title: Why are autism spectrum conditions more prevalent in males?
abstract: Autism Spectrum Conditions (ASC) are much more common in males, a bias that may offer clues to the etiology of this condition. Although the cause of this bias remains a mystery, we argue that it occurs because ASC is an extreme manifestation of the male brain. The extreme male brain (EMB) theory, first proposed in 1997, is an extension of the Empathizing-Systemizing (E-S) theory of typical sex differences that proposes that females on average have a stronger drive to empathize while males on average have a stronger drive to systemize. In this first major update since 2005, we describe some of the evidence relating to the EMB theory of ASC and consider how typical sex differences in brain structure may be relevant to ASC. One possible biological mechanism to account for the male bias is the effect of fetal testosterone (fT). We also consider alternative biological theories, the X and Y chromosome theories, and the reduced autosomal penetrance theory. None of these theories has yet been fully confirmed or refuted, though the weight of evidence in favor of the fT theory is growing from converging sources (longitudinal amniocentesis studies from pregnancy to age 10 years old, current hormone studies, and genetic association studies of SNPs in the sex steroid pathways). Ultimately, as these theories are not mutually exclusive and ASC is multi-factorial, they may help explain the male prevalence of ASC.
authors.affiliation: Autism Research Centre, Department of Psychiatry, University of Cambridge, Cambridge, United Kingdom. sb205@cam.ac.uk
authors.forename: Simon
authors.initials: S
authors.lastname: Baron-Cohen
authors.forename: Michael V
authors.initials: MV
authors.lastname: Lombardo
authors.forename: Bonnie
authors.initials: B
authors.lastname: Auyeung
authors.forename: Emma
authors.initials: E
authors.lastname: Ashwin
authors.forename: Bhismadev
authors.initials: B
authors.lastname: Chakrabarti
authors.forename: Rebecca
authors.initials: R
authors.lastname: Knickmeyer
mesh_terms: D001921:Brain / Q000378:metabolism; D002648:Child; D002659:Child Development Disorders, Pervasive / Q000453:epidemiology*; D005260:Female; D006801:Humans; D008297:Male; D020641:Polymorphism, Single Nucleotide; D011247:Pregnancy; D015995:Prevalence; D013739:Testosterone / Q000378:metabolism
chemical_list: D013739:Testosterone