4 ms·

I had heard that alcoholics who drink coffee have a markedly decreased chance of developing cirrhosis, something like a 60% reduction. But only for regular caff

I had heard that alcoholics who drink coffee have a markedly decreased chance of developing cirrhosis, something like a 60% reduction. But only for regular caffeinated coffee- not tea, not decaf coffee. Do you have any insight into why or is this not true?

qiqing 11y ago
Huh, I hadn't seen that until just now, but I looked up this paper (http://www.ncbi.nlm.nih.gov/pubmed/11557177 http://www.ncbi.nlm.nih.gov/pubmed/11557177) and a more recent one that cited that one: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4110174/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4110174/ Notes for below: * CHB/CHC -> chronic hepatitis B/C * NAFLD -> Non-alcoholic fatty liver disease When discussing possible mechanisms for their findings: "We postulate that the observation of the benefit of coffee on the progression of liver disease may be due to its effects on the oxidative stress/lipotoxicity pathway, which underlie the pathogenesis of cirrhosis related to alcohol, NAFLD and possibly, in part, CHC. However, since oxidative stress is not the predominant mechanism of injury seen in CHB, coffee has no beneficial effect. Polyphenols and melanoidins, which are major components of coffee, have been shown to mediate multiple protective mechanisms in a rat model of steatohepatitis, ranging from increased fatty acid β oxidation, mitigating oxidative stress and curtailing liver inflammation (47). The other components of coffee, cafestol and kahwoel, can induce phase II detoxifying enzymes, including sulfotransferase, UDP-glucuronosyl transferase, glutathione transferase and peroxidase, and thus contribute to the anti-oxidant properties of coffee (14, 48). In addition, chemicals in coffee such as polyphenols and the diterpenes have been shown to down-regulate proinflammatory, fibrogenic cytokines such as transforming growth factor beta (TGF-β) and its downstream modulator, connective tissue growth factor (CTGF), collagen and stellate cell activation (13–16). Epidemiologic studies on caffeine have been inconsistent in demonstrating a protective effect in liver disease since other caffeine-containing beverages such as tea have not shown to be protective (19–21). Similarly, in our study, the inverse association with caffeine became null after adjustment for coffee, suggesting that ingredients of coffee other than caffeine appear to be responsible for this beverage’s effect on risk reduction. Furthermore, other caffeine-containing beverages like green tea and black tea had no significant effects with cirrhosis mortality in this study."

qiqing 11y ago

Huh, I hadn't seen that until just now, but I looked up this paper (http://www.ncbi.nlm.nih.gov/pubmed/11557177 http://www.ncbi.nlm.nih.gov/pubmed/11557177) and a more recent one that cited that one: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4110174/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4110174/ Notes for below: * CHB/CHC -> chronic hepatitis B/C * NAFLD -> Non-alcoholic fatty liver disease When discussing possible mechanisms for their findings: "We postulate that the observation of the benefit of coffee on the progression of liver disease may be due to its effects on the oxidative stress/lipotoxicity pathway, which underlie the pathogenesis of cirrhosis related to alcohol, NAFLD and possibly, in part, CHC. However, since oxidative stress is not the predominant mechanism of injury seen in CHB, coffee has no beneficial effect. Polyphenols and melanoidins, which are major components of coffee, have been shown to mediate multiple protective mechanisms in a rat model of steatohepatitis, ranging from increased fatty acid β oxidation, mitigating oxidative stress and curtailing liver inflammation (47). The other components of coffee, cafestol and kahwoel, can induce phase II detoxifying enzymes, including sulfotransferase, UDP-glucuronosyl transferase, glutathione transferase and peroxidase, and thus contribute to the anti-oxidant properties of coffee (14, 48). In addition, chemicals in coffee such as polyphenols and the diterpenes have been shown to down-regulate proinflammatory, fibrogenic cytokines such as transforming growth factor beta (TGF-β) and its downstream modulator, connective tissue growth factor (CTGF), collagen and stellate cell activation (13–16). Epidemiologic studies on caffeine have been inconsistent in demonstrating a protective effect in liver disease since other caffeine-containing beverages such as tea have not shown to be protective (19–21). Similarly, in our study, the inverse association with caffeine became null after adjustment for coffee, suggesting that ingredients of coffee other than caffeine appear to be responsible for this beverage’s effect on risk reduction. Furthermore, other caffeine-containing beverages like green tea and black tea had no significant effects with cirrhosis mortality in this study."