RT Journal
A1 Smith KA, Fairburn CG, Cowen PJ
T1 SYmptomatic relapse in bulimia nervosa following acute tryptophan depletion
JF Archives of General Psychiatry
JO Archives of General Psychiatry
YR 1999
FD February 1
VO 56
IS 2
SP 171
OP 176
DO 10.1001/archpsyc.56.2.171
UL http://dx.doi.org/10.1001/archpsyc.56.2.171
AB Background 
    Preclinical and clinical studies suggest that lowered brain serotonin neurotransmission may contribute to the pathophysiology of bulimia nervosa (BN). The aim of our study was to test this hypothesis by examining the psychological effects of a dietary-induced impairment in serotonin activity in subjects known to be at risk for manifestation of the clinical syndrome of BN.Methods 
    An 85.8 g amino acid mixture lacking the serotonin precursor tryptophan and a balanced mixture were administered to 10 clinically recovered, medication-free female subjects with a history of BN in a double-blind, crossover design. Twelve healthy female subjects with no history of psychiatric disorder were studied as a comparison group. Observer and self-rated measures of mood and eating disorder cognitions were made for the 7 hours following administration of each amino acid mixture.Results 
    Compared with healthy controls, subjects with a history of BN had significant lowering of mood, increases in ratings of body image concern, and subjective loss of control of eating following the tryptophan-free mixture.Conclusions 
    Our results suggest that diminished serotonin activity may trigger some of the cognitive and mood disturbances associated with BN. Our findings support suggestions that chronic depletion of plasma tryptophan may be one of the mechanisms whereby persistent dieting can lead to the development of eating disorders in vulnerable individuals.