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research-article2016

TAG0010.1177/1756283X16636765Therapeutic Advances in GastroenterologyO. Kennedy et al.

Therapeutic Advances in Gastroenterology

Letter to the Editor

Coffee, caffeine and non-alcoholic fatty liver disease? Oliver John Kennedy, Paul Roderick, Robin Poole and Julie Parkes

We read with interest the meta-analysis [Shen et al. 2016] in Therapeutic Advances in Gastroenterology regarding the association between caffeine and non-alcoholic fatty liver disease (NAFLD). The authors analysed separately the associations of (1) caffeine from ‘regular coffee’, which has been described elsewhere as ‘filtrated coffee’ [Anty et al. 2012], and (2) ‘total caffeine’, which included all coffee types, including espresso, and non-coffee caffeine (e.g. tea and soda). The authors found that ‘regular coffee caffeine’ but not ‘total caffeine’ was inversely associated with NAFLD fibrosis severity, and that neither was associated with NAFLD prevalence. Coffee is a complex mixture of biologically active compounds, including caffeine, chlorogenic acid, cafestol and kahweol. These compounds possess anti-oxidative and anti-fibrotic properties and may protect against a range of liver diseases, including fibrosis, cirrhosis and hepatocellular carcinoma [Saab et al. 2014]. Caffeine is thought to prevent fibrosis by antagonism of adenosine receptor A2a [Feld et  al. 2015], which inhibits hepatic stellate cells: the primary mediators of hepatic fibrosis [Wang et  al. 2014]. Therefore, it is surprising that the meta-analysis found an inverse association between NAFLD hepatic fibrosis severity and ‘regular coffee caffeine’ but not ‘total caffeine’. One possible explanation for this is that a compound in regular coffee other than caffeine is responsible. An equally plausible explanation is that no association between ‘total caffeine’ and NAFLD fibrosis severity was found because the data in the meta-analysis was unadjusted for confounders, such as type 2 diabetes mellitus (T2DM) and body mass index (BMI). This was apparent in an additional sensitivity analysis we performed on these data, which involved rerunning the meta-analysis while excluding the individual studies one at a time to examine their influence on the pooled association. When we

excluded the study by Bambha and colleagues [Bambha et al. 2014], we found a statistically significant association between ‘total caffeine’ and NAFLD hepatic fibrosis severity. However, when we included the study by Bambha and colleagues, the association was null, as reported in the metaanalysis. This is paradoxical since Bambha and colleagues reported that the sole measured source of caffeine (i.e. ‘coffee’ described as ‘coffee {unspecified}’ in the meta-analysis) was actually inversely associated with fibrosis, but only after adjustment for confounders. Unfortunately, the adjustment was not incorporated into the metaanalysis because ‘total caffeine’ was calculated from raw unadjusted coffee consumption. Another notable finding from the meta-analysis is the lack of an association between either ‘regular coffee caffeine’ or ‘total caffeine’ and NAFLD prevalence. The risk of NAFLD is increased in T2DM. Observational studies report inverse associations between coffee and T2DM [Ding et al. 2014]. The mechanism of action is thought to be largely mediated by chlorogenic acid, which improves glucose metabolism by inhibiting gut absorption and gluconeogenesis [Ding et  al. 2014]. Chlorogenic acid is present in regular coffee, so a protective effect against diabetes and, thus, reduced NAFLD prevalence might be expected. The lack of an association may reflect the study designs (e.g. cross-sectional and case control) which provide low levels of evidence (e.g. due to selection/information bias and lack of temporality). However, above all it underscores the need for robust randomized trials to investigate the effects of coffee on liver disease and other health outcomes.

Ther Adv Gastroenterol 2016, Vol. 9(3) 417­–418 DOI: 10.1177/ 1756283X16636765 © The Author(s), 2016. Reprints and permissions: http://www.sagepub.co.uk/ journalsPermissions.nav

Correspondence to: Oliver John Kennedy, BSc, PhD Primary Care & Population Sciences, Faculty of Medicine, University of Southampton, Southampton SO16 6YD, UK [email protected] Paul Roderick, MBBS, MA, MSc, MD Primary Care & Population Sciences, Faculty of Medicine, University of Southampton, Southampton, UK Robin Poole, MB, ChB, MRCGP, MSc, MFPH Primary Care & Population Sciences, Faculty of Medicine, University of Southampton, Southampton, UK Julie Parkes, BM, Bch, Msc, PhD, FFPH Primary Care & Population Sciences, Faculty of Medicine, University of Southampton, Southampton, UK

Funding This research received no specific grant from any funding agency in the public, commercial, or notfor-profit sectors.

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Therapeutic Advances in Gastroenterology 9(3) Conflict of interest statement The authors declare that there is no conflict of interest.

coffee consumption and risk of type 2 diabetes: a systematic review and a dose-response meta-analysis. Diabetes Care 37: 569–586. Feld, J., Lavoie, E., Michel, F. and Dranoff, J. (2015) I drink for my liver, Doc: emerging evidence that coffee prevents cirrhosis. F1000Research 4: 95.

References Anty, R., Marjoux, S., Iannelli, A., Patouraux, S., Schneck, A., Bonnafous, S. et al. (2012) Regular coffee but not espresso drinking is protective against fibrosis in a cohort mainly composed of morbidly obese European women with NAFLD undergoing bariatric surgery. J Hepatol 57: 1090–1096.

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Bambha, K., Wilson, L., Unalp, A., Loomba, R., Neuschwander-Tetri, B., Brunt, E. et al. (2014) Coffee consumption in NAFLD patients with lower insulin resistance is associated with lower risk of severe fibrosis. Liver Int 34: 1250–1258. Ding, M., Bhupathiraju, S., Chen, M., Van Dam, R. and Hu, F. (2014) Caffeinated and decaffeinated

Saab, S., Mallam, D., Cox, G. and Tong, M. (2014) Impact of coffee on liver diseases: a systematic review. Liver Int 34: 495–504. Shen, H., Rodriguez, A., Shiani, A., Lipka, S., Shahzad, G., Kumar, A. et al. (2016) Association between caffeine consumption and nonalcoholic fatty liver disease: a systemic review and meta-analysis. Ther Adv Gastroenterol 9: 113–120. Wang, H., Guan, W., Yang, W., Wang, Q., Zhao, H., Yang, F. et al. (2014) Caffeine inhibits the activation of hepatic stellate cells induced by acetaldehyde via adenosine A2a receptor mediated by the cAMP/PKA/ SRC/ERK1/2/P38 MAPK signal pathway. PloS One 9: e92482.

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Coffee, caffeine and non-alcoholic fatty liver disease?

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