6.3 Epigenetic effects and human mental disorders
McGowan et al. (2009) looked at post-mortem hippocampal tissue from humans, comparing three groups: (i) suicide victims with a history of child abuse; (ii) suicide victims without a history of child abuse, and (iii) non-suicide controls, people with no history of child abuse who had died suddenly.
The researchers found that glucocorticoid receptor (GR) gene expression in the hippocampus of abused suicide victims was lower than in the hippocampus of non-abused suicide victims or controls. In other words, glucocorticoid receptors are proteins made by the cells of the brain (neurons), so they are coded for by genetic information. The epigenetic mechanism silencing GR gene expression was methylation (Box 3). McGowan and colleagues found higher levels of GR gene methylation in abused suicide victims than in non-abused suicide victims or in controls.
The effects of epigenetic modification in humans are undoubtedly hugely complex, as a great many genes besides the GR gene are known to be epigenetically modified by experiential factors. However McGowan et al.’s findings suggest that epigenetic mechanisms could be implicated in the long-term effects of adverse early experience on mental health in humans.
Activity 11 Genes and environment
On balance, does the evidence suggest that emotional disorders such as depression and anxiety are caused by genetic factors or by factors in the environment?
The weight of evidence suggests that both types of factors play a role. Combinations of genetic vulnerabilities and environmental factors may lead to the development of disorders. Environmental factors may also affect the sensitivity of systems such as the stress response system via changes in gene expression (epigenetic effects). Hence both genes and environment play a part in emotional disorders.