- Design
- Population-based cohort, Danish National Health Surveys
- Population
- 354,624 adults without cirrhosis
- Primary outcome
- 10-year cirrhosis risk by alcohol and cardiometabolic factors
- Effect
- 0.14% (1–7 drinks/wk) to 4.6% (>42); PAF alcohol 59.9%
This Danish population cohort followed 354,624 adults without cirrhosis from national health surveys (2010–2017) over 3.3 million person-years; 1211 developed cirrhosis. It was published in the Journal of Hepatology in August.
Ten-year cirrhosis risk rose steeply with alcohol: 0.14% at 1–7 drinks a week, 0.29% at 8–14, 0.68% at 15–28, 2.0% at 29–42 and 4.6% above 42. Obesity, diabetes, hypertension and smoking each carried a two- to threefold higher risk. Obesity, diabetes and hypertension added risk at up to 28 drinks a week but not above it; smoking added risk at every level. About 60% of cirrhosis was attributable to alcohol, 29% to hypertension, 21% to smoking and 14% to obesity.
In MetALD terms, metabolic risk factors matter most in moderate drinkers, while in heavy drinkers alcohol overwhelms everything else. The priority order for prevention is alcohol reduction first, then smoking and cardiometabolic control.
- Quantify drinks per week in every patient with fatty liver or abnormal liver tests.
- In moderate drinkers with obesity, diabetes or hypertension, treat both together.
- In heavy drinkers, alcohol reduction is the intervention that matters most.
- Offer smoking cessation; it adds risk at every drinking level.
Why it matters
It clarifies where metabolic risk factors add to alcohol's liver risk and where they do not.
Don't overread it
This is observational; attributable fractions assume causation the design cannot prove.
The statistics, in plain English
Population attributable fractions estimate how much disease would disappear if an exposure were removed, assuming the association is causal. Self-reported drinking usually underestimates true intake, which would make the alcohol effect, if anything, larger.
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