Behavioral and Brain Sciences

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Psychosis and autism as diametrical disorders of the social brain

Bernard Crespia1 and Christopher Badcocka2

a1 Killam Research Professor, Department of Biosciences, Simon Fraser University, Burnaby, BC V5A 1S6, Canada crespi@sfu.ca http://www.sfu.ca/biology/faculty/crespi/

a2 Department of Sociology, London School of Economics, London WC2A 2AE, United Kingdom C.Badcock@lse.ac.uk http://www.lse.ac.uk/collections/sociology/whoswho/badcock.htm

Abstract

Autistic-spectrum conditions and psychotic-spectrum conditions (mainly schizophrenia, bipolar disorder, and major depression) represent two major suites of disorders of human cognition, affect, and behavior that involve altered development and function of the social brain. We describe evidence that a large set of phenotypic traits exhibit diametrically opposite phenotypes in autistic-spectrum versus psychotic-spectrum conditions, with a focus on schizophrenia. This suite of traits is inter-correlated, in that autism involves a general pattern of constrained overgrowth, whereas schizophrenia involves undergrowth. These disorders also exhibit diametric patterns for traits related to social brain development, including aspects of gaze, agency, social cognition, local versus global processing, language, and behavior. Social cognition is thus underdeveloped in autistic-spectrum conditions and hyper-developed on the psychotic spectrum.;>We propose and evaluate a novel hypothesis that may help to explain these diametric phenotypes: that the development of these two sets of conditions is mediated in part by alterations of genomic imprinting. Evidence regarding the genetic, physiological, neurological, and psychological underpinnings of psychotic-spectrum conditions supports the hypothesis that the etiologies of these conditions involve biases towards increased relative effects from imprinted genes with maternal expression, which engender a general pattern of undergrowth. By contrast, autistic-spectrum conditions appear to involve increased relative bias towards effects of paternally expressed genes, which mediate overgrowth. This hypothesis provides a simple yet comprehensive theory, grounded in evolutionary biology and genetics, for understanding the causes and phenotypes of autistic-spectrum and psychotic-spectrum conditions.

Bernard Crespi, Professor of Evolutionary Biology at Simon Fraser University, has authored more than 100 publications and 4 books in the areas of social behavior, life-history evolution, and evolutionary genetics. He conducted his doctoral work with William Hamilton and Richard Alexander at the University of Michigan, followed by postdoctoral studies at Oxford and Cornell. Dr. Crespi has received the Theodosius Dobzhansky Prize and the E. O. Wilson Award from the Society for the Study of Evolution; and a Killam Fellowship from the Canada Council has allowed him to apply his expertise to the evolution of human cognition and psychiatric disorders.

Christopher Badcock was born in 1946 and studied for his first degree and Ph.D. at the London School of Economics, where he is now a Reader in the Department of Sociology. Following a private didactic analysis with Anna Freud, he published a number of books and papers on Freud, evolutionary psychology, and genetics, and is now completing a book on the wider implications of the theory outlined in this paper. He is author of Evolutionary Psychology: A Critical Introduction (Polity Press, 2000), and currently teaches graduate and undergraduate courses on evolution and genetics.

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