123Autism and Environmental Factors, First Edition. Omar Bagasra and Cherilyn Heggen.
© 2018 John Wiley & Sons, Inc. Published 2018 by John Wiley & Sons, Inc.
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We are accustomed to look for the gross and immediate effects and to
ignore all else. Unless this appears promptly and in such obvious form
that it cannot be ignored, we deny the existence of hazard. Even research
men suffer from the handicap of inadequate methods of detecting the
beginnings of injury. The lack of sufficiently delicate methods to detect
injury before symptoms appear is one of the great unsolved problems in
medicine.
Rachel Carson, 1962, Silent SpringThere is an inexplicable bias toward males in classical autism by a ratio of
~4:1, and ~10:1 in Asperger syndrome [1]. The diagnosis of autism spectrum
disorder (ASD) is based on developmental history and the presence of abnor-
mal behaviors. The clinical picture is heterogeneous and the etiology is
unknown. We believe that the real genesis of the “spectrum” is based on three
basic elements: (1) the timing of fetal testosterone (or other synthetic chemi-
cals that a fetal brain would encounter during gestation), early higher than
normal exposure may lead to a worse outcome; (2) the amount (dose) of testos-
terone (or other neuromodifying agents); and (3) the exposure to testosterone
(or other male hormone‐like chemicals) has a selective neuromodifying effect.
Of note, when we mention testosterone it does not imply that fetal testosterone
is chemically unique from adult testosterone. It is the same chemical, secreted
by the fetal cells or, according to some reports, from the placental part that is
fetal in origin. We have discovered that testosterone (and numerous other syn-
thetic chemicals) selectively kills oxytocin‐ and arginine vasopressin‐receptor
positive neurons. The complete elimination of these neurons (if exposure
occurred in the early stage of neurodevelopment) results in classical autism.
This is due to the fact that in the early stage of gestation (i.e., weeks 8–24),