The fetal origins of adult mental illness

Abstract

This chapter critically examines the hypothesis that the origins of some adult mental illnesses such as schizophrenia, which is the focus of this review, derive from adverse events in utero, such as maternal nutrition deficiency, infection and hypoxia. The hypothesis was originally derived from neuropathological changes in patients with established schizophrenia that are highly suggestive of impaired neural development occurring around mid-gestation. Increasingly it appears that gestational timing and the severity of the insult, rather than type of insult, plays a critical role in subsequent behavioural outcome. Supporting the neurodevelopmental hypothesis, recent studies have demonstrated that serious mental illnesses such as schizophrenia and afferent disorders are associated firstly with behavioural abnormalities that are present from early childhood, and secondly with ongoing neural injury on serial magnetic resonance imaging through late childhood and adolescence. These data suggest that alterations in brain development during fetal life lead to an evolving damage over the course of childhood before finally being overtly expressed in early adulthood. Current data suggest that the initial loss of cells in utero leads to a long-term remodelling of the brain that is mediated by upregulation of physiological apoptosis. That such adult illnesses present with early behavioural and physiological clues, are progressive and not static in nature, and that the process is potentially governed by common mechanisms regardless of cause, offers significant new opportunities for intervention and treatment. ©2006 Eurekah.com and Springer Science+Business Media.