Tryptophan is an
essential amino acid whose metabolites play key roles in diverse physiological processes. Due to low reserves in the body, especially under various catabolic conditions,
tryptophan deficiency manifests itself rapidly, and both the
serotonin and
kynurenine pathways of metabolism are clinically significant in
critically ill patients. In this review, we highlight these pathways as sources of
serotonin and
melatonin, which then regulate neurotransmission, influence circadian rhythm, cognitive functions, and the development of
delirium. Kynurenines serve important signaling functions in inter-organ communication and modulate endogenous
inflammation. Increased plasma
kynurenine levels and
kynurenine-
tryptophan ratios are early indicators for the development of
sepsis. They also influence the regulation of skeletal muscle mass and thereby the development of polyneuromyopathy in
critically ill patients. The modulation of
tryptophan metabolism could help prevent and treat age-related disease with low grade chronic
inflammation as well as
post intensive care syndrome in all its varied
manifestations: cognitive decline (including
delirium or
dementia), physical impairment (catabolism,
protein breakdown, loss of muscle mass and tone), and mental impairment (depression, anxiety or
post-traumatic stress disorder).