Lifestyle, Dietary Interventions, and Biochemical Markers in the Management of Chronic Hepatobiliary and Gastric Diseases

Abstract

Introduction: Chronic hepatobiliary diseases — including metabolic dysfunction-associated steatotic liver disease (MASLD), chronic viral hepatitis, cirrhosis, and cholelithiasis — and chronic gastric diseases — including gastroesophageal reflux disease (GERD), peptic ulcer disease (PUD), and Helicobacter pylori-associated gastritis — share modifiable risk factors centered on diet, body weight, alcohol, tobacco, and sedentary lifestyle. Despite expanding pharmacotherapy, lifestyle and dietary interventions remain first-line for many conditions and adjunctive across all of them. Objective: To synthesize current evidence on lifestyle and dietary interventions, supported by biochemical markers, in the management of chronic hepatobiliary and gastric diseases in adults, and to propose an integrated nutrology-informed framework. Methods: A structured narrative review was conducted using PubMed/MEDLINE, Scopus, Web of Science, and the Cochrane Library for studies published between January 2000 and December 2025. Search terms combined "diet," "lifestyle," "Mediterranean diet," "weight loss," "physical activity" with "MASLD," "chronic hepatitis," "cirrhosis," "gallstones," "GERD," "peptic ulcer," and "Helicobacter pylori," together with "biochemical markers," "FIB-4," "ALT," and "AST." Randomized controlled trials, cohort studies, systematic reviews, and authoritative guidelines published in English were eligible. Results: In MASLD, weight loss of ≥5% reduces hepatic steatosis, ≥7% improves necroinflammation, and ≥10% stabilizes or reverses fibrosis; the Mediterranean diet reduces hepatic fat by approximately 39% over 12 weeks. In cirrhosis, individualized protein-energy nutrition, branched-chain amino acid supplementation, and sarcopenia prevention improve survival. In gallstone disease, gradual weight loss, high-fiber, low-refined-carbohydrate diets, coffee, and physical activity reduce incidence, whereas crash dieting precipitates stones. In GERD and PUD, weight reduction, smoking cessation, alcohol moderation, and avoidance of trigger foods complement acid suppression In H. pylori-associated gastritis, polyphenol-rich diets (broccoli sprouts, green tea, cranberry) and probiotics improve eradication and reduce gastric inflammation. Across all conditions, simple biochemical and non-invasive markers (ALT/AST, GGT, FIB-4, lipid panel, HbA1c, hsCRP) provide objective monitoring. Conclusion: Lifestyle and dietary interventions — Mediterranean-style nutrition, gradual weight management, physical activity, alcohol moderation, and tobacco cessation — combined with monitoring of accessible biochemical markers, form a unifying nutrological strategy across the hepatobiliary–gastric disease spectrum and should be systematically integrated into routine practice.