Different types of sweetened coffee consumption, genetic predictor of gut microbe, and the risk of metabolic dysfunction-associated steatotic liver disease

BACKGROUND & AIMS: Associations between different types of coffee consumption and metabolic dysfunction-associated steatotic liver disease (MASLD) remained inconsistent. We aimed to assess the longitudinal associations of coffee consumption (including unsweetened, sugar-sweetened, artificially sweetened, caffeinated and decaffeinated coffee) with the risk of MASLD, while also exploring the potential coffee type-gut microbial abundance interactions. METHODS: The present cohort study included 185,437 participants free of MASLD at baseline in the UK Biobank. Dietary consumption of different types of coffee was collected through 24-hour dietary recall questionnaires. Incident cases of MASLD were ascertained through linked hospital records and death registries. Genetic risk scores (GRSs) of the relative abundance of intestinal microbiota and the risk of MASLD were calculated using 19 and 5 single nucleotide polymorphisms, respectively. Cox proportional hazards regression model was employed to estimate the hazard ratios (HRs) and 95% confidence intervals (CIs) for the associations. RESULTS: During a median follow-up of 10.49 years, we documented 1,536 MASLD cases. Compared with non-consumers, individuals consuming more than 2.5 servings per day of unsweetened coffee, caffeinated coffee, or a combination of both had a lower risk of MASLD, with adjusted HRs (CIs) of 0.70 (0.60-0.82), 0.78 (0.67-0.91), and 0.69 (0.58-0.82), respectively. No significant association was found between sugar-sweetened and artificially sweetened coffee consumption and the risk of MASLD. These associations were consistent across genetic risk levels of abundance of intestinal microbiota and MASLD itself, with no significant interaction observed (all P values for interactions ≥ 0.05). CONCLUSION: Higher intake of unsweetened coffee, particularly the caffeinated variety, was significantly associated with a reduced risk of MASLD, irrespective of genetic predisposition related to the abundance of intestinal microbiota or MASLD itself.