Feld Jordan J, Lavoie Élise G, Fausther Michel, Dranoff Jonathan A
Toronto Western Hospital Liver Center, Toronto, ON, M5G 2M9, Canada.
Division of Gastroenterology and Hepatology, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
F1000Res. 2015 Apr 21;4:95. doi: 10.12688/f1000research.6368.2. eCollection 2015.
Evidence demonstrating that regular ingestion of coffee has salutary effects on patients with chronic liver disease is accumulating rapidly. Specifically, it appears that coffee ingestion can slow the progression of liver fibrosis, preventing cirrhosis and hepatocellular carcinoma (HCC). This should excite clinicians and scientists alike, since these observations, if true, would create effective, testable hypotheses that should lead to improved understanding on fibrosis pathogenesis and thus may generate novel pharmacologic treatments of patients with chronic liver disease. This review is designed to examine the relevant clinical and epidemiological data in critical fashion and to examine the putative pharmacological effects of coffee relevant to the pathogenesis of liver fibrosis and cirrhosis. We hope that this will inspire relevant critical analyses, especially among "coffee skeptics". Of note, one major assumption made by this review is that the bulk of the effects of coffee consumption are mediated by caffeine, rather than by other chemical constituents of coffee. Our rationales for this assumption are threefold: first, caffeine's effects on adenosinergic signaling provide testable hypotheses; second, although there are myriad chemical constituents of coffee, they are present in very low concentrations, and perhaps more importantly, vary greatly between coffee products and production methods (it is important to note that we do not dismiss the "botanical" hypothesis here; rather, we do not emphasize it at present due to the limitations of the studies examined); lastly, some (but not all) observational studies have examined both coffee and non-coffee caffeine consumption and found consistent effects, and when examined, no benefit to decaffeinated coffee has been observed. Further, in the interval since we examined this phenomenon last, further evidence has accumulated supporting caffeine as the effector molecule for coffee's salutary effects.
越来越多的证据表明,经常饮用咖啡对慢性肝病患者有有益影响。具体而言,饮用咖啡似乎可以减缓肝纤维化的进展,预防肝硬化和肝细胞癌(HCC)。这应该会让临床医生和科学家都感到兴奋,因为这些观察结果如果属实,将产生有效且可检验的假设,有助于增进对纤维化发病机制的理解,从而可能产生针对慢性肝病患者的新型药物治疗方法。本综述旨在批判性地审视相关临床和流行病学数据,并研究咖啡与肝纤维化和肝硬化发病机制相关的假定药理作用。我们希望这将激发相关的批判性分析,尤其是在“咖啡怀疑论者”当中。值得注意的是,本综述做出的一个主要假设是,咖啡消费的大部分影响是由咖啡因介导的,而非咖啡的其他化学成分。我们做出这一假设的理由有三点:第一,咖啡因对腺苷能信号传导的影响提供了可检验的假设;第二,虽然咖啡有无数化学成分,但它们的浓度非常低,而且更重要的是,不同咖啡产品和生产方法之间差异很大(需要注意的是,我们在此并未摒弃“植物学”假设;而是由于所研究的研究存在局限性,目前我们没有强调这一点);最后,一些(但并非全部)观察性研究同时考察了咖啡和非咖啡咖啡因的消费情况,发现了一致的效果,并且在研究时,未观察到脱咖啡因咖啡有任何益处。此外,自我们上次研究这一现象以来,又积累了更多证据支持咖啡因是咖啡有益作用的效应分子。