Associations between prediagnostic blood glucose levels, diabetes, and glioma
Abstract Previous literature indicates that pre-diagnostic diabetes and blood glucose levels are inversely related to glioma risk. To replicate these findings and determine whether they could be attributed to excess glucose consumption by the preclinical tumour, we used data from the Apolipoprotein...
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Nature Portfolio
2017-05-01
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Series: | Scientific Reports |
Online Access: | https://doi.org/10.1038/s41598-017-01553-2 |
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author | Judith Schwartzbaum Michael Edlinger Victoria Zigmont Pär Stattin Grzegorz A. Rempala Gabriele Nagel Niklas Hammar Hanno Ulmer Bernhard Föger Göran Walldius Jonas Manjer Håkan Malmström Maria Feychting |
author_facet | Judith Schwartzbaum Michael Edlinger Victoria Zigmont Pär Stattin Grzegorz A. Rempala Gabriele Nagel Niklas Hammar Hanno Ulmer Bernhard Föger Göran Walldius Jonas Manjer Håkan Malmström Maria Feychting |
author_sort | Judith Schwartzbaum |
collection | DOAJ |
description | Abstract Previous literature indicates that pre-diagnostic diabetes and blood glucose levels are inversely related to glioma risk. To replicate these findings and determine whether they could be attributed to excess glucose consumption by the preclinical tumour, we used data from the Apolipoprotein MOrtality RISk (AMORIS) (n = 528,580) and the Metabolic syndrome and Cancer project (Me-Can) cohorts (n = 269,365). We identified individuals who were followed for a maximum of 15 years after their first blood glucose test until glioma diagnosis, death, emigration or the end of follow-up. Hazard ratios (HRs), 95% confidence intervals (CIs) and their interactions with time were estimated using Cox time-dependent regression. As expected, pre-diagnostic blood glucose levels were inversely related to glioma risk (AMORIS, P trend = 0.002; Me-Can, P trend = 0.04) and pre-diagnostic diabetes (AMORIS, HR = 0.30, 95% CI 0.17 to 0.53). During the year before diagnosis, blood glucose was inversely associated with glioma in the AMORIS (HR = 0.78, 95% CI 0.66 to 0.93) but not the Me-Can cohort (HR = 0.99, 95% CI 0.63 to 1.56). This AMORIS result is consistent with our hypothesis that excess glucose consumption by the preclinical tumour accounts for the inverse association between blood glucose and glioma. We discuss additional hypothetical mechanisms that may explain our paradoxical findings. |
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language | English |
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spelling | doaj.art-f5bad9db859b4922934baf2ba57637002022-12-21T19:08:33ZengNature PortfolioScientific Reports2045-23222017-05-01711910.1038/s41598-017-01553-2Associations between prediagnostic blood glucose levels, diabetes, and gliomaJudith Schwartzbaum0Michael Edlinger1Victoria Zigmont2Pär Stattin3Grzegorz A. Rempala4Gabriele Nagel5Niklas Hammar6Hanno Ulmer7Bernhard Föger8Göran Walldius9Jonas Manjer10Håkan Malmström11Maria Feychting12Division of Epidemiology, College of Public Health, Ohio State UniversityDepartment of Medical Statistics, Informatics, and Health Economics, Medical UniversityDivision of Epidemiology, College of Public Health, Ohio State UniversityDepartment of Surgical and Perioperative Sciences, Urology and Andrology, Umeå UniversityDivision of Epidemiology, College of Public Health, Ohio State UniversityInstitute of Epidemiology and Medical Biometry, Ulm UniversityMedical Evidence & Observational Research, Global Medical Affairs, Astra Zeneca R&DDepartment of Medical Statistics, Informatics, and Health Economics, Medical UniversityAgency for Preventive and Social MedicineUnit of Cardiovascular Epidemiology, Institute of Environmental Medicine, Karolinska InstitutetDepartment of Surgery, Skåne University HospitalUnit of Epidemiology, Institute of Environmental Medicine, Karolinska InstitutetUnit of Epidemiology, Institute of Environmental Medicine, Karolinska InstitutetAbstract Previous literature indicates that pre-diagnostic diabetes and blood glucose levels are inversely related to glioma risk. To replicate these findings and determine whether they could be attributed to excess glucose consumption by the preclinical tumour, we used data from the Apolipoprotein MOrtality RISk (AMORIS) (n = 528,580) and the Metabolic syndrome and Cancer project (Me-Can) cohorts (n = 269,365). We identified individuals who were followed for a maximum of 15 years after their first blood glucose test until glioma diagnosis, death, emigration or the end of follow-up. Hazard ratios (HRs), 95% confidence intervals (CIs) and their interactions with time were estimated using Cox time-dependent regression. As expected, pre-diagnostic blood glucose levels were inversely related to glioma risk (AMORIS, P trend = 0.002; Me-Can, P trend = 0.04) and pre-diagnostic diabetes (AMORIS, HR = 0.30, 95% CI 0.17 to 0.53). During the year before diagnosis, blood glucose was inversely associated with glioma in the AMORIS (HR = 0.78, 95% CI 0.66 to 0.93) but not the Me-Can cohort (HR = 0.99, 95% CI 0.63 to 1.56). This AMORIS result is consistent with our hypothesis that excess glucose consumption by the preclinical tumour accounts for the inverse association between blood glucose and glioma. We discuss additional hypothetical mechanisms that may explain our paradoxical findings.https://doi.org/10.1038/s41598-017-01553-2 |
spellingShingle | Judith Schwartzbaum Michael Edlinger Victoria Zigmont Pär Stattin Grzegorz A. Rempala Gabriele Nagel Niklas Hammar Hanno Ulmer Bernhard Föger Göran Walldius Jonas Manjer Håkan Malmström Maria Feychting Associations between prediagnostic blood glucose levels, diabetes, and glioma Scientific Reports |
title | Associations between prediagnostic blood glucose levels, diabetes, and glioma |
title_full | Associations between prediagnostic blood glucose levels, diabetes, and glioma |
title_fullStr | Associations between prediagnostic blood glucose levels, diabetes, and glioma |
title_full_unstemmed | Associations between prediagnostic blood glucose levels, diabetes, and glioma |
title_short | Associations between prediagnostic blood glucose levels, diabetes, and glioma |
title_sort | associations between prediagnostic blood glucose levels diabetes and glioma |
url | https://doi.org/10.1038/s41598-017-01553-2 |
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