January 2020
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Full text: Tracy, D., Joyce, D., Shergill, S., & Albertson, D. (2020). Kaleidoscope. The British Journal of Psychiatry, 216(1), 62-63. doi:10.1192/bjp.2019.258
Read the full January 2020 Kaleidoscope column in BJPsych for free
This month's Highlights column (A3) notes a reversing of clinical emphasis to sociopsychobio, but we never fully escape biology: why do psychoses persist? Given the young age of onset and the often-devastating impact on social interaction, presumably they should face significant negative evolutionary pressures. Previous Kaleidoscopes have described genetic links with creativity and early hominin language development; Mike Owen, in the Royal Society of Medicine's 2019 Darwin lecture, explained that new mutations continue to arise that will predispose to schizophrenia. Taking an evolutionary perspective, van den Heuvel et al contrast neuroimaging connectome data between homo sapiens and chimpanzee, and the changes observed in schizophrenia.1 They found that the evolutionary advancements in human brain connectivity significantly overlap with the regions of dysconnectivity seen in schizophrenia, an effect not observed in other, less species-specific, mental illnesses – such as depression. These core regions are involved in semantic comprehension, language processing, cognitive control, social cognition, emotional processing and affiliative behaviour: all functions, the authors note, which can be disrupted in psychoses. It is the connections found only in sapiens that are most associated with problems in schizophrenia. Our enriched, specialised brain connectivity, the most complex parts that literally make us human, are those that predispose us to psychosis. For more evolutionary perspectives we commend Riadh Abed's discussions on outgroup intolerance theory2 and the writings of Randy Nesse.3