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Effect of acute tryptophan depletion on CO₂-induced anxiety in patients with panic disorder and normal volunteers^*

Department of Psychiatry, Manchester Royal Infirmary, Manchester

J. F. W. DEAKIN, PhD and I. M. ANDERSON, MD

Department of Psychiatry, University of Manchester, Manchester

Declaration of interest This study was supported by an MRC project grant.

^* Previously presented at the Annual Meeting of the British Association for Psychopharmacology in association with the British Neuropsychiatry Association, 16-19 July 1995, Cambridge.

Correspondence: Dr I. M. Anderson, University of Manchester Department of Psychiatry, Room 9809, Stopford Building, University of Manchester, Oxford Road, Manchester M13 9PT, UK. Tel: 0161 276 5396; Fax: 0161 273 2135; e-mail: ian.anderson{at}man.ac.uk

Background Uncertainties remain about the role of serotonin in the aetiology and treatment of panic disorder.

Aims To investigate the effect of reducing brain serotonin function on anxiety at rest, and following 5% CO₂ provocation in normal controls and patients with panic disorder.

Method Twenty drug-free patients with DSM — III — R panic disorder and 19 controls received a tryptophan-free amino acid drink on one occasion and a control drink on the other in a double-blind, balanced protocol. 5% CO₂ was given as a panic challenge after 270 minutes.

Results Plasma tryptophan fell by more than 80% both patients and controls after the tryptophan-free drink. Tryptophan depletion did not alter resting anxiety. In patients alone, tryptophan depletion caused a greater anxiogenic response and an increased rate of panic attacks (9 v. 2, P<0.05) after 5% CO₂ challenge. No normal volunteers panicked.

Conclusions Serotonin may directly modulate panic anxiety in patients with panic disorder. This may underlie the efficacy of serotonergic antidepressants in treating panic disorder.

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