Readers of this blog will be familiar with my model of Autism/ Schizophrenia and I recently found an online article by Crespi et al that elegantly summarizes the theory that autism and Schizophrenia are on a continuum of phenotypic variations related to cognition and the social brain.
I will be using images and text from that article heavily, so go ahead and read the original article too, which is very well-written and thought provoking.
The Authors contend that autism and schizophrenia are on a continuum where cognition is concerned with Autistics leaning towards mechanistic cognition, while schizophrenics leaning towards mentalistic cognition. This should be a familiar story to readers of this blog.
They discuss the various contrasting features of Autism and Schizophrenia. They contend that Autism is made up of three dimensions: language and communication difficulties, social reciprocity difficulties and creative or imaginative difficulties (which they term as repetitive and restricted behavior) .
They contrast this with the psychotic spectrum in which they include the three corresponding dimensions as Unipolar depression, bipolar disorder and Schizophrenia.
They then go ahead and list a variety of evidence from studies of growth, development, neuroanatomy, cognition, behavior, and epidemiology for diametric phenotypes in autism and psychosis. I reproduce below the table (click to enlarge – the tables are a must read!!) which highlights salient differences in phenotypes:
The authors have their own theory (which seems very plausible to me) regarding why Autism and Schizophrenia are diametrically opposite. This they contend is due to evolutionary arms race between the child and mother for scarce resources mediated by maternal and paternal imprinting genes.
They do a brilliant job of describing their theory so I quote from them:
Further hints that imprinted genes may have something to do with autism and psychosis come from the finding that autistics have heavier birth-weight(especially males) while schizophrenics are lighter – just as you would expect if paternal genes were more prominent in autism. Again, more paternal and/or less maternal genetic influence is sometimes implicated in cancer(another form of over-growth) and here the striking finding is that schizophrenics have less cancer than autistics despite the fact that the former smoke much more. Again, there is evidence that autistics by contrast to psychotics show early brain growth at the expense of the mother.
The article’s discussion is enlightening as it also throws light on other previous researchers who have hypothesized along similar lines. Alas The Mouse Trap doesn’t get a mention, But Nettle , regarding whom I have blogged before gets a mention.
Our hypothesis can be conceptualized at two interacting levels: (1) the diametric architecture of autistic and psychotic-spectrum conditions (Badcock 2004), and (2) the underpinnings of this structure in dysregulated genomic imprinting. A diametric structure to autism and schizophrenia has been considered for some traits before: thus, Abu-Akel (1999) and Abu-Akel & Bailey (2000) suggested that autism and schizophrenia represent extremes on a continuum of theory of mind skills from hypodevelopment to hyper-development, Frith (2004b) described ‘under-mentalizing’ in autism and ‘over-mentalizing’ in schizophrenia, and Nettle (2006) anticipated an autism psychosis spectrum in noting that “autistic traits are in many ways the converse of the unusual experiences component of schizotypy”. However, most previous research on autism and psychosis has considered the disorders to be etiologically unrelated (or has considered the negative symptoms of schizophrenia in terms of autism), although both disorders are believed to be underlain by dysregulated development of the social brain (Broks 1997; Emery 2000; Burns 2004, 2006). By our hypothesis, autism and psychosis represent extremes on continua of human cognitive architecture from mechanistic to mentalistic cognition, with balanced cognition at the center (Figure 4). Each set of conditions is extremely heterogeneous but also highly convergent, in that diverse genetic, epigenetic and environmental effects can generate similar cognitive phenotypes (Happé 1994, p. 2; Keverne 1999; Seeman et al. 2005; Badcock & Crespi 2006; Happé et al.2006). These striking convergences are mediated, in our view, by the dynamics of social brain development, with under-development in autistic conditions and hyperdevelopment in psychotic conditions (Badcock 2004), Further tests of this hypothesis should focus on assessing the breadth and depth of diametric phenotypic structure to autistic and psychotic spectrum conditions, and testing for tradeoffs between mentalistic and mechanistic thought and ability.
I am thrilled to see my theory also being investigated in parallel and worked on by distinguished scientists and am grateful for the scientific work going in this area. I am sure we will soon see more research supporting my thesis.