Myths and facts about diet in metabolic dysfunction-associated steatotic liver disease—part II: Nutrition during incretin-based therapy

Incretin-based therapies, including glucagon-like peptide-1 (GLP-1) receptor agonists and GLP-1-based co-agonists, have shown histological benefit in metabolic dysfunctionassociated steatotic liver disease (MASLD); semaglutide has received regulatory approval for non-cirrhotic steatohepatitis with F2-F3 fibrosis, and current guidance recommends nutritional and sarcopenia assessment during treatment.However, marked appetite suppression may compromise diet quality and increase the risk of inadequate protein and micronutrient intake and of lean mass loss, particularly when weight loss is rapid or unsupervised.In this review, part II of our myths-and-facts series, we address a single myth: That incretin therapy makes nutritional care unnecessary.Withdrawal trials show that weight and cardiometabolic benefits are not maintained after discontinuation and that lifestyle intervention alone does not replace the drug's effect; whether structured nutritional care limits weight regain remains unknown.We propose 11 literatureinformed, risk-stratified practical recommendations covering baseline nutritional and body-composition assessment; alcohol screening; a Mediterranean-style pattern adapted to local foods; individualized protein targets (usually 1.2-1.5 g/kg/day) with progressive resistance training; micronutrient and bone monitoring; hydration and fiber strategies; and dietary management of gastrointestinal events.These are not consensus-based guidelines and are mostly extrapolated from obesity and general incretin-treated populations.Patient experience and lean MASLD remain underexplored in incretin research.