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Disturbed Endocrine Function in the Psychoses

I: Disordered Homeostasis or Disease Process?

Published online by Cambridge University Press:  02 January 2018

L. J. Whalley ,
J. E. Christie ,
D. H. R. Blackwood ,
J. Bennie ,
H. Dick ,
I. M. Blackburn  and
G. Fink
L. J. Whalley*
Affiliation:
MRC Brain Metabolism Unit, University Department of Psychiatry, Royal Edinburgh Hospital, Morningside Park, Edinburgh EH10 5HF
J. E. Christie
Affiliation:
MRC Brain Metabolism Unit, University Department of Psychiatry, Royal Edinburgh Hospital, Morningside Park, Edinburgh EH10 5HF
D. H. R. Blackwood
Affiliation:
MRC Brain Metabolism Unit, University Department of Psychiatry, Royal Edinburgh Hospital, Morningside Park, Edinburgh EH10 5HF
J. Bennie
Affiliation:
MRC Brain Metabolism Unit, University Department of Psychiatry, Royal Edinburgh Hospital, Morningside Park, Edinburgh EH10 5HF
H. Dick
Affiliation:
MRC Brain Metabolism Unit, University Department of Psychiatry, Royal Edinburgh Hospital, Morningside Park, Edinburgh EH10 5HF
I. M. Blackburn
Affiliation:
MRC Brain Metabolism Unit, University Department of Psychiatry, Royal Edinburgh Hospital, Morningside Park, Edinburgh EH10 5HF
G. Fink
Affiliation:
MRC Brain Metabolism Unit, University Department of Psychiatry, Royal Edinburgh Hospital, Morningside Park, Edinburgh EH10 5HF
*
∗Correspondence
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Abstract

Plasma concentrations of prolactin, growth hormone, cortisol, TSH, and the neurophysins were measured over 17 hours in 98 newly admitted psychiatric patients and 35 control subjects. Seventy patients had been free of psychotropic medication for three months. Patients with schizoaffective mania (SAM) differed significantly from control subjects by increased plasma Cortisol concentrations and decreased night-time TSH concentrations. The latter were also significantly lower than in both schizophrenic and manic disorder patients. Plasma Cortisol was increased to a lesser extent in other psychotic subgroups, and increases in prolactin were most marked in the affective psychoses. There was little diagnostic specificity for psychoses other than SAM. Higher Cortisol and prolactin levels may be due to the stimulatory effect of serotonergic pathways, but the neural mechanisms underlying lower night-time TSH levels in SAM are not known. The findings are not consistent with the view (a) that the hormonal changes of the psychoses simply reflect a non-specific response to stress, or (b) that the biological abnormalities of the psychoses can be accounted for by a single continuum of disturbance.

Type
Papers
Information
The British Journal of Psychiatry , Volume 155 , Issue 4 , October 1989 , pp. 455 - 461
Copyright
Copyright © Royal College of Psychiatrists 1989 

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