Evidence map›Paper›PMID 42385787›Full record

ArticleClinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association2026

Coffee Consumption and Improved Liver Outcomes: Clinical, Imaging, and Proteomic Evidence From the UK Biobank.

Hyun-Seok Kim, Mohammad Saeid Rezaee-Zavareh, Yufeng Wang, Abdelrahman M Attia, Minsun Kwak, Seungwon Burm, Derin Celtik, Daniel Legaspi, Osama Khattab, Naomy Kim and 13 more

Abstract read
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In one paragraph

Article in Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

23 authors.

Hyun-Seok KimKarsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, California. Electronic address: hyunseok.kim@cshs.org.
Mohammad Saeid Rezaee-ZavarehMiddle East Liver Diseases (MELD) Center, Tehran, Iran.
Yufeng WangBiomedical Imaging Research Institute, Cedars-Sinai Medical Center, Los Angeles, California.
Abdelrahman M AttiaKarsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, California.
Minsun KwakKarsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, California.
Seungwon BurmKarsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, California.
Derin CeltikKarsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, California.
Daniel LegaspiKarsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, California.
Osama KhattabKarsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, California.
Naomy KimKarsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, California.
Beza M MengistuBiomedical Imaging Research Institute, Cedars-Sinai Medical Center, Los Angeles, California.
Kelsey N LariosBiomedical Imaging Research Institute, Cedars-Sinai Medical Center, Los Angeles, California.
David Sooik KimUniversity of California Los Angeles Medical School, Los Angeles, California; Department of Gastroenterology and Hepatology, University of Southern California, Los Angeles, California.
Walid AyoubKarsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, California.
Alexandar KuoKarsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, California.
Paul MartinKarsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, California.
Aarshi VipaniKarsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, California.
Yun WangKarsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, California.
Suthat LiangpunsakulDivision of Gastroenterology and Hepatology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; Roudebush Veterans Administration Medical Center, Indianapolis, Indiana.
Debiao LiBiomedical Imaging Research Institute, Cedars-Sinai Medical Center, Los Angeles, California.
Shelly C LuKarsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, California.
Stephen PandolKarsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, California.
Ju Dong YangKarsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, California; Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, California.

Funding

Enhancing Risk Stratification in Alcoholic Hepatitis: Integrating AI-Based Radiomics with Clinical PredictorsK23AA032572 · NIAAA · CEDARS-SINAI MEDICAL CENTER · PI Hyunseok Kim · 2026 to 2026
$197k
NIAAA NIH HHS K23 AA032572
6 · The paper itself

Abstract

BACKGROUND &

aimsCoffee consumption has been linked to a reduced risk of liver disease, but large-scale prospective studies integrating imaging biomarkers, proteomics, and intake patterns remain limited. The effects of coffee type, additives, and metabolic modifiers are also unclear.

methodsWe analyzed 354,957 UK Biobank participants without baseline cirrhosis or hepatocellular carcinoma. Coffee consumption, type (caffeinated/decaffeinated), and additives (sugar/sweeteners) were assessed by questionnaire. Incident cirrhosis, hepatocellular carcinoma, and liver-related mortality were ascertained through linked records. In a subcohort (n = 28,961) undergoing magnetic resonance imaging, hepatic fat (proton density fat fraction), iron, and fibroinflammation (iron-corrected T1) were evaluated. Proteomic profiling (n = 44,633) used Olink assays. Models were adjusted for demographic, behavioral, metabolic, and genetic covariates.

resultsOver a median 13-year follow-up, higher coffee intake showed a graded reduction in liver outcomes, with ≥5 cups/day group having risk reductions of cirrhosis (hazard ratio, 0.68; 95% confidence interval, 0.58-0.79), hepatocellular carcinoma (hazard ratio, 0.53; 95% confidence interval, 0.34-0.83), and liver-related mortality (hazard ratio, 0.58; 95% confidence interval, 0.45-0.74). Protective associations were similar for caffeinated and decaffeinated coffee and persisted among those adding sugar or artificial sweeteners, although additive use correlated with modestly higher iron-corrected T1. Higher coffee intake corresponded to lower hepatic fat, iron, and fibroinflammation. Proteomic analysis revealed consistent patterns: higher levels of hepatocellular synthesis and complement proteins (transthyretin, selenoprotein P, complement factor H-related protein4/5) and lower levels of fibrogenic and macrophage-activation markers (microfibril-associated protein 4, colony stimulating factor 1 receptor, ectonucleotide pyrophosphatase/phosphodiesterase 2, transthyretin) with coffee drinking.

conclusionsHigher coffee intake was associated with favorable clinical, imaging, and proteomic indicators of liver health. These multidimensional findings support moderate unsweetened coffee as a simple strategy for liver disease prevention.

Indexed as

CirrhosisCoffee ConsumptionHepatocellular CarcinomaLiver DiseaseUK Biobank

Identifiers

PMID42385787
PMCPMC13505578

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.