The Evolutionary Biology of Autism Risk

Session Date: 
Oct 5, 2012

I describe a simple model, based in evolutionary biology, neurodevelopment, and genetics, for understanding how the primary features of autism are related to the major neuroanatomical and cognitive traits that are highly-developed or unique to the human lineage. By this model, human-specific adaptations, especially brain size and brain structures that subserve social interactions, are explicitly connected with their alterations in autism spectrum conditions. This evolutionary-medical perspective has several important implications for understanding and analyzing autism and other psychological variation in humans. First, autism can be conceived as a relative extreme of natural, evolved variation, which involves reduced development of some traits, enhancements of other traits, and trade-offs between different abilities. This means that genes ‘for’ autism represent genes underlying the bases and facets of social cognition, and genes mediating trade-offs between social and other skills. Genetic studies and studies of 'autism gene' functions may be guided by this inference. Second, by this model, psychotic-affective conditions (including schizophrenia, bipolar disorder, depression, and borderline personality) represent diametric opposites to autism spectrum conditions, with neurotypical development and cognition at the centre. This bidirectional spectrum of psychological variation leads to reciprocal illumination of research findings across autism and psychotic-affective conditions, with practical implications regarding such issues as the increases in autism diagnoses and the development of treatments. I present data salient to these points, from the literature and from my laboratory, with a focus on rigorous application of evolutionary concepts and tools to understanding the causes of autism.

File 2012_10_05_09_Crespi.mp4162.08 MB