Black Coffee Consumption and Liver Health: A Comparative Review of Observational, Interventional, Mechanistic, and Mendelian Randomization
Black Coffee Consumption and Liver Health: Interventional and Mendelian Randomization
DOI:
https://doi.org/10.54393/df.v7i2.222Keywords:
Black Coffee, Dose-Response Relationship, Liver Health, Liver-Related MortalityAbstract
Coffee is one of the most widely consumed beverages in the world and has been studied many times for its positive liver effects in epidemiological research. Black coffee, made with no sugar, cream, or milk, is the best representation of a pure coffee dose of bioactive compounds, such as caffeine, chlorogenic acids, cafestol, and kahweol. With the amount of recent evidence available, synthesis is warranted to ascertain whether this association is causal, dose-dependent, and clinically relevant throughout the spectrum of chronic liver disease. It is a review of 35 peer-reviewed publications published between 2021 and 2025 from large prospective cohorts (UK Biobank, n ≈ 355,000–495,000; NHANES), systematic reviews and meta-analyses, randomized controlled trials on caffeine or chlorogenic acid supplementation, Mendelian randomization studies, disease-specific cohorts (hepatitis B, cirrhosis, metabolic syndrome), and mechanistic pharmacological reviews. The studies were assessed in five domains: MASLD risk, liver fibrosis and stiffness, cirrhosis, HCC, and liver-related mortality; biochemical evidence; interventional evidence; and molecular mechanisms. Observational data consistently show a lower risk of advanced fibrosis, cirrhosis, HCC, and liver-related mortality, while the strongest associations with coffee consumption are with fibrosis and cirrhosis rather than in relation to the incidence of steatosis. The dose-response relationship is not really dependent upon caffeine content; this suggests that chlorogenic acid and other polyphenols are likely to be the major mediators. However, there are inconsistent short-term biochemical effects from RCTs, mixed causal evidence from Mendelian randomization, and one large inverse-probability-weighted analysis suggested that the liver-specific mortality benefit was highly dependent on extensive adjustment for confounding factors.
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