Prolonged sleep deprivation in rats causes an unexplained hypercatabol
ic state, secondary malnutrition symptoms, and mortality. The nature o
f the vital impairment has long been a mystery. Its determination woul
d help to elucidate the type of organic dysfunction that sleep prevent
s. There are no gross detectable disturbances in intermediary metaboli
sm, clinical chemistry, or hematological indexes that provide substant
ial clues to the mediation of sleep-deprivation effects. Furthermore,
postmortem examinations reveal no systematic morphological or histopat
hological findings. Taken together, the cachexia and the absence of ev
idence of structural damage or organ dysfunction pointed to involvemen
t of a regulatory system that was diffuse, possibly the immune system.
Blood cultures revealed invasion by opportunistic microbes to which t
here was no febrile response. These results suggest that the life-thre
atening condition of prolonged sleep deprivation is a breakdown of hos
t defense against indigenous and pathogenic microorganisms.