In an epidemiology study, Klatsky et al1 have convincingly demonstrated a dose-response inverse association between coffee drinking and alcoholic cirrhosis and to a lesser extent between coffee drinking and nonalcoholic cirrhosis. In a cross-sectional study, coffee consumption was also significantly related to a lower prevalence of transaminase enzymes (markers of liver damage), with a stronger association for those who drank large quantities of alcohol. Tea drinking was not related to cirrhosis, but the numbers of heavy tea drinkers were small in this population. The authors speculate that the active principle may be caffeine. We strongly support the hypothesis that it is the polyphenol antioxidant compounds in coffee that are the causative agents and that they may act in concert with caffeine, which is also hepatoprotective.2 Coffee has phenolic acids in high concentrations such that usual coffee consumption (2-3 cups/d) provides over 500 mg3 of these and other phenolic compounds. Although teas are high in polyphenols, they do not contain these phenolic acid compounds. In fact, we have found that coffee is the number 1 single source of phenolic antioxidants in the US diet.4 A phenolic acid found in coffee protected animals against liver damage induced by acetaminophen and carbon tetrachloride,5 and coffee intake decreased hepatotoxic effects from D-galactosamine.6 The mechanism of action of coffee's phenolic acids for liver protection is hypothesized as inhibiting the inflammatory transcription factor nuclear factor κB, enhancing expression of phase 2 detoxifying enzymes and antioxidant enzymes, and improving insulin resistance.6 Further coffee research is certainly warranted, especially human intervention studies.
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