Epigenetic mechanisms as mediators of environmental risks for psychiatric disorders

Mental illness is a major cause of morbidity and mortality, contributing greatly to public health expenditure across the globe. Accumulating epidemiological data implicate various environmental insults in the aetiology of mental illness. One handicap, limiting the utility of research into the environmental causes of mental illness, is that the mechanisms by which environmental factors mediate susceptibility, either directly or via interactions with genetic polymorphisms, are not well understood. This article discusses the potential role of epigenetic mechanisms in mediating environmentally induced risk via long-lasting changes in gene expression. Epigenetics refers to the heritable, but reversible, regulation of gene function mediated principally through changes in DNA methylation and chromatin structure. Mounting evidence suggests that epigenetic processes can be influenced by exposure to a range of environmental factors external to the organism or cell, especially during key developmental periods such as embryogenesis. Because, unlike pathogenic DNA sequence mutations, epigenetic changes are potentially reversible, they provide a realistic target for the development of novel pharmacological interventions for psychiatric disorders.