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Cigarette Smoking, Coffee Consumption, Alcohol Intake, and Risk of Crohn’s Disease and Ulcerative Colitis: A Mendelian Randomization Study
Abstract
Background: Crohn’s disease (CD) and ulcerative colitis (UC) are widely associated with smoking in epidemiological studies, whereas there are conflicting results for the association between CD and UC for both coffee and alcohol consumption. Herein, we aimed to investigate whether cigarette smoking and alcohol and coffee consumption are causally associated with either CD or UC. Methods: We utilized 540 genome-wide significant single-nucleotide polymorphisms for 3 potentially addictive substances—nicotine, alcohol, and caffeine—to assess the association of smoking, coffee, and alcohol consumption with CD and UC (12,194 CD cases, 12,366 UC cases, and 25,042 controls of European ancestry), using Mendelian randomization analysis. Mendelian randomization estimates were used to evaluate the effect of the exposure factors on CD and UC risk. Sensitivity analysis was employed to test for any directional pleiotropy. Results: We found evidence for a positive causal association between the age of smoking initiation and UC risk and between alcohol consumption and CD risk, which disappeared after sensitivity analysis for both associations (P > 0.05). No evidence for a causal association between cigarettes per day, smoking initiation, smoking cessation, and coffee consumption variables and UC or CD was found. Conclusions: We found no clear evidence that either genetically predicted smoking, coffee consumption, or alcohol consumption are causally associated with the risk for CD or UC, although our findings indicate a potential positive association between the age of smoking and UC and between alcohol consumption and CD.
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“A Mendelian randomization study found no evidence that genetically predicted coffee consumption could be causally linked to the occurrence of IBD [135].”
From Effects of Coffee on the Gastro-Intestinal Tract: A Narrative Review and Literature Update (2022) · cites this paper as [135]
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Bowden, J., Davey Smith, G., & Burgess, S. (2015) · International Journal of Epidemiology · doi:10.1093/ije/dyv080 · Cited by 9,816
Bowden, J., Davey Smith, G., Haycock, P. C., & Burgess, S. (2016) · Genetic Epidemiology · doi:10.1002/gepi.21965 · Cited by 8,922
Abraham, C., & Cho, J. H. (2009) · New England Journal of Medicine · doi:10.1056/nejmra0804647 · Cited by 2,712 · cited 1×
“2, 3 The mechanism triggering IBDs involves the inappropriate inflammatory response to intestinal microbes, which is mediated by the complex interplay between genetic susceptibility, environmental factors, and microbial dysbiosis.”
BackgroundMeta-analysis: Principles and procedures
Egger, M., Smith, G. D., & Phillips, A. N. (1997) · BMJ · doi:10.1136/bmj.315.7121.1533 · Cited by 2,415
PhenoScanner: a database of human genotype-phenotype associations.
Staley, J. R., Blackshaw, J., Kamat, M. A., Ellis, S., Surendran, P., Sun, B. B., Paul, D. S., Freitag, D., Burgess, S., Danesh, J., et al. (2016) · Bioinformatics · doi:10.1093/bioinformatics/btw373 · Cited by 1,479
Using multiple genetic variants as instrumental variables for modifiable risk factors
Palmer, T. M., Lawlor, D. A., Harbord, R. M., Sheehan, N. A., Tobias, J. H., Timpson, N. J., Smith, G. D., & Sterne, J. A. (2012) · Statistical Methods in Medical Research · doi:10.1177/0962280210394459 · Cited by 1,289
Burgess, S., Daniel, R. M., Butterworth, A. S., Thompson, S. G., & the EPIC-InterAct Consortium (2015) · International Journal of Epidemiology · doi:10.1093/ije/dyu176 · Cited by 543
Ng, S. C., Tang, W., Leong, R. W., Chen, M., Ko, Y., Studd, C., Niewiadomski, O., Bell, S., Kamm, M. A., de Silva, H. J., et al. (2015) · Gut · doi:10.1136/gutjnl-2014-307410 · Cited by 443
Biedermann, L., Brülisauer, K., Zeitz, J., Frei, P., Scharl, M., Vavricka, S. R., Fried, M., Loessner, M. J., Rogler, G., & Schuppler, M. (2014) · Inflammatory Bowel Diseases · doi:10.1097/mib.0000000000000129 · Cited by 178
Research works printed but not linked: 25
- Kaser, 2010, Inflammatory bowel disease, Annu Rev Immunol., 28, 573, 10.1146/annurev-immunol-030409-101225 · DOI · Paper page
- Khor, 2011, Genetics and pathogenesis of inflammatory bowel disease, Nature., 474, 307, 10.1038/nature10209 · DOI
- Khalili, 2018, The role of diet in the aetiopathogenesis of inflammatory bowel disease, Nat Rev Gastroenterol Hepatol., 15, 525, 10.1038/s41575-018-0022-9 · DOI · Paper page
- Nie, 2017, Beverage consumption and risk of ulcerative colitis: Systematic review and meta-analysis of epidemiological studies, Medicine (Baltimore)., 96, e9070, 10.1097/MD.0000000000009070 · DOI
- Shouval, 2017, The role of environmental factors in the pathogenesis of inflammatory bowel diseases: a review, JAMA Pediatr., 171, 999, 10.1001/jamapediatrics.2017.2571 · DOI
