Effects of Prenatal and Postnatal Sex Steroid Hormones on the Development of Autistic Traits in Children At 18-24 Months of Age

Thursday, May 17, 2012
Sheraton Hall (Sheraton Centre Toronto)
9:00 AM
B. Auyeung1, J. Ahluwalia2, L. Thomson3, K. Taylor4, G. Hackett5 and S. Baron-Cohen1, (1)Autism Research Centre, University of Cambridge, Cambridge, United Kingdom, (2)Medical Director's Office, Cambridge University Hospitals NHS Foundation Trust, Cambridge, United Kingdom, (3)Cambridge University Hospitals NHS Foundation Trust, Cambridge, United Kingdom, (4)Department of Clinical Biochemistry, Cambridge University Hospitals NHS Foundation Trust, Cambridge, United Kingdom, (5)Obstetrics and Gynaecology, Cambridge University Hospitals NHS Foundation Trust, Cambridge, United Kingdom
Background: It has been suggested that autism may be an extreme manifestation of specific (but not all) male-typical traits, both in terms of cognition and neuroanatomy. Studies of prenatal exposure to sex steroid hormones during critical periods of development are related to specific (but not all) sexually dimorphic aspects of cognition and behaviour. However, it is not known whether postnatal exposure to these hormones has a similar effect. The critical periods for sexual differentiation of the brain are thought to be when sex differences in serum levels of sex steroids (e.g., testosterone) are highest. During human development, there is a prenatal surge in testosterone at around weeks 8-24 of gestation and a postnatal (neonatal) surge is also thought to occur shortly after birth when the child reaches 3-4 months of age.

Objectives: To examine how prenatal and postnatal sex steroid hormone levels are associated with individual differences in autistic traits in 18-24 month old children.

Methods: Fetal testosterone (fT) and fetal estradiol (fE) levels were measured in amniotic fluid using radioimmunoassay from pregnant women following routine second-trimester amniocentesis in n=129 toddlers. Saliva samples were collected from a subset of these children (n=35) when they reached 3-4 months of age. Salivary samples were assayed (without separation or extraction) for neonatal testosterone (nT) levels using commercially available immunoassay protocols.  When the children reached 18-24 months of age, mothers were asked to complete the Quantitative Checklist for Autism in Toddlers (Q-CHAT), a measure which has been shown to be effective in detecting the presence of autistic traits.

Results: fT levels were positively associated with scores on the Q-CHAT. For the smaller subset of children for which nT was measured, nT levels showed no significant sex differences and no relationships with FT levels or with Q-CHAT scores. The same subset retained the relationship between fT levels and Q-CHAT scores, despite the smaller sample size.

Conclusions: These findings are consistent with the hypothesis that prenatal (but not postnatal) androgen exposure (coinciding with a critical phase in sexual differentiation of the brain) is associated with the development of autistic traits in 18-24 month old toddlers. The present results should be followed up in a larger sample to examine whether individuals with clinical diagnoses of autism had elevated levels of fT.

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