In this recent paper the authors argue that “multi-organ failure secondary to sepsis may actually represent an adaptive hypometabolic response to preserve ATP homeostasis in the face of a prolonged inflammatory insult.” Unlike organ specific diseases, mitochondrial dysfunction in multiple organ failure may be potentially reversible by careful timing of proper treatment. The authors warn against conventional attempts to jumpstart these “hibernating” organs back to life.

A similar situation may exist during stabilization of some cryonics patients. Instead of delivering oxygen to dysfunctional mitochondria that will only leak from the respiratory chain to generate harmful oxygen and nitrogen species, stabilization technologies may benefit from research into novel strategies to reduce metabolic demand by inhibition of non-essential functional processes in the brain. Systematic study of the biochemistry of hypometabolism in hibernating and estivating animals may provide important clues for such a research agenda.