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Impact of Alcohol and Coffee Intake on the Risk of Advanced Liver Fibrosis: A Longitudinal Analysis in HIV-HCV Coinfected Patients (ANRS HEPAVIH CO-13 Cohort).
Yaya, I, Marcellin, F, Costa, M, Morlat, P, Protopopescu, C, Pialoux, G, Santos, ME, Wittkop, L, Esterle, L, Gervais, A, et al
Nutrients. 2018;(6)
Abstract
BACKGROUND Coffee intake has been shown to modulate both the effect of ethanol on serum GGT activities in some alcohol consumers and the risk of alcoholic cirrhosis in some patients with chronic diseases. This study aimed to analyze the impact of coffee intake and alcohol consumption on advanced liver fibrosis (ALF) in HIV-HCV co-infected patients. METHODS ANRS CO13-HEPAVIH is a French, nationwide, multicenter cohort of HIV-HCV-co-infected patients. Sociodemographic, behavioral, and clinical data including alcohol and coffee consumption were prospectively collected using annual self-administered questionnaires during five years of follow-up. Mixed logistic regression models were performed, relating coffee intake and alcohol consumption to ALF. RESULTS 1019 patients were included. At the last available visit, 5.8% reported high-risk alcohol consumption, 27.4% reported high coffee intake and 14.5% had ALF. Compared with patients with low coffee intake and high-risk alcohol consumption, patients with low coffee intake and low-risk alcohol consumption had a lower risk of ALF (aOR (95% CI) 0.24 (0.12–0.50)). In addition, patients with high coffee intake had a lower risk of ALF than the reference group (0.14 (0.03–0.64) in high-risk alcohol drinkers and 0.11 (0.05–0.25) in low-risk alcohol drinkers). CONCLUSIONS High coffee intake was associated with a low risk of liver fibrosis even in HIV-HCV co-infected patients with high-risk alcohol consumption.
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Systematic review with meta-analysis: coffee consumption and the risk of cirrhosis.
Kennedy, OJ, Roderick, P, Buchanan, R, Fallowfield, JA, Hayes, PC, Parkes, J
Alimentary pharmacology & therapeutics. 2016;(5):562-74
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BACKGROUND Liver cirrhosis is a large burden on global health, causing over one million deaths per year. Observational studies have reported an inverse association between coffee and cirrhosis. AIMS To perform a systematic review and meta-analysis to characterise the relationship between coffee consumption and cirrhosis. METHODS We searched for studies published until July 2015 that reported odds ratios, relative risks (RR) or hazard ratios for cirrhosis stratified by coffee consumption. We calculated RRs of cirrhosis for an increase in daily coffee consumption of two cups for each study and overall. We performed analyses by study design, type of cirrhosis and mortality. We assessed the risk of bias in each study and the overall quality of evidence for the effect of coffee on cirrhosis. RESULTS We identified five cohort studies and four case-control studies involving 1990 cases and 432 133 participants. We observed a dose-response in most studies and overall. The pooled RR of cirrhosis for a daily increase in coffee consumption of two cups was 0.56 (95% CI 0.44-0.68; I(2) 83.3%). The RR pooled from cohort studies for a daily increase of two cups was 0.58 (95% CI 0.41-0.76; I(2) 91.1%) and from case-control studies it was 0.52 (95% CI 0.40-0.63; I(2) 0.0%). The pooled RR of alcoholic cirrhosis for a daily increase of two cups was 0.62 (95% CI 0.51-0.73; I(2) 0%) and of death from cirrhosis it was 0.55 (95% CI 0.35-0.74; I(2) 90.3%). CONCLUSION This meta-analysis suggests that increasing coffee consumption may substantially reduce the risk of cirrhosis.
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Association of Coffee Consumption With Overall and Cause-Specific Mortality in a Large US Prospective Cohort Study.
