Coffee Consumption and C-reactive Protein

Author(s):  
Ngoc M. Pham ◽  
Victor R. Preedy
Circulation ◽  
2021 ◽  
Vol 143 (Suppl_1) ◽  
Author(s):  
Carolina Ochoa-Rosales ◽  
Niels van der Schaft ◽  
Kim V Braun ◽  
Frederick Ho ◽  
Fanny Petermann ◽  
...  

Background: Coffee intake has been linked to lower type 2 diabetes (T2D) risk. We hypothesized this may be mediated by coffee’s effects on inflammation. Methods: Using participants from the UK Biobank (UKB n=145370) and Rotterdam Study (RS n=7172) cohorts, we studied associations of coffee intake with incident T2D; longitudinally measured insulin resistance (HOMA IR); serum levels of inflammation markers; and the mediating role of inflammation. Statistical regression models were adjusted for sociodemographic, lifestyle and health factors. Results: The median follow up was 7 (UKB) and 9 (RS) years. 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]); with lower C reactive protein (CRP) and higher adiponectin (Figure1). Consumers of filtered coffee had the lowest T2D risk (UKB HR=0.88 [0.83; 0.93]). CRP levels mediated 9.6% (UKB) and 3.4% (RS) of the total effect of coffee on T2D (Figure 1). Conclusions: We suggest that coffee’s beneficial effects on lower T2D risk are partially mediated by improvements in systemic inflammation.Figure 1. a CRP and a adiponectin refer to the effect of coffee intake on CRP and adiponectin levels. a CRP RS : β=-0.014 (-0.022; -0.005); UKBB a CRP UKB : β=-0.011 (-0.012; -0.009) and RS a adiponectin : β=0.025 (0.007; 0.042). b CRP and b adiponectin refer to the effect of coffee related levels in CRP and adiponectin on incident T2D, independent of coffee. RS b CRP : HR=1.17 (1.04; 1.31); UKB b CRP : HR=1.45 (1.37; 1.54); and b adiponectin : HR=0.58 (0.32; 0.83). c′ refers to coffee’ effect on T2D going directly or via others mediators. UKB c′ independent of CRP : HR=0.96 (0.94; 0.99); RS c′ independent of CRP : HR=0.94 (0.90; 0.99); and RS c′ independent of CRP+adiponectin : HR=0.90 (0.80; 1.01). Coffee related changes in CRP may partially explain the beneficial link between coffee and T2D, mediating a 3.4% (0.6; 4.8, RS) and 9.6% (5.7; 24.4, UKB). Evidence of mediation was also found for adiponectin.


2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 1070-1070
Author(s):  
Carolina Ochoa-Rosales ◽  
Niels van der Schaft ◽  
Kim Braun ◽  
Frederick Ho ◽  
Fanny Petermann ◽  
...  

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.


Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1349 ◽  
Author(s):  
Elizabeth D. Moua ◽  
Chenxiao Hu ◽  
Nicole Day ◽  
Norman G. Hord ◽  
Yumie Takata

Coffee contains bioactive compounds with anti-inflammatory properties, and its consumption may reduce c-reactive protein (CRP) levels, a biomarker of chronic inflammation. A previous meta-analysis reported no overall association between blood CRP level and coffee consumption by modeling the coffee consumption in categories, with substantial heterogeneity. However, the coffee cup volume was not considered. We conducted a systematic review and dose–response meta-analysis investigating the association between coffee consumption and CRP levels reported in previous observational studies. A dose–response meta-analysis was conducted by mixed-effects meta-regression models using the volume of coffee consumed as metric. Eleven studies from three continents were identified using the PubMed database, totaling 61,047 participants. Three studies with the largest sample sizes observed a statistically significant association between coffee and CRP levels, which was inverse among European and United States (US) women and Japanese men (1.3–5.5% decrease in CRP per 100 mL of coffee consumed) and positive among European men (2.2% increase). Other studies showed no statistically significant associations. When all studies were combined in the dose–response meta-analysis, no statistically significant associations were observed among all participants or when stratified by gender or geographic location, reflecting the conflicting associations reported in the included studies. Further studies are warranted to explore these inconsistent associations.


2010 ◽  
Vol 41 (2) ◽  
pp. 345-352 ◽  
Author(s):  
O. Bjerkeset ◽  
U. Romild ◽  
G. Davey Smith ◽  
K. Hveem

BackgroundElevated levels of circulating C-reactive protein (CRP) have been associated with coronary heart disease and, in some studies, depression. Most studies have been of populations selected by age and/or gender. We investigate these associations with depression, myocardial infarction (MI), or both, in a large general population sample.MethodA cross-sectional population study of 9258 women and men aged ⩾20 years. The study included clinical examination, self-report of MI and depression and factors known to confound their associations. The Hospital Anxiety and Depression Scale was used to assess severity of depressive symptoms. Elevated high sensitive-CRP was defined as values >2.2 mg/l.ResultsThe association of elevated CRP with depression was attenuated towards the null [from odds ratio (OR) 1.28, p=0.001 to OR 1.08, p=0.388] following extensive adjustment, while associations with MI (adjusted OR 1.42, p=0.032) and co-morbid MI and depression (adjusted OR 2.66, p=0.003) persisted. Confounders associated with elevated CRP levels were smoking (OR 1.66; p<0.001), chronic physical illness (OR 1.34, p<0.001), BMI ⩾30 (OR 1.13, p<0.001), employment (OR 0.70, p<0.001) and high coffee consumption (OR 0.83, p=0.017). Interaction tests indicated a lower effect of old age (OR 0.54, p<0.001) and smoking (OR 0.63, p<0.001) on elevated CRP levels in women compared with men.ConclusionsCRP levels were raised in those with MI and co-morbid MI and depression; the positive association with depression was explained by confounding factors. We found new evidence that might help understand gender-specific patterns. Future studies should explore the neurobiological mechanisms underpinning these interrelations and their relevance for treatment of these conditions.


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