More Than 1,000 Genetic and Genomic Disorders and Still Counting 25account for 85–90% or more of ASD cases [41,42]. Most significantly, trio
exome sequencing investigation, where the complete exome (messenger RNA
or the genes that carry out the daily functions of a living being) or exomes of
both normal parents and their autistic child are fully sequenced. These
sequencing studies have revealed that the child’s genes show de novo functional
loss variants that do not exist in either parent [89–92]. ASD is complex, and it
is estimated that there are hundreds of genetic loci or genes and a thousand or
more SNPs that may have a causative impact on ASD development. It should
be noted that SNPs are noted to be 10–20 times more common in ASD than in
the normal control children. The higher the number of SNPs, the worse the
degree of autism (i.e., higher prevalence of intellectual disability). If we look at
the three characteristics of teratogenic effects, we can see that there appears to
be a dose relationship as well as timing when a synthetic chemical imparts it
effects on a developing fetus.
In an effort to pull together all possible genes and recurring genomic imbal
ances that have been posited to contribute to the etiology of ASD, a recent
exhaustive summary of literature research, both of the basic research and clinical
varieties, has identified 44 genomic loci and 103 disease‐implicated genes for
subjects with autistic or ASD behaviors [93–103]. These loci and genes have
each been in some way causally implicated in the intellectual disability associ
ated with ASD or autism, which suggests that this related pair of neurodevel
opmental disorders have genetic bases in common. For epilepsy and ASD,
there is also genetic overlap in many instances. All things considered, these
findings have demonstrated convincingly that autism cannot be categorized as
a single unique clinical entity but rather as a complex behavioral manifestation
of many, perhaps even hundreds, of genomic and genetic genomic disorders
[104]. The exploration of these exhaustive analyses, with their supporting data,
evidences the likelihood that such a large number of genetic mutations is not
the sole cause of ASD. Rather, secondary effects seem to be at work, mutagenic
agents that harm the developing fetus as gestation progresses [8–13]. Most of
these thousands of suspect genes may, in fact, not relate to ASD. They may
simply be part of abnormal developmental processes resulting from exposure
to synthetic chemicals, and investigators may be pursuing false leads on unpro
ductive trails. Similar false leads have occurred throughout recent human
medical history; this is not a new phenomenon.
A glaring example is the misinformation about the cause of AIDS. Initially, it
was believed that AIDS was caused by homosexual activity and that the semen/
sperm of those involved caused AIDS [105]. Then, Professor Peter Duesberg
put forward the hypothesis that “all AIDS diseases in America and Europe that
exceed their long‐established, normal backgrounds are caused by the long‐
term consumption of illicit recreational drugs and by AZT and its analogs:
Hemophilia‐AIDS, transfusion‐AIDS, and the extremely rare AIDS cases of
the general population reflect the normal incidence of the AIDS‐defining