Integrating downstream mediators of omega-3 fatty acids into enteral nutrition for improved patient care: an expert panel consensus

Abstract

Acute inflammation is a crucial biological response necessary for host defense and tissue repair, but unresolved inflammation can contribute to adverse outcomes across critical illness, cardiovascular disease, neurodegeneration, and cancer. Emerging evidence emphasizes that the resolution of inflammation is an active biosynthetic process mediated in part by specialized pro-resolving mediators (SPMs), lipid-derived molecules generated from omega-3 polyunsaturated fatty acids (PUFAs) such as eicosapentaenoic acid (C20:5n-3, EPA) and docosahexaenoic acid (C22:6n-3, DHA). These mediators—including resolvins, protectins, and maresins—exert potent immunomodulatory actions that restore tissue homeostasis and attenuate inflammation without immunosuppression. Despite the established role of SPMs, clinical and preclinical studies demonstrate that SPM biosynthesis is often impaired in disease states, limiting the efficacy of omega-3 PUFA-based nutritional interventions. To explore the potential of standardized SPM enrichment in enteral nutrition (EN), a multidisciplinary panel of experts conducted a Delphi-based consensus process. Consensus statements were developed supporting the rationale for enriching EN with preformed SPMs or their stable precursors to overcome compromised endogenous biosynthesis and enhance clinical benefits. Preliminary human studies suggest that such enrichment may reduce inflammation, improve immune function, and contribute to better outcomes in conditions such as obesity, atherosclerosis, infections, and chronic pain. The panel emphasized the need for rigorously designed clinical trials to determine whether enteral SPMs have measurable clinical effects and, if so, to define effective dosing strategies. Overall, SPM-enriched EN represents a potential advancement in the nutritional modulation of inflammation, warranting further investigation to guide evidence-based clinical application.

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ORCID for Philip C. Calder: orcid.org/0000-0002-6038-710X

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