Psychosis and Autism as Diametrical Disorders of the Social Brain

Psychosis and Autism as Diametrical Disorders of the Social Brain  Bernard Crespi [1]  and Christopher Badcock [2 ]

1  Killam Research Professor, Department of Biosciences, Simon Fraser University, Burnaby, BC, V5A 1S6, Canada    
crespi@sfu.ca

2  Department of Sociology, London School of Economics, London, U. K.
C.Badcock@lse.ac.uk

HOME PAGE URLs:
B. Crespi: http://www.sfu.ca/biology/faculty/crespi/
C. Badcock:  http://www.lse.ac.uk/collections/sociology/whoswho/badcock.htm

KEYWORDS: autism, cognition, genomic conflict, genomic imprinting, psychosis, schizophrenia, hyper-mentalism 

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 behaviour 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 vs. 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 vs. global processing, language, and behaviour.  Social cognition is thus under-developed 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 support 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.    

Behavioral and Brain Sciences, IN PRESS, 10 October 2007