A recent study by Prof. Wai-Kay Seto (The University of Hong Kong) and Prof. Jie Li (Drum Tower Hospital, Nanjing University Medical School), published in Alimentary Pharmacology & Therapeutics, systematically reviewed the epidemiology, pathogenic mechanisms, and prognostic impact of alcohol use in patients with metabolic dysfunction-associated steatotic liver disease (MASLD), showing that alcohol consumption significantly complicates disease progression and prognosis.
- Alcohol use is common in MASLD, but studies vary across regions.
International studies report 9% of MASLD patients drink at low levels and 14% at moderate levels, while a study of Hispanic Americans found 33% had a history of alcohol use. In the U.S., NHANES data show 27.3% of NAFLD patients drink moderately, and in the UK, up to 85% of MASLD patients have a history of alcohol consumption. These differences highlight the impact of cultural, economic, and healthcare factors, as well as inconsistent definitions of “safe drinking.” A unified alcohol assessment standard would help evaluate risk and manage health in MASLD patients worldwide.
- Alcohol is not just a co-factor but a potent accelerator of MASLD progression.
Alcohol accelerates MASLD progression through multiple mechanisms, such as oxidative stress, mitochondrial damage, fat accumulation, and gut barrier disruption, fueling inflammation. Genetic predispositions, such as PNPLA3 I148M, and sex differences further compound risk, emphasizing the need for personalized risk assessment.
- Even low-dose alcohol increases risks in MASLD patients.
Recent evidence shows even one drink per day significantly raises cirrhosis risk. Low-to-moderate drinking (women 100–130 g/week, men 100–200 g/week) is linked to fibrosis progression, and <20 g/day increases risk of advanced liver disease and HCC. Current evidence indicates that any alcohol consumption elevates adverse liver outcomes, supporting complete abstinence for MASLD patients.
- Alcohol’s impact on MASLD-related comorbidities
Obesity: Daily intake ≥7 g promotes fat synthesis, inhibits breakdown, and increases appetite, raising obesity and metabolic syndrome risk.
Diabetes: Short-term use may improve insulin sensitivity, but long-term drinking impairs pancreatic β-cell function; some drinks cause rapid blood sugar spikes.
Hypertension: Alcohol has dose-dependent effects—low doses minimal, moderate transiently lower BP, high doses cause delayed hypertension; chronic heavy drinking raises long-term BP.
Dyslipidemia: Moderate drinking may lower triglycerides via lipoprotein lipase, but frequent low-dose alcohol increases free fatty acids, LDL, VLDL, and triglycerides.
- Using subjective tools like AUDIT together with biomarkers such as PEth improves accurate detection of alcohol use in MASLD patients.
Subjective tools include AUDIT, AUDIT-C, SIAC, TLFB, drinking diaries, and Drinkaware apps, with AUDIT as the global standard for screening risky or dependent drinking. Objective biomarkers include direct markers (ethanol, urinary/hair EtG, PEth) and indirect markers (GGT, AST, ALT, MCV, CDT). PEth is highly specific, detects drinking over 2–4 weeks, and is unaffected by disease severity, making it valuable for monitoring abstinence and distinguishing MASLD, MetALD, and ALD.
Experts recommend complete abstinence from alcohol for MASLD patients. Combining questionnaires with biomarkers enables precise risk assessment, and interventions should consider individual metabolic and genetic factors. Further research into mechanisms and targeted therapies is needed to guide personalized clinical management and improve outcomes
