26 Introduction to Autism Spectrum Disorders
diseases, plus the AZT‐induced incidence of these diseases under a new name.”
The key to this so called drug‐aids hypothesis was the assumption that chronic
AIDS‐defining illnesses were only suffered by those who consumed illicit
drugs, with an underlying sub‐thesis that HIV‐1 does not exist! Unfortunately,
this hypothesis received support from the well‐known researcher Dr Kary B.
Mullis, who received the Nobel Prize in 1993 for his discovery of the polymer
ase chain reaction (PCR) method. Believing this false dogma, the South African
government ignored the AIDS crisis and the evolving treatment that became
available, thereby contributing to the spread of the AIDS pandemic. We recount
these events to show that how sometimes the paradigm can be wrong, and that
clinging to false paradigms can take a heavy toll on global health [105].
Removal of the shaded lenses of genetic bias and an unbiased examination of
scientific facts invites us to turn the traditional genetic dogma with regard to
ASD on its head, and focus on the environmental factors that have caused ASD
cases to skyrocket in recent decades. Such pollutants can induce genetic muta
tions in fetal brain cells at the early and most crucial stages of brain develop
ment. Twin studies clearly refute the idea that genetic inheritance is primarily
responsible for ASD; if it were, why do so many genetically identical (maternal)
or monozygotic twins not share the same ASD experience? Figure 1.14 supports
the idea that environmental causes of birth defects are well established, and
these defects are not primarily genetic diseases. Literally hundreds of environ
mental agents can cause genetically mediated malformations [63]. Therefore,
ASD may well owe its complex origins to complex toxic interactions in a
threatening chemical environment. ASD appears to be much more a matter of
public pollutants than of genetic inheritance (Figure 1.14).
Fetal malformations that result from a wide variety of drugs (i.e., valporic
acid), numerous infectious agents, hormones (or synthetic chemicals that dis
turb the hormonal balance), heavy metals, radiation, and alcohol are well
known and documented. With few exceptions, these causal factors have been
linked to specific malformations. Figure 1.15 summarizes various teratogenic
agents (i.e., those that cause damage to a fetus).
Due to astonishing progress in developmental biology and diagnostic proce
dures, researchers can now precisely identify pathways that have been modi
fied during the time of human fetal development (ontogenesis), and the precise
timing of teratogenic interference that resulted in malformations. Figure 1.16
displays the times at which various parts of the developing fetus are highly
susceptible to such interference (Figure 1.17).
We maintain that ASD is the cumulative result of exposure to various toxic
chemical agents that affect certain cell types in the brain during specific peri
ods of fetal development. Considering this logically, we see that the agents
mentioned below do, in fact, promote fetal brain malformation and do so in a
patently obvious fashion. For autistic children, brain size is larger, and this has
been traced to specific parts of the brain. The most significantly affected areas