Jorrit L Opstelten1, Max Leenders, Vincent K Dik, Simon S M Chan, Fiona D M van Schaik, Kay-Tee Khaw, Robert Luben, Göran Hallmans, Pontus Karling, Stefan Lindgren, Olof Grip, Timothy J Key, Francesca L Crowe, Heiner Boeing, Manuela M Bergmann, Kim Overvad, Domenico Palli, Giovanna Masala, Antoine Racine, Franck Carbonnel, Marie-Christine Boutron-Ruault, Anne Tjønneland, Anja Olsen, Vibeke Andersen, Rudolf Kaaks, Verena A Katzke, Rosario Tumino, Antonia Trichopoulou, Peter D Siersema, H Bas Bueno-de-Mesquita, Andrew R Hart, Bas Oldenburg. 1. 1Department of Gastroenterology and Hepatology, University Medical Center Utrecht, Utrecht, the Netherlands; 2Department of Medicine, Norwich Medical School, University of East Anglia, Norwich, United Kingdom; 3Department of Gastroenterology, Norfolk and Norwich University Hospital NHS Trust, Norwich, United Kingdom; 4Strangeways Research Laboratory, Institute of Public Health, University of Cambridge, Cambridge, United Kingdom; 5Department of Public Health and Clinical Medicine, Nutritional Research, Umeå University, Umeå, Sweden; 6Department of Public Health and Clinical Medicine, GI Unit, Umeå University, Umeå, Sweden; 7Department of Clinical Sciences, Lund University, Lund, Sweden; 8Gastroenterology-Hepatology Division, University Hospital Skane, Malmö, Sweden; 9Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom; 10Department of Epidemiology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), Potsdam, Germany; 11Section for Epidemiology, Department of Public Health, Aarhus University, Aarhus, Denmark; 12Molecular and Nutritional Epidemiology Unit, Cancer Research and Prevention Institute (ISPO), Florence, Italy; 13French Institute of Health and Medical Research (INSERM), Centre for Research in Epidemiology and Population Health, Institut Gustave Roussy, Villejuif, France; 14Université Paris Sud, Paris, France; 15Department of Gastroenterology, Bicêtre University Hospital, Assistance Publique des Hôpitaux de Paris, Paris, France; 16Diet, Genes and Environment, Danish Cancer Society Research Center, Copenhagen, Denmark; 17Institute of Regional Research, Center Sønderjylland, University of Southern Denmark, Odense, Denmark; 18Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany; 19Cancer Registry and Histopathology Unit, "Civic-M.P. Arezzo" Hospital, Ragusa, Italy; 20Department of Hygiene and Epidemiology, WHO Collaborating Center for Food and Nu
Abstract
BACKGROUND: Dairy products may be involved in the etiology of inflammatory bowel disease by modulating gut microbiota and immune responses, but data from epidemiological studies examining this relationship are limited. We investigated the association between prediagnostic intake of these foods and dietary calcium, and the subsequent development of Crohn's disease (CD) and ulcerative colitis (UC). METHODS: In total, 401,326 participants were enrolled in the European Prospective Investigation into Cancer and Nutrition cohort. At recruitment, consumption of total and specific dairy products (milk, yogurt, and cheese) and dietary calcium was measured using validated food frequency questionnaires. Cases developing incident CD (n = 110) or UC (n = 244) during follow-up were matched with 4 controls. Conditional logistic regression analyses were used to calculate odds ratios (ORs) with 95% confidence intervals (CIs), adjusted for total energy intake and smoking. RESULTS: Compared with the lowest quartile, the ORs for the highest quartile of total dairy products and dietary calcium intake were 0.61 (95% CI, 0.32-1.19, p trend = 0.19) and 0.63 (95% CI, 0.28-1.42, p trend = 0.23) for CD, and 0.80 (95% CI, 0.50-1.30, p trend = 0.40) and 0.81 (95% CI, 0.49-1.34, p trend = 0.60) for UC, respectively. Compared with nonconsumers, individuals consuming milk had significantly reduced odds of CD (OR 0.30, 95% CI, 0.13-0.65) and nonsignificantly reduced odds of UC (OR 0.85, 95% CI, 0.49-1.47). CONCLUSIONS: Milk consumption may be associated with a decreased risk of developing CD, although a clear dose-response relationship was not established. Further studies are warranted to confirm this possible protective effect.
BACKGROUND: Dairy products may be involved in the etiology of inflammatory bowel disease by modulating gut microbiota and immune responses, but data from epidemiological studies examining this relationship are limited. We investigated the association between prediagnostic intake of these foods and dietary calcium, and the subsequent development of Crohn's disease (CD) and ulcerative colitis (UC). METHODS: In total, 401,326 participants were enrolled in the European Prospective Investigation into Cancer and Nutrition cohort. At recruitment, consumption of total and specific dairy products (milk, yogurt, and cheese) and dietary calcium was measured using validated food frequency questionnaires. Cases developing incident CD (n = 110) or UC (n = 244) during follow-up were matched with 4 controls. Conditional logistic regression analyses were used to calculate odds ratios (ORs) with 95% confidence intervals (CIs), adjusted for total energy intake and smoking. RESULTS: Compared with the lowest quartile, the ORs for the highest quartile of total dairy products and dietary calcium intake were 0.61 (95% CI, 0.32-1.19, p trend = 0.19) and 0.63 (95% CI, 0.28-1.42, p trend = 0.23) for CD, and 0.80 (95% CI, 0.50-1.30, p trend = 0.40) and 0.81 (95% CI, 0.49-1.34, p trend = 0.60) for UC, respectively. Compared with nonconsumers, individuals consuming milk had significantly reduced odds of CD (OR 0.30, 95% CI, 0.13-0.65) and nonsignificantly reduced odds of UC (OR 0.85, 95% CI, 0.49-1.47). CONCLUSIONS: Milk consumption may be associated with a decreased risk of developing CD, although a clear dose-response relationship was not established. Further studies are warranted to confirm this possible protective effect.
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