Background: Patients with metabolic syndrome represent a particularly vulnerable population for alcohol-related liver disease progression. However, real-world longitudinal data evaluating the impact of alcohol abstinence on liver fibrosis dynamics in this group remain limited. Methods: We conducted a prospective observational study including hospitalized adults with metabolic syndrome and chronic alcohol consumption. Clinical, laboratory, and non-invasive fibrosis markers—fibrosis-4 index (FIB-4), aspartate aminotransferase-to-platelet ratio index (APRI), and transient elastography—were assessed at baseline and after 6 and 12 months of individual follow-up. Patients were classified according to alcohol consumption status during follow-up. Longitudinal and comparative analyses were performed. Results: At baseline, patients were classified as having alcoholic steatosis (56.3%), alcoholic steatohepatitis (25.0%), or alcoholic cirrhosis (18.7%). During follow-up, 72.9% of patients achieved sustained alcohol abstinence. Abstinent patients demonstrated significant improvements in liver stiffness, FIB-4, and APRI scores at 12 months (all p < 0.001), while non-abstinent patients showed progressive worsening of fibrosis markers. Gamma-glutamyl transferase levels were independently associated with fibrosis severity at baseline. Conclusions: This prospective real-world study suggests that alcohol abstinence is associated with favorable longitudinal changes in non-invasive liver fibrosis markers in patients with metabolic syndrome. Given the non-invasive nature of the diagnostic approach and the relatively small sample size, these findings should be considered hypothesis-generating. Further studies with larger cohorts are warranted to better elucidate the interaction between metabolic risk factors, alcohol consumption, and liver disease progression.

Background: Metabolic syndrome (MetS) and alcohol-related liver disease (ALD) are increasingly recognized as interconnected disorders linked by shared mechanisms of lifestyle-driven metabolic reprogramming. Alterations in systemic and hepatic metabolic pathways—including insulin signaling, lipid metabolism, mitochondrial bioenergetics, and redox homeostasis—reduce hepatic resilience to alcohol exposure and accelerate liver disease progression. Objective: This narrative review aims to integrate clinical, epidemiological, and mechanistic evidence published over the past two decades to examine how modifiable lifestyle factors contribute to metabolic reprogramming linking metabolic syndrome and alcohol-related liver disease with prioritization of high-level clinical evidence (cohort studies, meta-analyses, and guidelines). Key Findings: Modifiable lifestyle exposures such as alcohol consumption, cigarette smoking, unhealthy dietary patterns, and physical inactivity converge on common metabolically mediated pathways, including insulin resistance, dysregulated lipid metabolism and lipotoxicity, mitochondrial dysfunction, oxidative stress, chronic low-grade inflammation, and gut–liver axis perturbations. These processes are reflected in altered metabolite profiles involving lipid species, bile acids, tricarboxylic acid cycle intermediates, and microbiota-derived metabolites, shaping a metabolic–hepatic continuum. Among these, alcohol consumption and metabolic dysfunction show the strongest and most consistent associations with liver disease progression, with evidence supporting synergistic rather than additive effects. Conclusions: The coexistence of metabolic dysfunction and alcohol exposure is consistently associated with synergistic worsening of liver-related outcomes, including fibrosis progression, cirrhosis, and hepatocellular carcinoma. Recognition of metabolic alcohol-related liver disease (MetALD) underscores the need for integrated lifestyle-based strategies targeting alcohol consumption, smoking cessation, dietary quality, and physical activity to modulate shared metabolic and inflammatory pathways. A metabolically informed, systems-level approach may improve risk stratification, prevention, and management across the metabolic–hepatic continuum.

Background: Physical activity and Mediterranean diet adherence are important components of lifestyle management in patients with metabolic syndrome (MetS) and alcohol-related liver disease (ALD). We evaluated 12-month changes in lifestyle, metabolic parameters, and non-invasive fibrosis-related markers and explored their associations. Methods: In this 12-month prospective observational study, 50 adults with MetS and ALD were assessed at baseline, 6 months, and 12 months. Physical activity (IPAQ-SF), Mediterranean diet adherence (MEDAS-14), alcohol consumption status, liver stiffness, FIB-4, and APRI were evaluated. Exploratory multivariable analyses adjusted for sustained alcohol abstinence, baseline liver disease severity, age, sex, and change in waist circumference. Results: Physical activity increased from 455.2 ± 154.1 to 910.3 ± 275.4 MET-min/week and MEDAS-14 from 4.32 ± 0.62 to 7.92 ± 0.92 (both p < 0.001). Waist circumference, fasting glucose, LDL cholesterol, and triglycerides decreased significantly (all p < 0.001). At 12 months, physical activity and Mediterranean diet adherence were inversely correlated with liver stiffness, FIB-4, and APRI (all p ≤ 0.010). However, changes in IPAQ-SF and MEDAS-14 were not significantly associated with changes in non-invasive fibrosis-related markers after multivariable adjustment. Sustained alcohol abstinence (74.0%) was consistently associated with more favorable changes in all three markers. Conclusions: Improvements in physical activity and Mediterranean diet adherence occurred alongside favorable metabolic and liver-related changes, but their associations with non-invasive fibrosis-related markers were not maintained after adjustment for major potential confounders. Sustained alcohol abstinence was consistently associated with more favorable changes in these markers.