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Carbohydrate intake in the etiology of Crohn's disease and ulcerative colitis
Simon S M Chan1, Robert Luben, Fiona van Schaik
11Norwich 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.
Background:
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).
Methods:
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.
Results:
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).
Conclusions:
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.
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