20 Introduction to Autism Spectrum Disorders
One can surmise that a well‐organized, effectively connected larger
brain could make an autistic child extraordinarily brilliant, with much
higher computational, engineering, mathematical, artistic, and other abili
ties. In fact, this is what one sometimes sees in people with Asperger syn
drome. However, such a pattern is not universal; the abnormal, haphazardly
connected brain results in an intellectual dysfunctional brain. In either
case, the person with ASD would still be missing or have smaller compart
ments of the brain that are involved in communication, empathy, eye con
tact, and the so called abilities of mind‐reading and body language
interpretation. Why? What may be the cause of essential missing pieces?
We argue that this is the result of the early death or reduction of special
ized progenitor neurons that did not live long enough to later give rise
to these social communication faculties, resulting in socially awkward
but at times brilliant people. What would cause the death or reduction of
such highly specialized neurons at very early and critical stages of fetal
development? What environmental factors can contribute to a premature
demise of such fundamental neurons, and how does this relate to male
brain development? Why are male fetal brains more susceptible to envi
ronmental insults?Why Is There a “Spectrum” in Autism?
It is well documented fact that teratogenic agents (chemicals or physical
insults) interfere with normal fetal growth, homeostasis, development, dif
ferentiation, and behavior. Teratogens are xenobiotics and other factors that
cause malformations in the developing fetus. There are six basic principles
of teratology that were proposed by James Wilson in 1959 and still hold to
be true [84,85]:1) Susceptibility to teratogenesis depends on the embryo’s genotype that inter
acts with adverse environmental factors (G×E interaction).
2) The developmental stage of exposure to the conceptus (fetus) determines
the outcome.
3) Teratogenic agents have specific mechanisms through which they exert
their pathogenic effects.
4) The nature of the teratogenic compound or factor determines its access to
the developing conceptus/tissue (fetus or specific fetal tissues, organs, or
even specific progenitor cell types).
5) The four major categories of manifestations of altered development are:
death; malformation; growth retardation; and functional deficits.
6) The manifestations of the altered development increase with increasing
dose (i.e., ranging from no effect to death and demise of a fetus).