90 Olfaction and Autism
progenitor neurons must have receptors for those smell chemicals. Therefore,
it is highly unlikely that all the odorant (~450 different kinds of ORs found in
humans) will be present in early fetal brain development. This is the key to the
autism spectrum. If only a few different types of odorants (fragrances) entered
at 5 weeks of gestation, the elimination of the mother cells or progenitor cells
for those particular odor neurons would be permanent. Moreover, other
synthetic chemicals can enter and kill other types of nonodorant progenitor
neurons. However, if the same degree of breach of the fetal brain occurred at
later stages (i.e., weeks 11, 15, 22, 30, etc.), the degree of damage would be
progressively less. Consequently, at any stage of breach, loss of odorant neu-
rons as well as other types of neurons would be less obvious, but still causing
ASD and in the smell area the symptoms would be highly heterogeneous.
Of note, we want to reinforce the point that ASD is primarily not a genetic
disease or disorder, but cellular damage by selective destruction of highly
specialized neurons disrupting the highly organized evolutionary brain devel-
opment cascade that is caused by manmade synthetic chemicals. These syn-
thetic chemicals have no evolutionary history and our species (Homo sapiens)
has never seen these chemicals (or rather, never previously smelled them dur-
ing our evolution). There is not enough time to adapt to them. We have no
efficient way to neutralize these chemicals.
Back to the process of smelling: various output neurons in the olfactory bulb
target different subregions of the cortex. Within just one or two synapses,
information originating in the olfactory bulb spreads to diverse cortical regions
that have diverse functional capacity. For example, signals sent from the olfac-
tory bulb to the amygdala affect emotional processing; those to the olfactory
tubercle affect motivated behavior; those to the entorhinal cortex‐hippocam-
pus affect working memory and memory of episodic occurrences; and those to
the orbitofrontal cortex affect the valuation of rewards and assistance with
decision making, and autonomic regulation. The communication is not a one‐
way process. Extensive reciprocity is involved as seen, for instance, in the bidi-
rectional flow of information between the entorhinal cortex and the piriform
cortex, or between the orbitofrontal cortex and the piriform cortex. Moreover,
the areas involved in olfactory processing are also often multisensory. The
olfactory tubercle, for instance, helps process sound and odors, at least, and the
piriform cortex deals with both taste and odor, at least. The entorhinal and
orbitofrontal cortices deal with most of the senses. According to recent esti-
mates, between 3% and 15% of the piriform cortical neurons are activated
when a “puff ” of odorant reaches them. While neuronal ensembles with only
50–100 neurons may be adequate for the encoding of particularly singular
odors, most require more complex ensembles to process a particular odorant.
Since the piriform cortex has a vast number of pyramidal neurons, perhaps as
many as 50,000, shifting coalitions of overlapping ensembles are available to
help identify the numerous odors extant in the modern world, which helps