Many Diseases That Were Considered Genetic are Being Reassessed 153explain these observations is that the environmental factors induced genetic
mutations, which would not be equally distributed due to slight variations in
maternal blood delivery to the twins. The unequal blood flow in maternal twin
pairs is well documented [34–37], see Figures 6.3 and 6.4. This may result in
unequal genetic mutations in each twin [38–41]. Since certain environmental
chemicals can interfere in neurodevelopment there will be discordant autism
symptoms in some maternal twin‐pair twins [34–36]. This phenomenon may
partially explain the paradox of discordant maternal twin‐pair twins, but also
shed light on our hypothesis that even perhaps a few molecules of a harmful
chemical reaching a fetal brain could deplete specific neurons and induce ASD.
Why has it taken so many decades for us to realize that ASD is not only
genetic but that environmental factors play a significant role? Part of the
answer is that in the 1970s, genetic engineering was in vogue in scientific
research. Everyone wanted to use the new tools for genetic sequencing and to
determine the role of genetic codes in diseases. Scientists in the 1980s and
1990s began to analyze genetics that could be associated with a particular ill-
ness. In some cases, they offered great insight. But, after decades of searching,
they were unable to identify any particular gene or genes that could be defi-
nitely liked to ASD. These efforts continue; scientists regularly publish articles
in prestigious journals showing a “likely association” of a particular gene to
autism! These efforts will most likely continue for decades since scientific cul-
ture is difficult to change, even though there are lonely voices that have chal-
lenged the single focus on genetics [42–48]. In a recent Letter to the Editor,
Waterhouse et al. [48] wrote:
“Syndromic ASD brain impairments vary from syndrome to syndrome,
and gene models of ASD brain impairment lack replication and cover-
age. The ASD diagnosis lacks boundary construct validity because 96%
of those with ASD have significant non‐diagnostic symptoms, including
many who have full comorbid disorders. In addition, the ASD spectrum
of disorders lacks construct validity. The spectrum has no shared early
brain or behavioral predictor, no shared consistent developmental
course, no shared Broader Autism Phenotype, no replicated subgroups,
and no shared recurrence risk rate. Crucially, the phenotypic brain and
behavior links between ASD and other neurodevelopmental disorders
remain unclear, and the real complexities of the interaction of develop-
mental risk factors also remain unclear. Taken together, the preponder-
ance of evidence argues that using the diagnosis of ASD in research is
fruitless because the diagnosis is an arbitrary unscientific “convenient
fiction” that has blocked the discovery of replicable neurobiological vari-
ation among individuals with serious neurodevelopmental social impair-
ment. Equally important, maintaining the ASD diagnosis supports the
impossible research goal of finding a unitary cause for ASD, and