Clarification of whether there is a hepatoprotective threshold and whether the benefits plateau with further consumption will be important for understanding the biology and potentially for therapeutic recommendations. Most
previous studies of caffeine’s health effects have focused largely on coffee consumption rather than total caffeine intake. The instrument developed for this study allowed for a relatively detailed breakdown of sources of dietary caffeine intake. However, for the purposes of analysis, it this website was necessary to assume that all caffeine sources of a given type contained equal amounts of caffeine irrespective of brand, the process of production, or other factors. The use of visual aids likely improved the reliability of estimates. Responses were consistent on repeat testing, suggesting that the instrument
can provide reproducible results, and that caffeine consumption stays relatively constant over time, at least for the study period. To tease apart whether the beneficial effects seen were related to caffeine or coffee intake, each component was evaluated individually. Consistent with previous reports, no beneficial effect was seen with green or black tea, LEE011 datasheet caffeinated soda, or any other sources of caffeine.5 However, a significant protective effect could have been missed because of small numbers; as 71% of total caffeine consumed came from coffee. Alternatively, if the beneficial effect of caffeine on fibrosis requires consumption above a threshold of daily caffeine, any benefit of non–coffee-related caffeine
may have been inapparent because the absolute amount of caffeine consumed from sources other than coffee was relatively low (75th percentile: 61 mg from noncoffee sources versus 270 mg from coffee). The observation that the association with less advanced liver fibrosis was seen only with caffeinated coffee implies either that the benefit is derived from caffeine (all caffeine or only that in coffee) or possibly from a substance removed by the decaffeination process. Different decaffeinating procedures were not evaluated. Race was an important effect modifier of the caffeine–fibrosis relationship. White patients consumed the most caffeine, and the protective association with advanced fibrosis was most apparent in this group. It is difficult medchemexpress to draw strong conclusions about the results in the nonwhite patients because of the relatively small numbers. The observation that nonwhite patients in the highest quartile of caffeine consumption for this group did not have lower odds of advanced fibrosis may simply be attributable to the fact that even the highest quartile in this group consumed much less caffeine than the apparent protective threshold. Previous studies have shown that increased coffee consumption is associated with lower liver enzymes, reduced rates of liver cancer, and possibly even reduced hepatic decompensation and liver-related mortality.
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