Loftfield, E, Freedman, ND, Graubard, BI, Guertin, KA, Black, A, Huang, WY, Shebl, FM, Mayne, ST, Sinha, R
American journal of epidemiology. 2015;(12):1010-22
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Concerns about high caffeine intake and coffee as a vehicle for added fat and sugar have raised questions about the net impact of coffee on health. Although inverse associations have been observed for overall mortality, data for cause-specific mortality are sparse. Additionally, few studies have considered exclusively decaffeinated coffee intake or use of coffee additives. Coffee intake was assessed at baseline by self-report in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. Hazard ratios were estimated using Cox proportional hazards models. Among 90,317 US adults without cancer at study baseline (1998-2001) or history of cardiovascular disease at study enrollment (1993-2001), 8,718 deaths occurred during 805,644 person-years of follow-up from 1998 through 2009. Following adjustment for smoking and other potential confounders, coffee drinkers, as compared with nondrinkers, had lower hazard ratios for overall mortality (<1 cup/day: hazard ratio (HR) = 0.99 (95% confidence interval (CI): 0.92, 1.07); 1 cup/day: HR = 0.94 (95% CI: 0.87, 1.02); 2-3 cups/day: HR = 0.82 (95% CI: 0.77, 0.88); 4-5 cups/day: HR = 0.79 (95% CI: 0.72, 0.86); ≥6 cups/day: HR = 0.84 (95% CI: 0.75, 0.95)). Similar findings were observed for decaffeinated coffee and coffee additives. Inverse associations were observed for deaths from heart disease, chronic respiratory diseases, diabetes, pneumonia and influenza, and intentional self-harm, but not cancer. Coffee may reduce mortality risk by favorably affecting inflammation, lung function, insulin sensitivity, and depression.
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Evaluation of various biomarkers as potential mediators of the association between coffee consumption and incident type 2 diabetes in the EPIC-Potsdam Study.
Jacobs, S, Kröger, J, Floegel, A, Boeing, H, Drogan, D, Pischon, T, Fritsche, A, Prehn, C, Adamski, J, Isermann, B, et al
The American journal of clinical nutrition. 2014;(3):891-900
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BACKGROUND The inverse association between coffee consumption and the risk of type 2 diabetes (T2D) is well established; however, little is known about potential mediators of this association. OBJECTIVE We aimed to investigate the association between coffee consumption and diabetes-related biomarkers and their potential role as mediators of the association between coffee consumption and T2D. DESIGN We analyzed a case-cohort study (subcohort: n = 1610; verified incident T2D cases: n = 417) nested within the European Prospective Investigation into Cancer and Nutrition-Potsdam study involving 27,548 middle-aged participants. Habitual coffee consumption was assessed with a validated, semiquantitative food-frequency questionnaire. We evaluated the association between coffee consumption and several T2D-related biomarkers, such as liver markers (reflected by γ-glutamyltransferase, fetuin-A, and sex hormone-binding globulin), markers of dyslipidemia (high-density lipoprotein cholesterol and triglycerides), inflammation [C-reactive protein (CRP)], an adipokine (adiponectin), and metabolites, stratified by sex. RESULTS Coffee consumption was inversely associated with diacyl-phosphatidylcholine C32:1 in both sexes and with phenylalanine in men, as well as positively associated with acyl-alkyl-phosphatidylcholines C34:3, C40:6, and C42:5 in women. Furthermore, coffee consumption was inversely associated with fetuin-A (P-trend = 0.06) and CRP in women and γ-glutamyltransferase and triglycerides in men. Coffee consumption tended to be inversely associated with T2D risk in both sexes, reaching significance only in men [HR (95% CI): women: ≥4 compared with >0 to <2 cups coffee/d: 0.78 (0.46, 1.33); men: ≥5 compared with >0 to <2 cups coffee/d: 0.40 (0.19, 0.81)]. The association between coffee consumption and T2D risk in men was slightly reduced after adjustment for phenylalanine or lipid markers. CONCLUSIONS Coffee consumption was inversely associated with a diacyl-phosphatidylcholine and liver markers in both sexes and positively associated with certain acyl-alkyl-phosphatidylcholines in women. Furthermore, coffee consumption showed an inverse trend with CRP in women and with triglycerides and phenylalanine in men. However, these markers explained only to a small extent the inverse association between long-term coffee consumption and T2D risk.