Cited by 231Sexual Differentiation and DisordersAutism Spectrum Disorder ResearchNeuroendocrine regulation and behavior

Topical Review: Fetal Testosterone and Sex Differences in Typical Social Development and in Autism

Knickmeyer, Rebecca Christine, Baron-Cohen, Simon·2006·Journal of Child Neurology

Abstract

Experiments in animals leave no doubt that androgens, including testosterone, produced by the testes in fetal and/or neonatal life act on the brain to induce sex differences in neural structure and function. In human beings, there is evidence supporting a female superiority in the ability to read nonverbal signals, specific language-related skills, and theory of mind. Even more striking than the sex differences seen in the typical population is the elevated occurrence of social and communicative difficulties in human males. One such condition, autism, occurs four times more frequently in boys than in girls. Recently, a novel theory known as the "extreme male brain" has been proposed. It suggests that the behaviors seen in autism are an exaggeration of typical sex differences and that exposure to high levels of prenatal testosterone might be a risk factor. In this article, we argue that prenatal and neonatal testosterone exposures are strong candidates for having a causal role in sexual dimorphism in human behavior, including social development, and as risk factors for conditions characterized by social impairments, particularly autism spectrum conditions.

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Crossref · 10.1177/08830738060210101601

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248 of 248 references verified0 citation errors · 0 not checkable

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  • Amniotic testosterone level is correlated with ASD-related traits in children regardless of diagnosis.

    “Amniotic testosterone level is correlated with ASD-related traits in children regardless of diagnosis (Auyeung et al., 2012, 2010; Chapman et al., 2006; Knickmeyer and Baron-Cohen, 2006; Lutchmaya et al., 2002a, 2002b).”

    From Excess Neonatal Testosterone Causes Male-Specific Social and Fear Memory Deficits in Wild-Type Mice (2025) · cites this paper as Knickmeyer and Baron-Cohen, 2006

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Authors
Knickmeyer, R. C., & Baron-Cohen, S.
Affiliations
  • University of North Carolina at Chapel Hill (US)
  • The Autism Research Centre Department of Psychiatry, University of Cambridge, Cambridge, UK
Corresponding author
Knickmeyer, Rebecca Christine
Venue
Journal of Child Neurology
Published
2006-10
Volume
21
Issue
10
Pages
825-845
ISSN
  • 0883-0738 (ISSN-L)
  • 1708-8283
OpenAlex
W2014925500
Cited by
230
References
250
Citations by year
2026: 2 · 2025: 7 · 2024: 6 · 2023: 10 · 2022: 9 · 2021: 13 · 2020: 11 · 2019: 9 · 2018: 9 · 2017: 10 · 2016: 14 · 2015: 17 · 2014: 15 · 2013: 13 · 2012: 11
FWCI
1.01
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Child Neurology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Sexual Differentiation and Disorders
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
  • Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
Keywords
prenatal testosterone, sex differences, autism spectrum disorder, social development (developmental psychology), extreme male brain theory, androgens, social communication deficits, theory of mind, sexual dimorphism, autism risk factors
MeSH terms
Animals, Autistic Disorder, Female, Fetus, Humans, Male, Pregnancy, Sex Characteristics, Social Change, Testosterone

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