**Methods:** This cross-sectional study included 2,622 participants aged 20–59 years with reliable VCTE results (≥10 valid LSM measurements after ≥3 hours fasting, IQR/median <30%). Marijuana use was self-reported and categorized as never user (no lifetime use), past user (lifetime use at least once, but not in the past 30 days), and current user (≥1 day in the last 30 days). Steatosis was defined as CAP ≥274 dB/m (S1 or higher), and significant fibrosis as LSM ≥8.2 kPa (F2 or higher). Multivariate logistic regression models were used to adjust for confounders including age, sex, BMI, ethnicity, education, marital status, poverty level, smoking, alcohol intake, and comorbidities (CVD, CKD, COPD, hypertension, diabetes, anemia, hepatitis B, hepatitis C). Subgroup analyses were performed by alcohol intake (never-to-moderate vs. heavy drinkers).
**Key Results:** Among 2,622 participants (mean age 40.0±11.7 years, 49.1% male), 45.9% were never users, 35.0% past users, and 19.1% current users. The prevalence of steatosis was 50.3% in never users, 35.0% in past users, and 14.7% in current users (P<0.001). Mean CAP values were 264.8±62.2 dB/m (never), 263.1±63.9 dB/m (past), and 246.6±64.0 dB/m (current) (P<0.001). In unadjusted analysis, current marijuana use was associated with lower odds of steatosis (OR 0.56, 95% CI 0.45–0.70, P<0.001). After full adjustment (Model III: age, sex, BMI, ethnicity, education, marital status, poverty, smoking, alcohol, CVD, CKD, COPD, hypertension, diabetes, anemia, hepatitis B, hepatitis C), current use remained significantly associated with lower odds of steatosis (OR 0.69, 95% CI 0.48–0.997, P=0.048). Past use was not significantly associated with steatosis in any model (Model III: OR 0.83, 95% CI 0.63–1.09, P=0.184). In subgroup analysis by alcohol intake, among never-to-moderate drinkers, current marijuana use was associated with lower odds of steatosis (adjusted OR 0.45, 95% CI 0.23–0.86, P=0.015), but this association was not significant among heavy drinkers (adjusted OR 0.83, 95% CI 0.52–1.34, P=0.449). For fibrosis, the prevalence was 8.2% in never users, 7.5% in past users, and 5.8% in current users (P=0.221). No significant association was found between marijuana use and fibrosis in any model (current use Model III: OR 0.69, 95% CI 0.36–1.30, P=0.248).
**Clinical Implications:** This study suggests that current marijuana use is inversely associated with liver steatosis in the general US adult population, independent of alcohol intake and other confounders. However, no association was found with liver fibrosis. These findings add to the evidence that cannabinoids may have a protective effect against fatty liver, possibly through modulation of the endocannabinoid system (CB1 and CB2 receptors). The clinical significance is limited by the cross-sectional design, which precludes causal inference, and by reliance on self-reported marijuana use. Further longitudinal studies are needed to confirm these findings and explore the potential therapeutic role of marijuana compounds in preventing or treating nonalcoholic fatty liver disease.