Patients with eating disorders (EDs) exhibit several clinical features and biologic
findings indicative of serotonin (5-hydroxytryptamine, 5-HT) dysregulation. These
include feeding disturbances, depression and suicide, impulsivity and violence, anxiety
and harm avoidance, obsessive-compulsive features, seasonal variation of symptoms,
as well as disturbances in neuroendocrine and vascular tissues, as well as other neurochemical
systems linked to 5-HT, such as temperature. This review attempts to integrate available
results from controlled studies in humans, with particular focus on cerebrospinal
fluid (CSF), platelet and plasma studies, as well as pharmacologic challenge strategies
using a variety of serotonergic agents. Taken together, these findings support the
concept of altered post-synaptic, hypothalamic 5-HT receptor sensitivity in bulimia
nervosa (BN), regardless of the presence of anorexia nervosa (AN) or major depression
(MD), although these conditions may be associated with other disturbances in 5-HT
function, perhaps pre-synaptic ones. The observation that different response measures
of 5-HT function in the same subjects may be simultaneously increased, decreased and
no different in patients compared to controls is consistent with a 5-HT dysregulation
hypothesis. It may be that a variety of psychobiological stressors, such as dieting,
binge-eating, purging, drug abuse, photoperiodic changes, as well as psychosocial-interpersonal
stressors, perturb and interact with an already vulnerable 5-HT system.