Despite increasing evidence for the role of psychosocial factors in the onset and
continuance of psychosis, the experiences involved are still largely considered the result of a
biogenetic anomaly for which medication is the first-line treatment response. This review
summarizes the extensive literature demonstrating that adverse events involving trauma, loss,
stress, and disempowerment have a central etiological role in psychosis. Evidence is further
presented to show that many neurological changes traditionally considered indicative of a
disease process can in fact be accounted for as secondary effects to the physiology of stress
or the residual of long-term neuroleptic prescription. Particular emphasis is given to the
traumagenic neurodevelopmental model of psychosis, which illustrates how many of the
structural and functional cerebral anomalies observed in adult patients with psychosis
(including dopamine dysregulation, atrophy, hippocampal damage, and overactivity of the
hypothalamic–adrenal–pituitary axis) closely correspond to those in the brains of abused
children. Finally, research is discussed that demonstrates how trauma may manifest in
characteristic symptoms of psychosis, particularly hallucinations and delusions. It is
suggested that if social adversities are of central importance in psychosis, then
psychotherapy that addresses the long term sequelae of those adversities should be
considered an essential aspect of treatment
