Chan Simon S M, Luben Robert, van Schaik Fiona, Oldenburg Bas, Bueno-de-Mesquita H Bas, Hallmans Göran, Karling Pontus, Lindgren Stefan, Grip Olof, Key Timothy, Crowe Francesca L, Bergmann Manuela M, Overvad Kim, Palli Domenico, Masala Giovanna, Khaw Kay-Tee, Racine Antoine, Carbonnel Franck, Boutron-Ruault Marie-Christine, Olsen Anja, Tjonneland Anne, Kaaks Rudolf, Tumino Rosario, Trichopoulou Antonia, Hart Andrew R
1Norwich Medical School, Department of Medicine, University of East Anglia, Norwich, United Kingdom; 2Department of Gastroenterology, Norfolk and Norwich University Hospital NHS Trust, Norwich, United Kingdom; 3Strangeways Research Laboratory, Institute of Public Health, University of Cambridge, United Kingdom; 4University Medical Center Utrecht, Department of Gastroenterology and Hepatology, Utrecht, the Netherlands; 5National Institute of Public Health and the Environment (RIVM), Bilthoven, the Netherlands; 6Department of Epidemiology and Biostatistics, The School of Public Health, Imperial College London, London, United Kingdom; 7Department of Public Health and Clinical Medicine, Nutritional Research, Umeå University, Umeå, Sweden; 8Department of Public Health and Clinical Medicine, GI Unit, Umeå University, Umeå, Sweden; 9Department of Clinical Sciences, University Hospital, Malmö, Sweden; 10Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom; 11Department of Epidemiology, German Institute of Human Nutrition, Potsdam, Germany; 12Department of Clinical Epidemiology, University of Aarhus, Denmark; 13Molecular and Nutritional Epidemiology Unit, Cancer Research and Prevention Centre, Florence, Italy; 14INSERM, Centre for Research in Epidemiology and Population Health, Institut Gustave Roussy, Paris, France; 15Université Paris Sud, UMRS 1018, Paris, France; 16Department of Gastroenterology, Bicêtre University Hospital, Assistance Publique des Hôpitaux de Paris, Paris, France; 17Institute of Cancer Epidemiology, Danish Cancer Society, Copenhagen, Denmark; 18Division of Clinical Epidemiology, DKFZ-German Cancer Research Centre, Heidelberg, Germany; 19Cancer Registry and Histopathology Unit, "Civic - M.P.Arezzo" Hospital, Ragusa, Italy; 20WHO Collaborating Center for Food and Nutrition Policies, Athens, Greece.
Inflamm Bowel Dis. 2014 Nov;20(11):2013-21. doi: 10.1097/MIB.0000000000000168.
Diet may have a role in the etiology of inflammatory bowel disease. In previous studies, the associations between increased intakes of carbohydrates, sugar, starch, and inflammatory bowel disease are inconsistent. However, few prospective studies have investigated the associations between these macronutrients and incident Crohn's disease (CD) or ulcerative colitis (UC).
A total of 401,326 men and women were recruited between 1991 and 1998. At recruitment, dietary intakes of carbohydrate, sugar, and starch were measured using validated food frequency questionnaires. The cohort was monitored identifying participants who developed incident CD or UC. Cases were matched with 4 controls, and odds ratios were calculated for quintiles of total carbohydrate, sugar, and starch intakes adjusted for total energy intake, body mass index, and smoking.
One hundred ten participants developed CD, and 244 participants developed UC during follow-up. The adjusted odds ratio for the highest versus the lowest quintiles of total carbohydrate intake for CD was 0.87, 95% CI = 0.24 to 3.12 and for UC 1.46, 95% CI = 0.62 to 3.46, with no significant trends across quintiles for either (CD, P trend = 0.70; UC, P trend = 0.41). Similarly, no associations were observed with intakes of total sugar (CD, P trend = 0.50; UC, P trend = 0.71) or starch (CD, P trend = 0.69; UC, P trend = 0.17).
The lack of associations with these nutrients is in agreement with many case-control studies that have not identified associations with CD or UC. As there is biological plausibility for how specific carbohydrates could have an etiological role in inflammatory bowel disease, future epidemiological work should assess individual carbohydrates, although there does not seem to be a macronutrient effect.
饮食可能在炎症性肠病的病因中起作用。在先前的研究中,碳水化合物、糖、淀粉摄入量增加与炎症性肠病之间的关联并不一致。然而,很少有前瞻性研究调查这些宏量营养素与克罗恩病(CD)或溃疡性结肠炎(UC)发病之间的关联。
1991年至1998年期间共招募了401326名男性和女性。在招募时,使用经过验证的食物频率问卷测量碳水化合物、糖和淀粉的饮食摄入量。对该队列进行监测,确定发生CD或UC的参与者。病例与4名对照进行匹配,并计算调整总能量摄入、体重指数和吸烟因素后的总碳水化合物、糖和淀粉摄入量五分位数的比值比。
在随访期间,110名参与者患了CD,244名参与者患了UC。CD患者中,总碳水化合物摄入量最高五分位数与最低五分位数相比,调整后的比值比为0.87,95%置信区间为0.24至3.12;UC患者为1.46,95%置信区间为0.62至3.46,两者在五分位数间均无显著趋势(CD,P趋势=0.70;UC,P趋势=0.41)。同样,未观察到总糖摄入量(CD,P趋势=0.50;UC,P趋势=0.71)或淀粉摄入量(CD,P趋势=0.69;UC,P趋势=0.17)与之存在关联。
这些营养素缺乏关联与许多未发现与CD或UC存在关联的病例对照研究结果一致。鉴于特定碳水化合物在炎症性肠病中可能具有病因学作用具有生物学合理性,未来的流行病学研究应评估单个碳水化合物,尽管似乎不存在宏量营养素效应。