Hostname: page-component-586b7cd67f-g8jcs Total loading time: 0 Render date: 2024-11-23T22:00:54.486Z Has data issue: false hasContentIssue false
  • English
  • Français

Abnormal response to metabolic stress in schizophrenia: marker of vulnerability or acquired sensitization?

Published online by Cambridge University Press:  13 August 2004

M. MARCELIS ,
E. CAVALIER ,
J. GIELEN ,
P. DELESPAUL  and
J. VAN OS
M. MARCELIS
Affiliation:
Department of Psychiatry and Neuropsychology, South Limburg Mental Health Research Network, EURON, Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands; Service de Chimie médicale, University Hospital Liège, Liège, Belgium; Division of Psychological Medicine, Institute of Psychiatry, De Crespigny Park, London SE5 8AF, UK
E. CAVALIER
Affiliation:
Department of Psychiatry and Neuropsychology, South Limburg Mental Health Research Network, EURON, Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands; Service de Chimie médicale, University Hospital Liège, Liège, Belgium; Division of Psychological Medicine, Institute of Psychiatry, De Crespigny Park, London SE5 8AF, UK
J. GIELEN
Affiliation:
Department of Psychiatry and Neuropsychology, South Limburg Mental Health Research Network, EURON, Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands; Service de Chimie médicale, University Hospital Liège, Liège, Belgium; Division of Psychological Medicine, Institute of Psychiatry, De Crespigny Park, London SE5 8AF, UK
P. DELESPAUL
Affiliation:
Department of Psychiatry and Neuropsychology, South Limburg Mental Health Research Network, EURON, Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands; Service de Chimie médicale, University Hospital Liège, Liège, Belgium; Division of Psychological Medicine, Institute of Psychiatry, De Crespigny Park, London SE5 8AF, UK
J. VAN OS
Affiliation:
Department of Psychiatry and Neuropsychology, South Limburg Mental Health Research Network, EURON, Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands; Service de Chimie médicale, University Hospital Liège, Liège, Belgium; Division of Psychological Medicine, Institute of Psychiatry, De Crespigny Park, London SE5 8AF, UK
Get access Rights & Permissions [Opens in a new window]

Abstract

Background. Previous work suggests that individuals with schizophrenia display an altered homovanillic acid (HVA) response to metabolic stress. The present study replicated and extended this paradigm, including individuals with elevated genetic risk for schizophrenia.

Method. Patients with psychosis (n=50), non-psychotic first-degree relatives of patients with psychosis (n=51) and controls without psychosis (n=50) underwent, in randomized order, double-blind administration of placebo and the glucose analogue 2-deoxy-D-glucose (2DG), which induces a mild, transient clinical state of glucoprivation. Plasma HVA and cortisol were assessed twice before the start of the 2DG/placebo infusion (baseline values), as well as four times post infusion. Data were analysed using multi-level random regression techniques.

Results. During the stress condition, significant increases in plasma HVA and cortisol were found. The increase in plasma HVA level during the stress condition was significantly stronger in patients than in controls, whereas this was not the case in relatives v. controls. The increase in plasma cortisol during the stress condition was significantly less in patients than controls, but no significant difference in the increase of plasma cortisol during stress was found in the comparison between relatives and controls.

Conclusions. Patients with psychosis, but not their non-psychotic first-degree relatives, show an altered neurobiological response to metabolic stress, suggesting that this dysregulation is not a genetically transmitted vulnerability, but an illness-related effect, possibly reflecting acquired sensitization of neuroendocrine systems by repeated environmental stressors or repeated stimulation with agonistic drugs.

Type
Research Article
Information
Psychological Medicine , Volume 34 , Issue 6 , August 2004 , pp. 1103 - 1111
Copyright
© 2004 Cambridge University Press

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)