population Health, U1018, Team 9, Institut Gustave Roussy, Villejuif, France; 18Université Paris Sud, UMRS 1018, Villejuif, France; 19Department of Gastroenterology, Bicêtre University Hospital, Assistance Publique des Hôpitaux de Paris, Le Kremlin Bicêtre, France; 20Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark; 21Focused Research Unit for Molecular and Clinical Research, Institute of Regional Research- Center Sønderjylland, University of Southern Denmark, Odense, Denmark; 22Laboratory Center, Hospital of Southern Jutland, Aabenraa, Denmark; 23Institute of Cancer Epidemiology, Danish Cancer Society, Copenhagen, Denmark; 24Division of Clinical Epidemiology, DKFZ-German Cancer Research Centre, Heidelberg, Germany; 25Cancer Registry and Histopathology Unit, "Civic-M.P.Arezzo" Hospital, ASP Ragusa, Italy; and 26WHO Collaborating Center for Food and Nutrition Policies, Athens, Greece.
Inflamm Bowel Dis. 2017 Dec;23(12):2072-2082. doi: 10.1097/MIB.0000000000001108.
Oxidative stress may be involved in the aetiology of inflammatory bowel disease and whether dietary polyphenols, which possess antioxidants properties, prevent its development is unknown.
A total of 401,326 men and women aged 20 to 80 years from 8 countries were recruited between 1991 and 1998 and at baseline completed validated food frequency questionnaires. Dietary polyphenol intake was measured using Phenol-Explorer, a database with information on the content of 502 polyphenols. Incident cases of Crohn's diseases (CD) and ulcerative colitis (UC) were identified during the follow-up period of up to December 2010. A nested case-control study using conditional logistic regression estimated the odds ratios (ORs), and 95% confidence intervals, for polyphenol intake (categories based on quartiles) and developing CD or UC.
In total, 110 CD (73% women) and 244 UC (57% women) cases were identified and matched to 440 and 976 controls, respectively. Total polyphenol intake was not associated with CD (P trend = 0.17) or UC (P trend = 0.16). For flavones and CD, there were reduced odds for all quartiles, which were statistically significant for the third (OR3rd versus 1st quartile = 0.33; 95% confidence interval, 0.15-0.69) and there was an inverse trend across quartiles (P = 0.03). Similarly, for resveratrol, there was an inverse association with CD (OR4th versus 1st quartile = 0.40; 95% confidence interval, 0.20-0.82) with an inverse trend across quartiles (P = 0.02). No significant associations between subtypes of polyphenols and UC were found. Effect modification by smoking in CD was documented with borderline statistical significance.
The data supports a potential role of flavones and resveratrol in the risk of developing CD; future aetiological studies should investigate these dietary components and further examine the potential for residual confounding.
氧化应激可能与炎症性肠病的病因有关，而膳食多酚具有抗氧化特性，其是否能预防其发生尚不清楚。
1991 年至 1998 年期间，从 8 个国家招募了 401326 名年龄在 20 至 80 岁之间的男性和女性，并在基线时完成了经过验证的食物频率问卷。膳食多酚的摄入量通过 Phenol-Explorer 进行测量，这是一个包含 502 种多酚含量信息的数据库。在截至 2010 年 12 月的随访期间，确定了克罗恩病（CD）和溃疡性结肠炎（UC）的发病病例。使用条件逻辑回归对病例对照研究进行嵌套，估计了多酚摄入量（基于四分位数的类别）与发生 CD 或 UC 的比值比（OR）及其 95%置信区间。
共确定了 110 例 CD（73%为女性）和 244 例 UC（57%为女性）病例，并分别与 440 例和 976 例对照相匹配。总的多酚摄入量与 CD（P 趋势=0.17）或 UC（P 趋势=0.16）无关。对于类黄酮和 CD，所有四分位数的优势比均降低，第三四分位数（OR3rd 与 1st 四分位数=0.33；95%置信区间，0.15-0.69）具有统计学意义，四分位数之间呈反向趋势（P=0.03）。同样，对于白藜芦醇，与 CD 呈负相关（OR4th 与 1st 四分位数=0.40；95%置信区间，0.20-0.82），四分位数之间呈反向趋势（P=0.02）。未发现多酚亚型与 UC 之间存在显著关联。CD 中吸烟的作用修饰具有边缘统计学意义。
数据支持类黄酮和白藜芦醇在 CD 发病风险中的潜在作用；未来的病因学研究应调查这些饮食成分，并进一步研究潜在的残余混杂因素。
