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Volume 149, Issue 1, Pages 97-104 (15 January 2007)


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Olfactory sensitivity through the course of psychosis: Relationships to olfactory identification, symptomatology and the schizophrenia odour

Warrick J. BreweraCorresponding Author Informationemail address, Stephen J. Woodbd, Christos Pantelisbe, Gregor E. Bergera, David L. Copolovc, Patrick D. McGorrya

Received 27 March 2005; received in revised form 22 December 2005; accepted 6 March 2006.

Abstract 

There is some evidence for an unusual body odour in schizophrenia that has been linked to a hexenoic acid derivative (trans-3-methyl-2-hexenoic acid; MHA). Poor body odour has been linked to increased negative symptoms and reduced olfactory identification ability. However, the relationship between these findings and MHA, including olfactory sensitivity for MHA, has not been examined. Olfactory sensitivity thresholds were assessed for MHA and n-butyl-alcohol (NBA), in normal controls (CTL; n=24), patients with chronic schizophrenia (CHR; n=32) and a first-episode psychosis cohort (FE; n=31). In addition, forced choice detection of the pheromonal steroids 5-α-androst-16-en-3-one, androsterone-sulphate and estrone-3-sulphate was performed along with a measure of olfactory identification. CHR patients had significantly reduced sensitivity to MHA, but not NBA, compared to FE and CTL subjects. While sensitivity to pheromones was not different between the groups, CHR patients who could not detect them also showed poorer sensitivity to MHA. Further, the CHR group showed a significant association between reduced MHA sensitivity and greater levels of disorganised and negative symptoms. No relationships between identification and sensitivity for any substance were found. Our findings are the first to report reduced sensitivity for MHA in chronic schizophrenia patients, in the absence of similar impairment for more traditionally used substances. This may be linked to olfactory habituation effects, abnormal chemical processing or a genetic predisposition.

a ORYGEN Research Centre, Melbourne, Victoria, Australia

b Melbourne Neuropsychiatry Centre, Department of Psychiatry, University of Melbourne, Victoria, Australia

c Monash University, Melbourne, Australia

d Brain Research Institute, Melbourne, Victoria, Australia

e Howard Florey Institute, University of Melbourne, Victoria, Australia

Corresponding Author InformationCorresponding author. ORYGEN Research Centre (Locked Bag 10), Parkville, Vic. 3052, Australia. Tel.: +61 3 9342 2800; fax: +61 3 9342 2858.

PII: S0165-1781(06)00077-1

doi:10.1016/j.psychres.2006.03.005


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