126 Male Gender Bias and Levels of Male Hormones During Fetal Development
Sex differences were observed, with boys scoring higher on the Q‐CHAT than
girls and a correlation was found between fetal testosterone and autistic traits
[3,4]. These studies suggest that higher levels of fetal testosterone play a role.
The connection between fetal testosterone and ASD has been supported by
numerous independent studies, both in humans and rodents [3–41], but fail to
explain the increased incidence of autism in the last three decades compared
with several decades ago [42,43]. We will discuss the role of the environmental
factors, especially the chemicals that act like testosterone or have similar
effects as testosterone in a later section and in Chapter 7 [2,14,44–60].
More recently, several studies have analyzed the Baron‐Cohen hypothesis
but found no evidence of a link with digital ratio. In an analysis of 6,015 ASD
children and controls, Guyatt et al. (42) did not find an association between
2D:4D and ASD in males or females. Most significant is the paper by Kung and
colleagues [43] which reported no relationship between prenatal androgen
exposure and autistic traits. They took their evidence from studies of children
with congenital adrenal hyperplasia and from studies of amniotic testosterone
concentrations in typically developing children. They employed a parent‐
report questionnaire, the Childhood Autism Spectrum Test (CAST), to meas-
ure autistic traits in both studies. The first study examined autistic traits in
young children with congenital adrenal hyperplasia, a condition causing unu-
sually high concentrations of testosterone prenatally in girls. They assessed
81 children with congenital adrenal hyperplasia (43 girls) and 72 unaffected
relatives (41 girls), aged 4–11 years. The second study examined autistic traits
in relation to amniotic testosterone in 92 typically developing children (48 girls),
aged 3–5 years. Findings from neither study supported the association between
prenatal testosterone exposure and autistic traits. Specifically, young girls with
and without congenital adrenal hyperplasia did not differ significantly in CAST
scores and amniotic testosterone concentrations were not significantly associ-
ated with CAST scores in boys, girls, or the whole sample. These studies do not
support a relationship between prenatal testosterone exposure and autistic
traits. This study may appear to be a clear‐cut refutation of EMB theory. This
is not the case. The most common form of congenital adrenal hyperplasia is
due to 21‐hydroxylase deficiency that converts 17‐hydroxyprogesterone to
11‐deoxycortisol. Obviously, this is not testosterone. In the human fetus there
are precise receptors for testosterone as well as for deoxycortisol and they have
different physiological roles [43].
Furthermore, Kung et al.’s studies [43] had numerous methodological flaws:
first, they measured testosterone concentration from umbilical cord blood.
This is an inexpensive methodology that facilitates data collection on a large
number of normal pregnancies. However, a limitation of this approach is that
cord blood androgen levels may not reflect concentrations during the first and
second trimesters of gestation, which is traditionally thought to be a critical
period during which prenatal hormone exposure has its most pronounced