Sirs,

The beneficial effects of coffee consumption for chronic liver disease have attracted increasing interest in recent years. I read with great interest the recent review article by Yesil and Yilmaz in which, after reviewing the experimental, epidemiological and clinical studies, they reported that coffee intake can reduce the risk of non‐alcoholic fatty liver disease (NAFLD) and also discussed the potential biological mechanisms underlying the benefits of coffee consumption for NAFLD,1 which include anti‐oxidation, inhibiting hepatic stellate cells and the expression of connective tissue growth factor, and lowering serum levels of aminotransferases, etc.

Here, I propose another important biological mechanism of the benefits of coffee consumption, that is, the gut microbiota modulation by the bioactive coffee components, on the basis of the following aspects.

Firstly, in recent years, there is a growing body of evidence supporting the association between gut microbiota and chronic liver disease initiation and progression.2-5 For instance, Mouzaki et al. recently reported differences in gut microbiota between patients with NAFLD and healthy controls and a diet‐/body mass index‐independent link between the proportion of Bacteroidetes and the presence of non‐alcoholic steatohepatitis (NASH) in a cross‐sectional study.4 De Minicis et al. found that microbiota may interfere with liver fibrogenesis.5 Through analysing microbiota in a high‐fat diet plus bile duct ligation vs. control plus bile duct ligation mice, they revealed an increase in percentage of Gram‐negative vs. Gram‐positive bacteria, a reduced Bacteroidetes‐Firmicutes ratio, and a significant increase in Gram‐negative Proteobacteria, while increasing the population of intestinal Gram‐negative endotoxin producers may accelerate liver fibrogenesis.5

Secondly, it is interesting to find that coffee and its bioactive coffee components can modulate gut microbiota. The study of Jaquet et al. with sixteen healthy adult volunteers consumed a daily dose of three cups of coffee for 3 weeks indicated that coffee consumption resulted in an increase in the metabolic activity and/or numbers of the Bifidobacterium spp. population, a bacterial group with reputed beneficial effects.6 Similarly, Nakayama and Oishi have reported that coffee consumption exhibits a regulative effect on gut microbiota and increased aquaporin8, both of which are of significance for maintaining intestinal balance.7

More recently, Cowan et al. found that chronic coffee consumption can modulate gut microbiota in high‐fat‐fed rats and attenuate the increase in ratio between Firmicutes and Bacteroidetes.8 Additionally, the pharmacological effects of coffee have been focused on caffeine, disregarding the fruitful types of bioactive constituents, including alkaloids and phenolic compounds. The regulative effect of alkaloids and phenolic compounds for gut microbiota in animals and humans has been demonstrated by increasing studies in recent years.9

Therefore, it is plausible to infer that the regulative effect of coffee consumption on the gut microbiota may potentially contribute to reducing the risk of NAFLD, although at present we cannot identify which coffee constituent exerts this effect. With better understanding of the mechanisms of action, we will be in a better position to design interventional studies of coffee in patients with chronic liver diseases.