Bio-social origins of depression in the community

Abstract

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-HT(2) receptor responsiveness to stress may play a role in the evolution of depression.