- Mahid, 2006, Smoking and inflammatory bowel disease: a meta-analysis, Mayo Clin Proc., 81, 1462, 10.4065/81.11.1462 · DOI
- Parkes, 2014, Smoking in inflammatory bowel disease: impact on disease course and insights into the aetiology of its effect, J Crohns Colitis., 8, 717, 10.1016/j.crohns.2014.02.002 · DOI
- Bergmann, 2017, No association of alcohol use and the risk of ulcerative colitis or Crohn’s disease: data from a European Prospective cohort study (EPIC), Eur J Clin Nutr., 71, 512, 10.1038/ejcn.2016.271 · DOI
- Porter, 2017, Epidemiology of inflammatory bowel disease among participants of the Millennium Cohort: incidence, deployment-related risk factors, and antecedent episodes of infectious gastroenteritis, Aliment Pharmacol Ther., 45, 1115, 10.1111/apt.13991 · DOI
- Wang, 2013, Multicenter case-control study of the risk factors for ulcerative colitis in China, World J Gastroenterol., 19, 1827, 10.3748/wjg.v19.i11.1827 · DOI
- Halfvarson, 2006, Environmental factors in inflammatory bowel disease: a co-twin control study of a Swedish-Danish twin population, Inflamm Bowel Dis., 12, 925, 10.1097/01.mib.0000228998.29466.ac · DOI
- Russel, 1998, Modern life’ in the epidemiology of inflammatory bowel disease: a case-control study with special emphasis on nutritional factors, Eur J Gastroenterol Hepatol., 10, 243, 10.1097/00042737-199803000-00010 · DOI
- Cornelis, 2015, Genome-wide meta-analysis identifies six novel loci associated with habitual coffee consumption, Molecular Psychiatry., 20, 647, 10.1038/mp.2014.107 · DOI · Paper page
- Liu, 2019, Association studies of up to 1.2 million individuals yield new insights into the genetic etiology of tobacco and alcohol use, Nat Genet., 51, 237, 10.1038/s41588-018-0307-5 · DOI · Paper page
- Li, 2002, An approximation to the F distribution using the chi-square distribution, Comput Stat Data Anal, 40, 21, 10.1016/S0167-9473(01)00097-4 · DOI
- de Lange, 2017, Genome-wide association study implicates immune activation of multiple integrin genes in inflammatory bowel disease, Nat Genet., 49, 256, 10.1038/ng.3760 · DOI · Paper page
- Nikolakopoulou, 2014, How to interpret meta-analysis models: fixed effect and random effects meta-analyses, Evid Based Ment Health., 17, 64, 10.1136/eb-2014-101794 · DOI · Paper page
- Pierce, 2013, Efficient design for Mendelian randomization studies: subsample and 2-sample instrumental variable estimators, Am J Epidemiol., 178, 1177, 10.1093/aje/kwt084 · DOI · Paper page
- Lee, 2018, Association between cigarette smoking status and composition of gut microbiota: population-based cross-sectional study, Journal of Clinical Medicine., 7:282
- Calkins, 1989, A meta-analysis of the role of smoking in inflammatory bowel disease, Dig Dis Sci., 34, 1841, 10.1007/BF01536701 · DOI · Paper page
- Yadav, 2017, Genetic factors interact with Tobacco smoke to modify risk for inflammatory bowel disease in humans and mice, Gastroenterology., 153, 550, 10.1053/j.gastro.2017.05.010 · DOI
- Nimmo, 2012, Genome-wide methylation profiling in Crohn’s disease identifies altered epigenetic regulation of key host defense mechanisms including the Th17 pathway, Inflamm Bowel Dis., 18, 889, 10.1002/ibd.21912 · DOI
- Salih, 2018, Smoking is associated with risk for developing inflammatory bowel disease including late onset ulcerative colitis: a prospective study, Scand J Gastroenterol., 53, 173, 10.1080/00365521.2017.1418904 · DOI
- El-Tawil, 2013, Epidemiology and inflammatory bowel diseases, World J Gastroenterol., 19, 1505, 10.3748/wjg.v19.i10.1505 · DOI
- Lee, 2014, Oral caffeine administration ameliorates acute colitis by suppressing chitinase 3-like 1 expression in intestinal epithelial cells, J Gastroenterol., 49, 1206, 10.1007/s00535-013-0865-3 · DOI
Cited by
Effects of Coffee on the Gastro-Intestinal Tract: A Narrative Review and Literature Update
Nehlig, A. (2022) · Nutrients · doi:10.3390/nu14020399 · Cited by 158
Metadata
- Authors
- Georgiou, A. N., Ntritsos, G., Papadimitriou, N., Dimou, N., & Evangelou, E.
- Affiliations
- Medical School, University of Cyprus , Nicosia, Cyprus
- Clinical and Molecular Epidemiology Unit, Department of Hygiene and Epidemiology, School of Medicine, University of Ioannina , Ioannina, Greece
- ORCID
- Georgiou, Andrea N
- Venue
- Inflammatory Bowel Diseases
- Publisher
- Oxford University Press (OUP)
- Published
- 2020-07-06
- Volume
- 27
- Issue
- 2
- Pages
- 162-168
- ISSN
- 1078-0998
- 1536-4844
- Cited by
- 45
- References
- 9
- Language
- en
- Funders
- European Social Fund
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- Georgiou, A. N., Ntritsos, G., Papadimitriou, N., Dimou, N., & Evangelou, E. (2021). Cigarette Smoking, Coffee Consumption, Alcohol Intake, and Risk of Crohn’s Disease and Ulcerative Colitis: A Mendelian Randomization Study. Inflammatory Bowel Diseases. https://doi.org/10.1093/ibd/izaa152
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