Male Gender Bias and Levels of Male Hormones During Fetal Development 127effect on neurodevelopment. Secondly, they used a very small sample size
which they acknowledged as a limitation in their studies [43]. Thirdly, there
was a lack of measurement of amniotic fluid from fetuses that were later diag-
nosed with ASD. Kung et al. [43] and Guyatt et al. [42] report that any link
between prenatal androgen levels and the ASD phenotype is not clear cut. Any
observer of ASD science over the past three decades should not be surprised by
the mixed findings; all hypotheses seeking to describe the etiological pathways
to ASD have endured similar inconsistent data. Here, we stress that ASD is a
spectrum and exhibits a great degree of heterogeneity. The etiological variabil-
ity observed in ASD exceeds any other known disorders [1]. The scientific
response has been to reduce the emphasis on distinctly outlined diagnostic
boundaries, and instead focus on understanding the simply definable causes
which requires thinking outside the box.
The heterogeneity of ASD is summarized in a recent article by Waterhouse
et al. [61]:
“ASD research is at an important crossroads. The ASD diagnosis is
important for assigning a child to early behavioral intervention and
explaining a child’s condition. But ASD research has not provided a
diagnosis‐specific medical treatment, or a consistent early predictor, or
a unified life course. If the ASD diagnosis also lacks biological and con-
struct validity, a shift away from studying ASD‐defined samples would
be warranted.... The findings reviewed indicate that the ASD diagnosis
lacks biological and construct validity.”Hypothesis We believe that the severity of ASD depends on the time when
the fetus was exposed to testosterone‐like chemicals during the gestation
period. One of the reasons that autism manifest as a “spectrum” is due to
the time of exposure of adverse neuromodifying synthetic chemicals during the
fetal neurodevelopment. For example, if a fetus is exposed to a neuromodifying
agent at an early stage of brain development (i.e., day 25, Figure 1.1) then the
neuromodifying agent would have serious impact on the normal development
of the exposed fetal primordial brain cells and may result in an autistic child.
However, if the exposure to the same neurotoxic chemicals occurred at a later
stage of brain development (i.e., days 35, 45, 55, etc.) the outcome will be differ-
ent since at each of these stages of fetal development the damage would be dif-
ferent and significantly less adverse than it would be at day 25 (if the concentration
of the neurotoxin was exactly the same at each stage). Elimination or a signifi-
cant reduction in specific types of neurons can have widespread adverse effects
on brain development. In humans, oxytocin‐ and arginine vasopressin (AVP)‐
receptor positive neurons play a central role in “social communication”. If a fetus
is exposed to the same or similar oxytocin‐ and AVP‐receptor positive damag-
ing neurotoxic agents, the result would be a “spectrum”. As shown in Figure 5.1,