C-Reactive Protein Partially Mediates the Inverse Association Between Coffee Consumption and Risk of Type 2 Diabetes: The UK Biobank and the Rotterdam Study Cohorts
Autor: | M. Arfan Ikram, Carlos Celis-Morales, Niels van der Schaft, Fanny Petermann, Frederick K. Ho, Jill P. Pell, Trudy Voortman, Carolina Ochoa-Rosales, Kim V.E. Braun |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
Oncology
medicine.medical_specialty Inverse Association Nutrition and Dietetics Adiponectin biology business.industry C-reactive protein Medicine (miscellaneous) Coffee consumption Type 2 diabetes medicine.disease Biobank Rotterdam Study Insulin resistance Internal medicine medicine biology.protein Nutritional Epidemiology business Food Science |
Zdroj: | Curr Dev Nutr |
Popis: | OBJECTIVES: Given its popularity, there is an increasing interest in the study of coffee intake and its effect on health. Previous studies linked coffee consumption to lower type 2 diabetes (T2D) risk. However, potential underlying mechanisms remain unclear. We hypothesized that coffee's effects on systemic inflammation may play a role. We studied cross sectional and longitudinal associations of habitual coffee consumption with T2D risk and inflammation. METHODS: Participants from UK Biobank (UKB, n = 145,370) and Rotterdam Study (RS, n = 7172) cohorts were included. Coffee intake data were collected through self-administrated food frequency questionnaire or during home interviews. We studied associations of coffee intake with incident T2D using cox proportional hazard models; with longitudinally measured insulin resistance (HOMA IR) through linear mixed effect models; with serum baseline levels of inflammation markers using linear regressions; and the role of inflammation in coffee-T2D associations using mediation analysis. Models were adjusted for sociodemographic, lifestyle and health factors. Results were respectively expressed as hazard ratio (HR); β log transformed HOMA IR level; β log transformed ug/mL; and percentage mediated; and 95% confidence interval [95% CI]. RESULTS: UKB participants were 58% female and 55.2 years in average; RS were 59.7% female and 65.1 years. The median follow up was 7 (UKB) and 9 (RS) years. The modal coffee consumption was 0.5–2 cups/day (UKB) and 3–4 cups/day (RS). An increase of one coffee cup/day was associated with 4–6% lower T2D risk (RS HR 0.94 [95% CI 0.90; 0.98]; UKB HR 0.96 [0.94; 0.98]); lower HOMA IR (RS β −0.017 [−0.024; −0.010]); lower C reactive protein (CRP, RS β −0.014 [−0.022; −0.005]; UKBB β −0.011 [−0.012; −0.009] and higher adiponectin (RS β 0.025 [0.007; 0.042]. About coffee types, habitual consumers of filtered coffee had the lowest T2D risk (UKB HR 0.88 [0.83; 0.93]), compared to decaffeinated or instantaneous coffee. CRP levels mediated 9.6% (UKB) and 3.4% (RS) of the total effect of coffee on T2D. Adiponectin also showed evidence for mediation. CONCLUSIONS: Coffee's beneficial effects on lower T2D risk may be partially mediated by improvements in systemic inflammation. Among coffee drinkers, filtered coffee may be of preference. FUNDING SOURCES: Partially funded by the Institute for Scientific Information on Coffee. |
Databáze: | OpenAIRE |
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