Combining proteins with n-3 PUFAs (EPA + DHA) and their inflammation pro-resolution mediators for preservation of skeletal muscle mass

• Published in: Critical care (London, England) Vol. 28; no. 1; p. 38
• Main Authors: Blaauw, Renée, Calder, Philip C, Martindale, Robert G, Berger, Mette M
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 01.02.2024; BioMed Central
• Subjects: Aging; Amino acids; Analysis; Care and treatment; Composition; Illnesses; Inflammation; Kidneys; Medical examination; Mortality; Muscles; Musculoskeletal system; Nutrition therapy; Older people; Omega-3 fatty acids; Parenteral nutrition; Protein biosynthesis; Protein synthesis; Proteins; Sepsis; Switzerland; Lean body mass; Critical illness; Inflammation; Nutrition; Protein
• ISSN: 1364-8535; 1466-609X; 1364-8535; 1366-609X
• DOI: 10.1186/s13054-024-04803-8

The optimal feeding strategy for critically ill patients is still debated, but feeding must be adapted to individual patient needs. Critically ill patients are at risk of muscle catabolism, leading to loss of muscle mass and its consequent clinical impacts. Timing of introduction of feeding and protein targets have been explored in recent trials. These suggest that "moderate" protein provision (maximum 1.2 g/kg/day) is best during the initial stages of illness. Unresolved inflammation may be a key factor in driving muscle catabolism. The omega-3 (n-3) fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are substrates for synthesis of mediators termed specialized pro-resolving mediators or SPMs that actively resolve inflammation. There is evidence from other settings that high-dose oral EPA + DHA increases muscle protein synthesis, decreases muscle protein breakdown, and maintains muscle mass. SPMs may be responsible for some of these effects, especially upon muscle protein breakdown. Given these findings, provision of EPA and DHA as part of medical nutritional therapy in critically ill patients at risk of loss of muscle mass seems to be a strategy to prevent the persistence of inflammation and the related anabolic resistance and muscle loss.