Key Facts
- metALD: OR 2.58 for advanced fibrosis vs. MASLD
- ALD: OR 4.55 for advanced fibrosis vs. MASLD
- Excessive binge (8+ drinks/24 hrs): OR 3.77 trend toward advanced fibrosis
- Data source: NHANES 2017–2023; n=5,093 with SLD

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Lee discusess DDW 2026 data linking binge drinking frequency to advanced hepatic fibrosis in SLD.
New cross-sectional data presented at Digestive Disease Week (DDW) 2026 suggest that binge alcohol intake frequency may be a clinically meaningful, currently underappreciated contributor to advanced hepatic fibrosis risk in patients with steatotic liver disease (SLD).1
The findings, drawn from the National Health and Nutrition Examination Survey (NHANES) 2017–2023 database, indicate that patients classified as having metabolic and alcohol-associated liver disease (metALD) or alcohol-associated liver disease (ALD) carry substantially increasd odds of advanced fibrosis compared with those with metabolic dysfunction-associated steatotic liver disease (MASLD) alone, even when overall weekly alcohol intake appears moderate by conventional metrics.1
"While we think of metALD and the spectrum of steatotic liver disease as maybe, quote, unquote moderate drinking as compared to the ALD category, if we take a step back and look at the WHO definitions and the CDC definitions and the NIAAA definitions of at-risk drinking or heavy drinking, really, the metALD population is drinking quite heavily," said Frances Lee, lead investigator and corresponding author of the study in an interview with HCPLive.
Current frameworks for categorizing SLD subtypes like MASLD, metALD, and ALD rely on quantified alcohol intake measured across days and weeks, typically expressed in grams per day or per week. However, this approach does not capture how alcohol is consumed within a given episode. For example, a patient who binge drinks several times per week may fall within the metALD threshold for total weekly intake, yet the hepatotoxic burden of concentrated alcohol exposure in a short window is not reflected in that classification. The National Institute on Alcohol Abuse and Alcoholism (NIAAA) defines binge drinking as consuming ≥5 drinks for men, or ≥ 4 drinks for women, within a 2-hour period.
Lee and colleagues sought to address this gap by using NHANES data to examine whether binge drinking frequency, independent of total weekly intake, is associated with liver stiffness as assessed by vibration-controlled transient elastography (VCTE).
Among 27,493 survey participants, 5093 (18.5%) met criteria for SLD. Of these, 872 (17.2%) were classified as MASLD, 64 (1.3%) as metALD, and 71 (1.4%) as ALD. Significant fibrosis was defined as a liver stiffness measurement (LSM) > 8.5 kPa; advanced fibrosis was defined as LSM ≥ 13.1 kPa. Binge drinking frequency was stratified as excessive (4 to 7 times per week), moderate (2 times per week to 2 times per month), or rare (≤ 1 time per month). 1
Compared with patients in the MASLD group, those with metALD had 2.58-fold higher odds of advanced fibrosis (Odds Ratio [OR], 2.58; 95% Confidence Interval [CI], 1.19–5.61), and those with ALD had 4.55-fold higher odds (OR 4.55; 95% CI, 1.35–15.26). Among binge-drinking frequency categories, excessive binge drinking, defined as consuming eight or more drinks within 24 hours, trended toward higher risk for advanced fibrosis compared with rare binge drinking, though this did not reach statistical significance (OR 3.77; 95% CI, 0.93–15.40).
The 4-to-5 drink within 2 hours pattern similarly trended upward (OR 1.55; 95% CI, 0.53–4.55). Survey-weighted generalized linear models with a quasibinomial link function were used, adjusting for sex, age, race, diabetes status, waist circumference, dyslipidemia, hypertension, and obesity. 1
The metALD classification, introduced with the updated SLD nomenclature, was designed to characterize patients whose liver disease reflects both metabolic dysfunction and alcohol-related injury. The present findings underscore that this group, though sometimes perceived as occupying a middle ground between MASLD and ALD as described by investigators, carries a meaningfully elevated fibrosis risk that warrants clinical attention.2
"My research really supports that it's that intersection of the heavy drinking with the metabolic risk factors that increase the risk of fibrosis progression," Lee said.
Patients with obesity, pre-diabetes, dyslipidemia, or hypertension who are also engaging in binge drinking patterns may face exponentially compounded hepatic injury risk, a dynamic that current classification schemas, anchored in weekly gram thresholds, may not fully surface.
Lee explains further practical implications for patient counseling. Clinicians frequently encounter patients who do not self-identify as heavy drinkers because their consumption is episodic rather than daily. A patient consuming 6 drinks in a single weekend sitting, with no drinking on other days, may not meet criteria for ALD or even metALD by weekly calculation, yet their liver may be exposed to concentrated hepatotoxic metabolites in a compressed period.
"Your liver is processing a larger amount of toxic metabolites and alcohol in a short amount of period, which can lead to further damage to the liver," Lee noted.
The study provides early data to ground these clinical conversations in evidence rather than inference alone. 3
Lee identified the critical next steps for the field, including future work should incorporate timeline follow-back methodology alongside biochemical markers of alcohol exposure, with serial elastography using VCTE or MRI elastography to capture fibrosis trajectory over time. Understanding the role of concomitant metabolic therapies, particularly GLP-1 receptor agonists, which are increasingly used in patients with obesity and metabolic comorbidities, will also be essential. Genetic data, such as that available from the UK Biobank, may ultimately help identify which patients are most susceptible to binge-related hepatic injury at a genomic level. 1
Lee and co-investigators concluded that binge drinking behavior should be incorporated as a routine and quantified element of alcohol intake assessment in patients with SLD, not as a replacement for weekly gram calculations, but as a complementary dimension that may identify patients at greater fibrosis risk than their aggregate intake alone would suggest.
Editor’s Note: Lee does not report any relevant disclosures.
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