© 2002 The Royal College of Psychiatrists
Bio-social origins of depression in the community
Interactions between social adversity, cortisol and serotonin neurotransmission
Neuroscience and Psychiatry Unit, University of Manchester, Manchester
Institute of Psychiatry, London
Correspondence: Dr Paul Strickland, Neuroscience and Psychiatry Unit, Stopford Building, University of Manchester, Oxford Road, Manchester M13 9PT. Tel: 0161 275 7427; fax: 0161 275 7429; e-mail: P.Strickland{at}man.ac.uk
Declaration of interest Wellcome Trust funding.
See editorial, pp.
99–100, this issue.
Background Social adversity may be a risk factor for depression, by increasing cortisol secretion, which impairs serotonin (5-HT) neurotransmission.
Aims To examine this causal pathway in a community setting.
Method Women who were currently ICD-10 depressed (n=94), vulnerable to depression but not depressed (n=166) and non-vulnerable controls (n=177) were recruited. We assessed social adversity and vulnerability (Life Events and Difficulties Schedule; Self Evaluation and Social Support Scales) and psychiatric state (Schedules for Clinical Assessment in Neuropsychiatry). Salivary cortisol concentrations were measured at 09.00 and 23.00 h. Serotonin function was assessed using prolactin responses to dexfenfluramine.
Results Cortisol concentrations were not increased in the depressed or vulnerable. Morning salivary and serum cortisol were reduced in depression. Evening cortisol was increased after recent life events. Life events and depression were associated with increased prolactin responses.
Conclusions The hypothalamic—pituitary—adrenal axis is sensitive to social stress but does not mediate vulnerability to depression. Exaggerated 5-HT2 receptor responsiveness to stress may play a role in the evolution of depression.
Related articles in BJP:
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- ELIZABETH WALSH
BJP 2002 180: 0.[Full Text] - Cortisol, serotonin and depression: all stressed out?
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BJP 2002 180: 99-100.[Full Text]
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