It is apparent that the metabolic response to injury as manifest in hypermetabolism and organ failure is a markedly different process from standard starvation. As such, it seems to have a different set of support principles that are probably better called metabolic support than nutritional support. The best treatment remains prevention by controlling the presence of dead tissue, injured tissue, and infection, and by appropriately restoring and maintaining oxygen transport. With control of the source and the restoration of oxygen transport, the primary mode of support becomes one of metabolic support. This modality is a support tool that appears to "buy time" and help control malnutrition as a comorbidity or comortality. The principles that have evolved in large part have been those of learning to do no harm. The prevention of substrate limited metabolism and effective support of visceral functions is now available until the late stage of the organ failure process. We still cannot control the catabolic stimulus and the autocannibalism of the skeletal muscle mass with the redistribution of nitrogen into the visceral protein mass and the use of amino acids as prime energy sources. The ability to control this stimulus will probably reside in our ability to understand and manipulate the mediator systems. We are now evolving effective support regimens for preserving organ structure and function and for promoting tissue repair. The route of administration as well as the time of administration of the regimen may have some impact on the disease course itself. When metabolic support has been applied in the setting of intelligent surgery and critical care, a progressive reduction in morbidity and mortality has been realized over the last several years such that the current mortality risk for the organ failure syndrome is in the 35 to 40 per cent range overall.