Medical nutrition therapy in incretin-treated obesity-related heart failure with preserved ejection fraction.

Glucagon-like peptide-1 receptor agonists and dual agonists of the glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 receptors, exemplified by semaglutide and tirzepatide, respectively, have reshaped care for obesity-related heart failure with preserved ejection fraction (HFpEF). Their benefits extend beyond weight reduction to symptoms and physical function and, for tirzepatide, a lower risk of worsening heart failure. Yet kilograms lost do not reveal whether treatment preferentially reduces harmful adiposity, preserves muscle function, or maintains nutritional adequacy. Against this background, we examine how medical nutrition therapy (MNT) can be integrated with incretin-based therapy to support high-quality weight loss-a working construct used here to denote loss of excess adiposity without avoidable compromise of nutritional status or functional reserve. The discussion centers on three linked questions: how appetite suppression and gastrointestinal intolerance alter nutritional risk; how body composition relates to muscle and patient-centered outcomes; and how nutrition care should evolve from treatment initiation through plateau, maintenance, and discontinuation. Available evidence supports early nutrition assessment, attention to protein and overall diet quality, and coordinated resistance and aerobic exercise, while showing that body composition cannot replace direct assessment of strength, walking capacity, symptoms, and health status. We therefore outline a phase-based MNT pathway for obesity-related HFpEF, while emphasizing that no randomized trial has tested a protocolized nutrition program alongside incretin-based therapy in this population. The next advance should be judged not only by the amount of weight lost, but by whether that loss is safe, function-preserving, durable, and meaningful to patients.