Barcelona snapshots

Prof. Sir Robin M. Murray

Sir Robin M. Murray psiquiatra Controversias Psiquiatría Barcelona
King's College London, Reino Unido
Ponencia Los modelos plausibles necesitan integrar lo psicosocial y lo biológico
Fecha Jueves, 19 de Abril 2018
Hora 18:00 a 18:45
Mesa redonda Modelos para explicar la complejidad

BIOGRAFÍA

Robin Murray is Professor of Psychiatric Research at the Institute of Psychiatry, Psychology and Neuroscience, Kings College, and indeed has spent most of his working life there apart from one year at NIMH in the USA; fortunately the latter did him relatively little harm. His particular interest is in psychosis. He was one of the first to suggest that schizophrenia was in part a neurodevelopmental disorder, and he and his colleagues have contributed to the understanding that environmental factors such as obstetric events, drug abuse and social adversity dysregulate striatal dopamine and thus increase the risk of psychosis; he is currently most interested in gene-environmental interactions. He is also involved in testing new treatments for psychotic illnesses, and cares for people with psychosis at the South London and Maudsley NHS Trust. He has written over 800 articles, not all of them boring! He is the most frequently cited psychosis researcher outside the USA, has supervised 72 PhDs and 12 MD Theses, and 40 of his students have become full professors. He was elected a Fellow of the Royal Society in 2010 and received a knighthood in 2011.

RESUMEN

A recent study encompassing 16 sites across 5 European countries shows that the incidence varied widely, with the figures for South London being 5-10 times higher than in some Southern European sites. These differences presumably reflect differences in exposure to risk factors.

In the last 15 years we have learned a great deal about the environmental risk factors for psychosis. Many of these are social – childhood adversity, migration/ethnic minority status/bullying/ adverse life events. However, there are also non-social factors such as obstetric events (e.g. prenatal infection, perinatal hypoxia), and drug misuse. Such environmental risk factors increase risk of psychosis by biological means. Some such as adverse obstetric events impair neurodevelopment. Others such as abuse of drugs such as amphetamines, cocaine and cannabis impact on striatal dopamine. Recent studies show that exposure to childhood adversity, migration and acute social stress also increase striatal dopamine.

However, it remains the case that only a minority of those exposed to the above risk factors become psychotic while others develop other psychiatric disorders (e.g. depression, drug dependence) and yet other remain perfectly healthy. Genetic factors are likely to play a role in this. The huge PGC study has now identified some 250 genetic loci significantly associated with schizophrenia. Each of these polygenes has only a very small effect but cumulatively they account for about 30% of the variance in occurrence of schizophrenia.

A crucial issue is to understand the interplay between genetic and environmental factors. Is the effect merely additive, or is there a biological synergism? And do environmental risk factors interact simply with the overall genetic loading (as measured by the polygenic risk score), or do different environmental risk factors interact with genetically determined pathways? One might suspect that the genes encoding vulnerability to child abuse will be different to those predisposing to cannabis-associated psychosis.

REFERENCIAS

[PDF] Murray R, et al (2017). 30 Years on: How the Neurodevelopmental Hypothesis of Schizophrenia Morphed into the Developmental Risk Factor Model of Psychosis, Schizophrenia Bulletin, Volume 43, Issue 6, 21 October 2017, Pages 1190–1196, https://doi.org/10.1093/schbul/sbx121

[web] Murray R (2016). Mistakes I Have Made in My Research Career, Schizophrenia Bulletin, Volume 43, Issue 2, 1 March 2017, Pages 253–256, https://doi.org/10.1093/schbul/sbw165

[web] Murray R, et al (2015). Bridging the gap between research into biological and psychosocial models of psychosis, Shanghai Archives of Psychiatry. 2015;27(3):139-143. doi:10.11919/j.issn.1002-0829.215067.

[web] Howes O, Murray R (2013). Schizophrenia: an integrated sociodevelopmental-cognitive model, Lancet. 2014;383(9929):1677-1687. doi:10.1016/S0140-6736(13)62036-X.