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. (shrink)

This dissertation explores philosophical issues in autism and defends a new version of the enactive approach to autism and social cognition. The discussion in this dissertation centres around the question “why do autistics encounter social interaction problems?”, addressing this question in ways that raise broader philosophical issues. Within the philosophy of mind, these include the problem of other minds, the nature of emotions, and narratives and their role in understanding the self. Beyond cognition, such issues are intertwined with questions in (...) metaphysics, philosophy of science, sociopolitical and moral philosophy, and disability studies. In responding to the question “why do autistics encounter social interaction problems?”, I argue that autistic social interaction problems result from the sensorimotor differences between autistics and non-autistics. This contrasts with the response to this question given by widely-endorsed views that emphasize instead the cognitive deficits that autistic people have. Such cognitivist views, such as the theory theory and simulation theory, are the focus of my first two critical chapters. I go on to offer a critique of two approaches that go beyond the focus on mindreading in appealing to sensorimotor problems as lying at the heart of the problem. These views, interaction theory and the original enactive approach, are the focus of the next two chapters. I then turn to defend a novel form of the enactive approach in the last part of the dissertation by emphasizing the role of emotions as the capacity for us to make sense of the world and to construct the sense of self from narratives. My new approach shifts the explanatory focus from perception and motion to emotion. This maintains the advantage of the original enactive approach, while avoiding its behaviouristically limited descriptions. My account thus expands the theory’s capacity to describe and explain internal states important to self-understanding and self-expression. This allows one to approach autistic social difficulties by attending to the first-person perspective, cohering with my reliance on first-person autistic narratives as a major source of evidence that supplements traditional scientific research on autism. (shrink)