W. Kaye et al., SEROTONIN NEURONAL FUNCTION AND SELECTIVE SEROTONIN REUPTAKE INHIBITOR TREATMENT IN ANOREXIA AND BULIMIA-NERVOSA, Biological psychiatry, 44(9), 1998, pp. 825-838
Anorexia nervosa (AN) and bulimia nervosa (BN) are disorders character
ized by aberrant patterns of feeding behavior and weight regulation, a
nd disturbances in attitudes toward weight and shape and the perceptio
n of body shape. Emerging data support the possibility that substantia
l biologic and genetic vulnerabilities contribute to the pathogenesis
of AN and BN. Multiple neuroendocrine and neurotransmitter abnormaliti
es have been documented in AN and BN, but for the most part, these dis
turbances are state-related and tend to normalize after symptom remiss
ion and weight restoration; however, elevated concentrations of 5-hydr
oxyindoleacetic acid in the cerebrospinal fluid after recovery suggest
that altered serotonin activity in RN and BN is a trait-related chara
cteristic. Elevated serotonin activity is consistent with behaviors fo
und after recovery from AN and BN, such as obsessionality with symmetr
y and exactness, harm avoidance, perfectionism, and behavioral overcon
trol. In BN, serotonergic modulating antidepressant medications suppre
ss symptoms independently of their antidepressant effects. Selective s
erotonin reuptake inhibitors (SSRIs) are not useful when AN subjects a
re malnourished and underweight; however, when given after weight rest
oration, fluoxetine may significantly reduce the extremely high rate o
f relapse normally seen in AN. Nonresponse to SSRI medication in ill A
N subjects could be a consequence of an inadequate supply of nutrients
, which are essential to normal serotonin synthesis and function. Thes
e data raise the possibility that a disturbance of serotonin activity
may create a vulnerability for the expression of a cluster of symptoms
that are common to both AN and BN and that nutritional factors may af
fect SSRI response in depression, obsessive-compulsive disorder, or ot
her conditions characterized by disturbances in serotonergic pathways.
(C) 1998 Society of Biological Psychiatry.