All coffee types decrease the risk of adverse clinical outcomes in chronic liver disease: a UK Biobank study.
Chronic liver disease
Cirrhosis
Coffee
Hepatocellular carcinoma
Journal
BMC public health
ISSN: 1471-2458
Titre abrégé: BMC Public Health
Pays: England
ID NLM: 100968562
Informations de publication
Date de publication:
22 06 2021
22 06 2021
Historique:
received:
19
01
2021
accepted:
06
05
2021
entrez:
22
6
2021
pubmed:
23
6
2021
medline:
2
7
2021
Statut:
epublish
Résumé
Chronic liver disease (CLD) is a growing cause of morbidity and mortality worldwide, particularly in low to middle-income countries with high disease burden and limited treatment availability. Coffee consumption has been linked with lower rates of CLD, but little is known about the effects of different coffee types, which vary in chemical composition. This study aimed to investigate associations of coffee consumption, including decaffeinated, instant and ground coffee, with chronic liver disease outcomes. A total of 494,585 UK Biobank participants with known coffee consumption and electronic linkage to hospital, death and cancer records were included in this study. Cox regression was used to estimate hazard ratios (HR) of incident CLD, incident CLD or steatosis, incident hepatocellular carcinoma (HCC) and death from CLD according to coffee consumption of any type as well as for decaffeinated, instant and ground coffee individually. Among 384,818 coffee drinkers and 109,767 non-coffee drinkers, there were 3600 cases of CLD, 5439 cases of CLD or steatosis, 184 cases of HCC and 301 deaths from CLD during a median follow-up of 10.7 years. Compared to non-coffee drinkers, coffee drinkers had lower adjusted HRs of CLD (HR 0.79, 95% CI 0.72-0.86), CLD or steatosis (HR 0.80, 95% CI 0.75-0.86), death from CLD (HR 0.51, 95% CI 0.39-0.67) and HCC (HR 0.80, 95% CI 0.54-1.19). The associations for decaffeinated, instant and ground coffee individually were similar to all types combined. The finding that all types of coffee are protective against CLD is significant given the increasing incidence of CLD worldwide and the potential of coffee as an intervention to prevent CLD onset or progression.
Sections du résumé
BACKGROUND
Chronic liver disease (CLD) is a growing cause of morbidity and mortality worldwide, particularly in low to middle-income countries with high disease burden and limited treatment availability. Coffee consumption has been linked with lower rates of CLD, but little is known about the effects of different coffee types, which vary in chemical composition. This study aimed to investigate associations of coffee consumption, including decaffeinated, instant and ground coffee, with chronic liver disease outcomes.
METHODS
A total of 494,585 UK Biobank participants with known coffee consumption and electronic linkage to hospital, death and cancer records were included in this study. Cox regression was used to estimate hazard ratios (HR) of incident CLD, incident CLD or steatosis, incident hepatocellular carcinoma (HCC) and death from CLD according to coffee consumption of any type as well as for decaffeinated, instant and ground coffee individually.
RESULTS
Among 384,818 coffee drinkers and 109,767 non-coffee drinkers, there were 3600 cases of CLD, 5439 cases of CLD or steatosis, 184 cases of HCC and 301 deaths from CLD during a median follow-up of 10.7 years. Compared to non-coffee drinkers, coffee drinkers had lower adjusted HRs of CLD (HR 0.79, 95% CI 0.72-0.86), CLD or steatosis (HR 0.80, 95% CI 0.75-0.86), death from CLD (HR 0.51, 95% CI 0.39-0.67) and HCC (HR 0.80, 95% CI 0.54-1.19). The associations for decaffeinated, instant and ground coffee individually were similar to all types combined.
CONCLUSION
The finding that all types of coffee are protective against CLD is significant given the increasing incidence of CLD worldwide and the potential of coffee as an intervention to prevent CLD onset or progression.
Identifiants
pubmed: 34154561
doi: 10.1186/s12889-021-10991-7
pii: 10.1186/s12889-021-10991-7
pmc: PMC8218514
doi:
Substances chimiques
Coffee
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
970Subventions
Organisme : Medical Research Council
ID : MC_PC_17228
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_QA137853
Pays : United Kingdom
Références
BMJ. 2018 Jun 5;361:k2158
pubmed: 29871897
Gastroenterology. 2015 Jan;148(1):118-25; quiz e15
pubmed: 25305507
Arch Toxicol. 2002 Jan;75(11-12):685-94
pubmed: 11876501
Food Funct. 2014 Aug;5(8):1695-717
pubmed: 24671262
Int J Cancer. 2007 Apr 1;120(7):1555-9
pubmed: 17205531
Therap Adv Gastroenterol. 2016 May;9(3):417-8
pubmed: 27134669
PLoS One. 2015 Nov 10;10(11):e0142457
pubmed: 26556483
Int J Epidemiol. 2016 Dec 1;45(6):1887-1894
pubmed: 28089956
Eur J Gastroenterol Hepatol. 2017 Jan;29(1):17-22
pubmed: 27676091
Eur J Nutr. 2021 Jun;60(4):1761-1767
pubmed: 32856188
J Am Coll Nutr. 2021 Mar-Apr;40(3):261-272
pubmed: 32343195
PLoS One. 2013 Jul 18;8(7):e69114
pubmed: 23874883
Liver Int. 2015 Sep;35(9):2063-71
pubmed: 26053588
Br J Cancer. 2005 Sep 5;93(5):607-10
pubmed: 16091758
Br J Cancer. 2013 Sep 3;109(5):1344-51
pubmed: 23880821
Nutr Res. 2019 Feb;62:78-88
pubmed: 30803509
Aliment Pharmacol Ther. 2016 Mar;43(5):562-74
pubmed: 26806124
BMJ Open. 2017 May 9;7(5):e013739
pubmed: 28490552
Lancet Gastroenterol Hepatol. 2020 Mar;5(3):245-266
pubmed: 31981519
J Hepatol. 2012 Nov;57(5):1090-6
pubmed: 22820478
Lancet. 2014 May 17;383(9930):1749-61
pubmed: 24480518
J Clin Epidemiol. 2008 Apr;61(4):344-9
pubmed: 18313558
Z Gastroenterol. 2007 Jan;45(1):25-33
pubmed: 17236118
Int J Clin Pract. 2017 Jan;71(1):
pubmed: 27933694
Hepatology. 2016 Dec;64(6):1969-1977
pubmed: 27301913