Feeding critically ill patients the right 'whey': thinking outside of the box. A personal view

Paul E Marik, Paul E Marik

Abstract

Atrophy of skeletal muscle mass is an almost universal problem in survivors of critical illness and is associated with significant short- and long-term morbidity. Contrary to common practice, the provision of protein/amino acids as a continuous infusion significantly limits protein synthesis whereas intermittent feeding maximally stimulates skeletal muscle synthesis. Furthermore, whey-based protein (high in leucine) increases muscle synthesis compared to soy or casein-based protein. In addition to its adverse effects on skeletal muscle synthesis, continuous feeding is unphysiological and has adverse effects on glucose and lipid metabolism and gastrointestinal function. I propose that critically ill patients' be fed intermittently with a whey-based formula and that such an approach is likely to be associated with better glycemic control, less hepatic steatosis and greater preservation of muscle mass. This paper provides the scientific basis for my approach to intermittent feeding of critically ill patients.

Figures

Fig. 1
Fig. 1
A simplified overview of the anabolic and catabolic pathways in skeletal muscle.AKT= protein kinase b;FOXO-1=forkhead box class O-1; IRS-1=insulin receptor substrate-1; MAFBx=muscle atrophy f-box-1; MURF-1=muscle ring finger protein 1; NF κB= nucelar factor κB; IKK = inhibitor of nuclear factor κB kinase; IκB=inhibitor of nuclear factor κB; 4E-BP1= eukaryotic initiation factor (eIF) 4E binding protein 1; P70S6K = 70-kDa ribosomal protein S6 kinase; mTOR= mammalian target of rapamycin; TNF-α= tumour necrosis factor-α

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