Alcohol Intake, Cardiometabolic Risk, Fibrosis, and Gut Microbiota in Steatotic Liver Disease: A Population-Based Health Checkup StudyOriginal paper
Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease, four years before the first published case study.
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Background: The real-world risk profiles of newly defined steatotic liver disease (SLD) subtypes-MASLD, MetALD, and ALD-remain incompletely described in community settings. Methods: A cross-sectional analysis of 950 health-checkup participants was conducted. SLD (CAP ≥ 248 dB/m) and significant fibrosis (LSM ≥ 7.0 kPa) were evaluated by transient elastography. Associations between alcohol intake, cardiometabolic factors, fibrosis, and gut microbiota (16S rRNA sequencing) were assessed. Results: Among 950 participants, 310 (33%) had SLD (MASLD, n = 222; MetALD, n = 41; ALD, n = 23). Treated as a continuous exposure, higher alcohol intake was significantly correlated with elevated systolic/diastolic blood pressure, triglycerides, AST, and γ-GTP, but inversely correlated with HOMA-IR (all p < 0.05). In multivariable logistic regression adjusting for cardiometabolic factors, BMI was the only independent predictor of fibrosis (adjusted OR 1.22, 95% CI 1.11-1.35, p < 0.01), whereas alcohol intake showed no independent association. Furthermore, microbiota analysis revealed that ALD-related SLD was characterized by significant depletion of Blautia and enrichment of Gemella (FDR q < 0.05) compared to non-SLD controls, indicating an alcohol-associated dysbiosis signature. Conclusions: In early-stage SLD, alcohol intake continuously exacerbates cardiometabolic risk factors, whereas fibrosis is predominantly driven by BMI. These findings support quantitative alcohol/BMI integration for risk stratification, alongside microbiota profiling to detect ALD-related dysbiosis.