Binge drinking, metabolic dysfunction, and the spectrum of steatotic liver disease in the USA: a cross-sectional and longitudinal analysis


Younossi Z. M., Krag A., Zelber-Sagi S., Kalligeros M., Arrese M., Diaz L. A., ...Daha Fazla

The lancet. Gastroenterology & hepatology, cilt.11, sa.6, ss.495-508, 2026 (SCI-Expanded, Scopus) identifier identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 11 Sayı: 6
  • Basım Tarihi: 2026
  • Doi Numarası: 10.1016/s2468-1253(25)00376-0
  • Dergi Adı: The lancet. Gastroenterology & hepatology
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, EMBASE, MEDLINE
  • Sayfa Sayıları: ss.495-508
  • Recep Tayyip Erdoğan Üniversitesi Adresli: Evet

Özet

BACKGROUND: Underreporting of alcohol intake can misclassify individuals with significant alcohol exposure as having metabolic dysfunction-associated steatotic liver disease (MASLD) instead of metabolic dysfunction-associated alcohol-related liver disease (MetALD) or alcohol-related liver disease (ALD). Such misclassification obscures the true burden of alcohol-related liver disease, biases mortality estimates, and misguides public health priorities. This study assessed how correcting for alcohol underreporting influences prevalence and premature mortality estimates across the steatotic liver disease spectrum. METHODS: We did a cross-sectional and longitudinal analysis using US National Health and Nutrition Examination Survey (NHANES) data from 1988 to 2023. Adults aged 20 years or older who completed both the interview and examination components and had sufficient data to define steatotic liver disease and alcohol consumption (obtained via self-report) were included. To investigate prevalence trends, we analysed repeated cross-sectional NHANES cycles from 1988 to 2023. For mortality analyses, we analysed data from participants from NHANES cycles with linkage to the national death index, NHANES III (1988-94), and NHANES 1999-2014. Alcohol intake was corrected for sex-specific and frequency-specific underreporting and calibrated to national per-capita ethanol consumption. Binge drinking was defined as consuming five or more drinks on a single occasion at least once in the past year. Steatotic liver disease was defined using ultrasound, the US Fatty Liver Index, or vibration-controlled transient elastography, depending on availability in each survey cycle. We used Cox proportional hazards models to estimate adjusted hazard ratios (HRs) for premature mortality (≤75 years for men and ≤80 years for women). Population attributable fractions were derived from adjusted HRs and exposure prevalence. FINDINGS: Among 41 100 adults, adjusted prevalence increased between 1988-90 and 2021-23 from 12·69% (95% CI 11·38-13·99) to 28·16% (26·07-30·25) for MASLD, 1·62% (1·22-2·02) to 4·10% (3·38-4·82) for MetALD, and 2·28% (1·57-3·00) to 4·59% (3·94-5·25) for ALD (p<0·0001 for MASLD, p<0·0001 for MetALD, and p<0·0001 for ALD). In 2021-23, uncorrected prevalence was 1·65% (1·19-2·11) for ALD and 2·14% (1·69-2·59) for MetALD, indicating substantial underreporting of alcohol use. With 410 293 person-years of follow-up, premature mortality rates were highest in ALD (14·91 per 1000 person-years; HR 2·21 [95% CI 1·45-3·37]; p=0·0002), followed by MetALD (8·74 per 1000 person-years; HR 1·45 [1·03-2·04]; p=0·031) and MASLD (7·86 [HR 1·39 [1·10-1·76]; p=0·0062) compared with abstainers without steatotic liver disease (4·76 per 1000 person-years). Type 2 diabetes was the strongest metabolic predictor of MASLD premature mortality (population attributable fraction between 13·25% [95% CI 3·74-24·32] and 44·80% [20·43-66·63]) and binge drinking was the dominant driver in MetALD (20·98% [6·27-39·63]) and ALD (92·85% [73·74-98·07]). The greatest mortality risks were among those with binge drinking coexisting with type 2 diabetes or hypertension. INTERPRETATION: Adjusting for alcohol underreporting reveals a higher burden of ALD and MetALD than was previously recognised. Type 2 diabetes and binge drinking were leading mortality risk factors. These findings underscore the urgent need for targeted public health and clinical interventions, which should include systematic screening for alcohol consumption, particularly binge drinking, as well as comprehensive assessment of cardiometabolic risk factors. Additionally, educational initiatives are needed to increase awareness of the synergistic and potentially deleterious interaction between alcohol use and type 2 diabetes in accelerating liver disease progression and worsening liver-related outcomes. FUNDING: Center for Outcomes Research in Liver Disease.