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Comment & Response
February 2016

Use of 5-Hydroxytryptophan Labeled With Carbon 11 in Social Anxiety Disorder

Author Affiliations
  • 1Duke University Medical Center, Department of Cell Biology, Durham, North Carolina

Copyright 2016 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.

JAMA Psychiatry. 2016;73(2):177. doi:10.1001/jamapsychiatry.2015.2466

To the Editor In their article, Frick et al1 reported increased brain uptake of a 5-hydroxytryptophan labeled with carbon 11 ([11C]5-HTP) tracer in social anxiety disorder (SAD). On this ground, and taking into consideration preliminary findings of reduced 5-HT1A receptor binding potential in SAD, Frick et al1 proposed that elevated extracellular serotonin causes SAD. Elevating extracellular serotonin (with a selective serotonin reuptake inhibitor) is also a US Food and Drug Administration–approved therapy for SAD. Hence, according to Frick et al,1 in SAD, cause and cure are the same, which, although not inconceivable, appears difficult to reconcile. The Frick et al1 findings are interesting; however, the finding that uptake of an exogenous [11C]5-HTP tracer is a good indicator of endogenous serotonin synthesis, let alone extracellular serotonin, is questionable. Given the complexity of serotonin neurobiology, the functional implications for serotonin function of altered [11C]5-HTP uptake are unclear.