Jorrit L Opstelten1, Simon S M Chan2,3, Andrew R Hart2,3, Fiona D M van Schaik1, Peter D Siersema4, Eef G W M Lentjes5, Kay-Tee Khaw6, Robert Luben6, Timothy J Key7, Heiner Boeing8, Manuela M Bergmann8, Kim Overvad9, Domenico Palli10, Giovanna Masala10, Antoine Racine11,12, Franck Carbonnel11,12, Marie-Christine Boutron-Ruault11, Anne Tjønneland13, Anja Olsen13, Vibeke Andersen14, Rudolf Kaaks15, Tilman Kühn15, Rosario Tumino16, Antonia Trichopoulou17, Petra H M Peeters18,19, W M Monique Verschuren18,20, Ben J M Witteman21,22, Bas Oldenburg1. 1. Department of Gastroenterology and Hepatology, University Medical Center Utrecht, Utrecht, the Netherlands. 2. Department of Medicine, Norwich Medical School, University of East Anglia, Norwich, United Kingdom. 3. Department of Gastroenterology, Norfolk and Norwich University Hospitals NHS Foundation Trust, Norwich, United Kingdom. 4. Department of Gastroenterology and Hepatology, Radboud University Medical Center, Nijmegen, the Netherlands. 5. Department of Clinical Chemistry and Hematology, University Medical Center, Utrecht, the Netherlands. 6. Strangeways Research Laboratory, Institute of Public Health, University of Cambridge, Cambridge, United Kingdom. 7. Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom. 8. Department of Epidemiology, German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), Nuthetal, Germany. 9. Section for Epidemiology, Department of Public Health, Aarhus University, Aarhus, Denmark. 10. Molecular and Nutritional Epidemiology Unit, Cancer Research and Prevention Institute (ISPO), Florence, Italy. 11. Center for Research in Epidemiology and Population Health, French Institute of Health and Medical Research (Inserm), Institut Gustave Roussy, Villejuif, France. 12. Department of Gastroenterology, University Hospital of Bicêtre, Assistance Publique - Hôpitaux de Paris, Université Paris-Sud, Le Kremlin Bicêtre, France. 13. Unit of Diet, Genes and Environment, Danish Cancer Society Research Center, Copenhagen, Denmark. 14. Institute of Regional Research-Center Sønderjylland, University of Southern Denmark, Odense, Denmark. 15. Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany. 16. Cancer Registry and Histopathology Unit, "Civic-M.P. Arezzo" Hospital, Ragusa, Italy. 17. Hellenic Health Foundation, Athens, Greece. 18. Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, the Netherlands. 19. MRC-PHE Centre for Environment and Health, Department of Epidemiology and Biostatistics, School of Public Health, Imperial College, London, United Kingdom. 20. Centre for Nutrition, Prevention and Health Services, National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands. 21. Department of Gastroenterology and Hepatology, Gelderse Vallei Hospital, Ede, the Netherlands. 22. Division of Human Nutrition, Wageningen University, Wageningen, the Netherlands.
Abstract
Background: A low vitamin D status has been put forward as a potential risk factor for the development of inflammatory bowel disease (IBD). This study investigated the association between prediagnostic circulating vitamin D concentrations and dietary intakes of vitamin D, and the risk of Crohn's disease (CD) and ulcerative colitis (UC). Methods: Among 359,728 participants of the European Prospective Investigation into Cancer and Nutrition cohort, individuals who developed CD or UC after enrollment were identified. Each case was matched with2 controls by center, gender, age, date of recruitment, and follow-up time. At cohort entry, blood samples were collected and dietary vitamin D intakes were obtained from validated food frequency questionnaires. Serum 25-hydroxyvitamin D levels were measured using liquid chromatography-tandem mass spectrometry. Conditional logistic regression was performed to determine the odds of CD and UC. Results: Seventy-two participants developed CD and 169 participants developed UC after a median follow-up of 4.7 and 4.1 years, respectively. Compared with the lowest quartile, no associations with the 3 higher quartiles of vitamin D concentrations were observed for CD (p trend = 0.34) or UC (p trend = 0.66). Similarly, no associations were detected when serum vitamin D levels were analyzed as a continuous variable. Dietary vitamin D intakes were not associated with CD (p trend = 0.39) or UC (p trend = 0.83). Conclusions: Vitamin D status was not associated with the development of CD or UC. This does not suggest a major role for vitamin D deficiency in the etiology of IBD, although larger studies are needed to confirm these findings.
Background: A low vitamin D status has been put forward as a potential risk factor for the development of inflammatory bowel disease (IBD). This study investigated the association between prediagnostic circulating vitamin D concentrations and dietary intakes of vitamin D, and the risk of Crohn's disease (CD) and ulcerative colitis (UC). Methods: Among 359,728 participants of the European Prospective Investigation into Cancer and Nutrition cohort, individuals who developed CD or UC after enrollment were identified. Each case was matched with2 controls by center, gender, age, date of recruitment, and follow-up time. At cohort entry, blood samples were collected and dietary vitamin D intakes were obtained from validated food frequency questionnaires. Serum 25-hydroxyvitamin D levels were measured using liquid chromatography-tandem mass spectrometry. Conditional logistic regression was performed to determine the odds of CD and UC. Results: Seventy-two participants developed CD and 169 participants developed UC after a median follow-up of 4.7 and 4.1 years, respectively. Compared with the lowest quartile, no associations with the 3 higher quartiles of vitamin D concentrations were observed for CD (p trend = 0.34) or UC (p trend = 0.66). Similarly, no associations were detected when serum vitamin D levels were analyzed as a continuous variable. Dietary vitamin D intakes were not associated with CD (p trend = 0.39) or UC (p trend = 0.83). Conclusions: Vitamin D status was not associated with the development of CD or UC. This does not suggest a major role for vitamin D deficiency in the etiology of IBD, although larger studies are needed to confirm these findings.
Authors: Berkeley N Limketkai; Manish B Singla; Benjamin Rodriguez; Ganesh R Veerappan; John D Betteridge; Miguel A Ramos; Susan M Hutfless; Steven R Brant Journal: Clin Gastroenterol Hepatol Date: 2019-10-04 Impact factor: 11.382
Authors: Christine Elisabeth Janssen; Anna Maria Globig; Andrea Busse Grawitz; Dominik Bettinger; Peter Hasselblatt Journal: PLoS One Date: 2019-05-23 Impact factor: 3.240
Authors: Craig Haifer; Ian C Lawrance; Jacqueline R Center; Michael W Clarke; Prue H Hart; John A Eisman; Robyn Lucas; Simon Ghaly Journal: Therap Adv Gastroenterol Date: 2019-07-26 Impact factor: 4.409