Demasculinized digit ratios in a sample of boys with childhood autism.

Some theories have proposed that children with autism spectrum disorder (ASD) may be exposed to increased levels of androgens during prenatal development, resulting in greater androgenization of testosterone-dependent traits including both peripheral (bodily) and central (brain-related) traits. Empirical support for this hypothesis is scant and inconsistent. In the present work, we studied an ostensible anatomical marker of testosterone exposure (sexually differentiated finger lengths) which develops during the first trimester or early second trimester of gestation. Participants were 25 boys with classic autism, recruited from the clinical practice of a local physician specializing in childhood autism, who met the standardized DSM (Diagnostic and Statistical Manual) criteria for ASD, and 57 normally-developing age- and sex-matched male and female controls (32 males, 25 females); N = 82; Mage = 7.30 yrs., SD = 4.18. Finger length was measured to the nearest 0.5 mm from digital images of the ventral surface of the hands using a validated measurement protocol. Consistent with past reports from adult samples, several of the finger length ratios were confirmed to display sex differences among control children, but the group of boys with ASD showed a female-like finger growth pattern, not the hypermasculine pattern predicted, and were found to differ statistically from the male controls. Boys with ASD thus showed a demasculinized pattern of finger differentiation. Our data do not support theories which suggest that greater fetal testosterone exposure occurs in boys with autism.