Are Autism and Schizophrenia at Opposite Ends of a Brain Disorder Spectrum?

A novel study tries to explain what appears to be the diametrically opposite nature of traits associated with autistic-spectrum disorders, on the one hand, and psychotic-spectrum disorders, on the other. With a particular focus on autism and on schizophrenia, the authors link social brain development and other phenotypic traits to evolutionary biology and genetics.

About the Study

The abstract for a paper called Psychosis and Autism as Diametrical Disorders of the Social Brain, by Bernard Crespi and Christopher Badcock, came across my desk a few weeks ago. Unfortunately, it languished in my inbox along with several other things that arrived while I was out of the office for a couple of weeks last month:

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 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 behavior. 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.

The paper has been selected as a target article for open peer commentary at the prestigious journal Behavioral and Brain Sciences, one of the foremost print publications in its field. If you’d like to have a look at the full text of the paper, it’s available here. This looks to me like a fascinating attempt to provide a low-level genomic explanation for observed traits at a much higher level of description (i.e., the psychological).

The journal has a fairly unique quality-control system whereby commentaries are accepted only from people called ‘BBS Associates’ or those nominated by BBS Associates; and to be eligible to become a BBS Associate, you must either have had work previously accepted for the journal (or refereed for them), or been nominated by someone who has. As a BBS Associate myself since the late 90s, I’m happy to nominate others to write commentary for the article. So if you have relevant expertise in this area, and no other BBS Associate is available to you, please drop me a note via the site’s contact page and let me know a bit about your background.

About the Journal

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Behavioral and Brain Sciences (BBS) is an international, interdisciplinary journal providing Open Peer Commentary on important and controversial current research in the biobehavioral and cognitive sciences. Commentators must be BBS Associates, or suggested by a BBS Associate. If you are not a BBS Associate, please follow the instructions linked below:

All clinical material on this site is peer reviewed by one or more clinical psychologists or other qualified mental health professionals. This specific article was originally published by on and was last reviewed or updated by Dr Greg Mulhauser, Managing Editor on .

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