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The effect of a nutritional source of tryptophan on dieting-induced changes in brain 5-HT function

Published online by Cambridge University Press:  30 October 2003

M.-J. ATTENBURROW
Affiliation:
University Department of Psychiatry, Warneford Hospital, Oxford; and Department of Psychology, University of Bangor
C. WILLIAMS
Affiliation:
University Department of Psychiatry, Warneford Hospital, Oxford; and Department of Psychology, University of Bangor
J. ODONTIADIS
Affiliation:
University Department of Psychiatry, Warneford Hospital, Oxford; and Department of Psychology, University of Bangor
J. POWELL
Affiliation:
University Department of Psychiatry, Warneford Hospital, Oxford; and Department of Psychology, University of Bangor
F. VAN DE OUDERAA
Affiliation:
University Department of Psychiatry, Warneford Hospital, Oxford; and Department of Psychology, University of Bangor
M. WILLIAMS
Affiliation:
University Department of Psychiatry, Warneford Hospital, Oxford; and Department of Psychology, University of Bangor
P. J. COWEN
Affiliation:
University Department of Psychiatry, Warneford Hospital, Oxford; and Department of Psychology, University of Bangor

Abstract

Background. Dieting in healthy women results in a decrease in the availability of tryptophan (TRP), the amino-acid precursor of serotonin (5-HT), for brain 5-HT synthesis. This is associated with increases in the prolactin response to 5-HT drug challenge suggesting a ‘supersensitivity’ of 5-HT neuroendocrine responses. The aim of the study was to assess whether increased TRP intake during dieting would prevent the changes in TRP availability and 5-HT neuroendocrine function.

Method. Fifty female subjects underwent a 1000 kcal daily diet for 3 weeks. In the final week of the diet subjects were randomly allocated to receive either nutritionally-sourced TRP (1·8 g daily) or placebo in a double-blind, parallel group, design.

Results. TRP supplementation failed to modify the dieting-induced reduction in fasting TRP availability to the brain. However, in contrast to placebo-treated subjects, subjects receiving additional TRP did not show enhanced prolactin responses to intravenous TRP challenge.

Conclusions. The decrease in TRP availability produced by dieting may be due to increased TRP metabolism rather than decreased TRP intake. While TRP treatment did not increase fasting TRP availability it may have modified the effect of dieting on brain 5-HT function. Further studies will be needed to see if this effect of TRP has consequences for the effectiveness of dieting as means of weight control.

Type
Research Article
Copyright
© 2003 Cambridge University Press

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