Kjetil Bjørnevik1, Trond Riise1, Inger Bostrom2, Ilaria Casetta3, Marianna Cortese1, Enrico Granieri3, Trygve Holmøy4, Margitta T Kampman5, Anne-Marie Landtblom6, Sandra Magalhaes7, Maura Pugliatti8, Christina Wolfson9, Kjell-Morten Myhr10. 1. Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway/The Norwegian Multiple Sclerosis Competence Center, Department of Neurology, Haukeland University Hospital, Bergen, Norway. 2. Division of Neurology, Department of Clinical and Experimental Medicine, University of Linköping, Linköping, Sweden. 3. Department of Biomedical and Specialist Surgical Sciences, Section of Clinical Neurology, University of Ferrara, Ferrara, Italy. 4. Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway/Department of Neurology, Akershus University Hospital, Lørenskog, Norway. 5. Department of Neurology, University Hospital of North Norway, Tromsø, Norway. 6. Division of Neurology, Department of Clinical and Experimental Medicine, University of Linköping, Linköping, Sweden/Department of Neuroscience/Neurology, Uppsala University, Uppsala, Sweden. 7. Department of Epidemiology and Biostatistics and Occupational Health, McGill University, Montreal, QC, Canada. 8. Department of Biomedical and Specialty Surgical Sciences, Section of Clinical Neurology, University of Ferrara, Ferrara, Italy/Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway. 9. Department of Epidemiology and Biostatistics and Occupational Health, McGill University, Montreal, QC, Canada/Research Institute of the McGill University Health Centre, Montreal, QC, Canada. 10. The Kristian Gerhard Jebsen Centre for MS-Research, Department of Clinical Medicine, University of Bergen, Bergen, Norway/The Norwegian Multiple Sclerosis Registry and Biobank, Department of Neurology, Haukeland University Hospital, Bergen, Norway.
Abstract
BACKGROUND: Results from previous studies on a possible interaction between smoking and Epstein-Barr virus (EBV) in the risk of multiple sclerosis (MS) are conflicting. OBJECTIVES: To examine the interaction between smoking and infectious mononucleosis (IM) in the risk of MS. METHODS: Within the case-control study on Environmental Factors In Multiple Sclerosis (EnvIMS), 1904 MS patients and 3694 population-based frequency-matched healthy controls from Norway, Italy, and Sweden reported on prior exposure to smoking and history of IM. We examined the interaction between the two exposures on the additive and multiplicative scale. RESULTS: Smoking and IM were each found to be associated with an increased MS risk in all three countries, and there was a negative multiplicative interaction between the two exposures in each country separately as well as in the pooled analysis ( p = 0.001). Among those who reported IM, there was no increased risk associated with smoking (odds ratio (OR): 0.95, 95% confidence interval (CI): 0.66-1.37). The direction of the estimated interactions on the additive scale was consistent with a negative interaction in all three countries (relative excess risk due to interaction (RERI): -0.98, 95% CI: -2.05-0.15, p = 0.09). CONCLUSION: Our findings indicate competing antagonism, where the two exposures compete to affect the outcome.
BACKGROUND: Results from previous studies on a possible interaction between smoking and Epstein-Barr virus (EBV) in the risk of multiple sclerosis (MS) are conflicting. OBJECTIVES: To examine the interaction between smoking and infectious mononucleosis (IM) in the risk of MS. METHODS: Within the case-control study on Environmental Factors In Multiple Sclerosis (EnvIMS), 1904 MS patients and 3694 population-based frequency-matched healthy controls from Norway, Italy, and Sweden reported on prior exposure to smoking and history of IM. We examined the interaction between the two exposures on the additive and multiplicative scale. RESULTS: Smoking and IM were each found to be associated with an increased MS risk in all three countries, and there was a negative multiplicative interaction between the two exposures in each country separately as well as in the pooled analysis ( p = 0.001). Among those who reported IM, there was no increased risk associated with smoking (odds ratio (OR): 0.95, 95% confidence interval (CI): 0.66-1.37). The direction of the estimated interactions on the additive scale was consistent with a negative interaction in all three countries (relative excess risk due to interaction (RERI): -0.98, 95% CI: -2.05-0.15, p = 0.09). CONCLUSION: Our findings indicate competing antagonism, where the two exposures compete to affect the outcome.
Authors: Tomas Olsson; Lars Alfredsson; Anna Karin Hedström; Jesse Huang; Nicole Brenner; Julia Butt; Jan Hillert; Tim Waterboer; Ingrid Kockum Journal: Sci Rep Date: 2020-07-03 Impact factor: 4.379
Authors: Elin Engdahl; Rasmus Gustafsson; Jesse Huang; Martin Biström; Izaura Lima Bomfim; Pernilla Stridh; Mohsen Khademi; Nicole Brenner; Julia Butt; Angelika Michel; Daniel Jons; Maria Hortlund; Lucia Alonso-Magdalena; Anna Karin Hedström; Louis Flamand; Masaru Ihira; Tetsushi Yoshikawa; Oluf Andersen; Jan Hillert; Lars Alfredsson; Tim Waterboer; Peter Sundström; Tomas Olsson; Ingrid Kockum; Anna Fogdell-Hahn Journal: Front Immunol Date: 2019-11-26 Impact factor: 7.561