Introduction to Autism Spectrum Disorders 3adaptation of sickled red blood cells is most common among people with
origins in malaria‐infested regions, such as the Western parts of Africa
and the Mediterranean. The people with sickle cell disease inherited a
copy of the recessive gene from both parents. Like a genetic Trojan horse,
they carry this seemingly harmless hemoglobin S (HbS) gene because one
copy of it brings a great survival benefit by reducing susceptibility to the
deadly form of malaria; two copies, however, threatens health and even
life. Zero copies of the HbS gene commonly resulted in infant mortality
from malaria, which increased the percentage of persons with at least one
copy of the HbS gene. In this case more is not better: children of two par
ents with the HbS gene are much more prone to die of sickle cell anemia,
which, again, leaves a greater living population of those who have just one
parent with the HbS gene [1].
Similar adaptations to new environments took place when our ancestors
moved from Africa and faced varying temperatures, altitudes, and a lower
degree of sun UV radiation than that of their progenitors in Africa. Our ances
tors adapted to the new mutagenic plants and chemicals that they came across
during their journey “out of Africa”. For example, skin pigmentation accompa
nied geographic mobility as our ancestors migrated to Asia, Europe, Australia,
and elsewhere.
Adaptation of lactose tolerance is another example of genetic inheritance,
where 65% of the human population is lactose intolerant. This appears to be a
relatively new mutation. The gene that allows human children to digest milk
shuts off after three years of age when they are weaned. Certain human popula
tions, however, evolved to be lactose tolerant. This rise of lifelong lactose toler
ance in particular is pronounced in populations whose ancestors experienced
the time in history when the domestication of cows and other herd animals
occurred, a time in which the populations needed supplemental proteins
throughout their lives.
Can autism be due to genetic mutations or deletions? Does this relate to
survival mechanisms? In reality, human communication and patterns of behav
ior are governed by a large number of genes and by a complex orchestra‐like
communication between these genes that are formed and organized during the
early stages of human fetal development. It appears unlikely that a large num
ber of genes involved in human communications and survival mechanisms
would just begin to mutate in a precise manner so suddenly. Counterintuitively,
and “so suddenly,” from the epidemiological point of view, has this improbable
mutation transpired and done so rapidly?
Autism was relatively rare about four decades ago. In 1960, only one child in
10,000 was diagnosed with autism. By 2011, one in 100 children (1%) was
diagnosed with ASD; in 2013, the ratio had worsened to one in 88; in 2014,
according to the Centers for Disease Control and Prevention (CDC), USA,
one in 68 children suffered from ASD; and, in 2015, one in 45 children were