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. (7th June 2021)

• Record Type: Journal Article
• Authors: Ochoa-Rosales, Carolina; van der Schaft, Niels; Braun, Kim; Ho, Frederick; Petermann, Fanny; Pell, Jill; Ikram, M Arfan; Celis-Morales, Carlos; Voortman, Trudy
• Is Part Of: Current developments in nutrition. Volume 5(2021)Supplement 2
• Page Start: 1070
• Page End: 1070
• Publication Date: 2021-06-07
• Subjects: Nutrition -- Periodicals; Nutritional Physiological Phenomena; Nutrition; Periodicals; Periodicals; Fulltext; Internet Resources; Periodicals; 612.3
• DOI: 10.1093/cdn/nzab053_063
• Languages: English
• ISSNs: 2475-2991

Abstract

Abstract: 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.