• Moonen Hanneke Pierre Franciscus Xaverius HPFX Department of Intensive Care Medicine, Gelderse Vallei Hospital, Ede, The Netherlands; Division of Human Nutrition and Heal and Arthur Raymond Hubert Van Zanten.
• Department of Intensive Care Medicine, Gelderse Vallei Hospital, Ede, The Netherlands; Division of Human Nutrition and Health, Wageningen University & Research, Wageningen, The Netherlands.
• Curr Opin Crit Care. 2020 Aug 1; 26 (4): 346-354.

Purpose Of ReviewMitochondrial dysfunction is associated with increased morbidity and mortality during and after critical illness. The concept of adaptive mitochondrial metabolic-bio-energetic downregulation rather than bio-energetic failure during the acute phase of critical illness has gained traction. As mitochondria are not able to utilize substrate during adaptive hibernation and aggressive feeding induces further harm, this condition has consequences for nutrition therapy.Recent FindingsMeeting resting energy expenditure in early critical illness is associated with enhanced oxidative stress and attenuation of autophagy, as is hyperglycemia. The negative effect of early high protein administration remains unclear, whereas fat appears bio-energetically inert. Although antioxidant micronutrients are essential to mitochondrial function, high-dosage studies of single vitamins (C and D) failed to show benefit. Convalescence probably requires increased micronutrient and macronutrient administration to aid anabolism and restore mitochondrial function, although robust data on requirements and actual intake are lacking.SummaryOptimal nutrition therapy in the early phase of critical illness should avoid overfeeding and preserve (adaptive) mitochondrial function. Micronutrient supplementation probably requires a strategic cocktail instead of a high dosage of a single nutrient. Focus on identification of distinct metabolic phases to adapt nutrition during and after critical illness is essential.

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