Unheard and impressive theory of autism

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There is only one autistic syndrome (including “Aspergers”,
dyslexia, and so on). There are many individuals each with their
own variety of autism causes and outcomes but they all fall within
the one syndrome and the one unifying principle explained here.
Autism is not a disorder. Rather it is an aspect of natural individual differences. Exactly the same factors which generally cause
high IQ also cause autism at higher levels, and enable potential
creative genius in a narrow intermediate range of levels. I have
named these factors antiinnatia factors, because they suppress or
reduce the gene(ome)-expression of innate tendencies or characteristics. Hence anti-innate.
A person with extreme-ish high antiinnatia will be autistic. A
person with extreme low antiinnatia will have “ordinary” low IQ.
Many autistics also have low IQ scores, but that is caused by a
different process than that which causes “ordinary” low IQ, as will
be explained.
Humans (and animals in general) have many innate characteristics such as a nose in the middle of their face, eating, breathing,
blushing, learning to walk and talk and relate to their own species
more than to others. All these innate characteristics depend on
gene(ome)-expression of information in the genes(/genome).
Certain factors both genetic and environmental have a tendency to reduce gene-expression not just in respect of individual
genes but more generally (though in a biased way as will be
explained). The gene-expression processes can be generally reduced
by many common factors such as deficiency of energy supply or
nutrients, interfering pathogens, gene-expression-controlling regulatory genes, and molecules part-time binding to DNA.
Disadvantageous characteristics are less reliably expressed
than advantageous ones. So they are more liable to be suppressed
by antiinnatia. These antiinnatia factors consequently have the
effect of a quality-controlling filter, preferentially suppressing disadvantageous characteristics while leaving relatively unaffected
those characteristics which have a greater evolutionary history of
advantageousness. And in consequence of this principle, antiinnatia
does not affect the more fundamental aspects of body composition
and functioning (which are highly conserved even between different
species), but instead particularly affects behaviour and appearance.
Thus antiinnatia would not in practice much affect the production of
hemoglobin for blood cells, myosin in muscles, collagen for the skin,
and so on.
In the normal range the level of antiinnatia has effect mostly in
its suppression of disadvantageous “junk” expressions producing
errors and slowing of mental functions (and so higher antiinnatia
causes higher IQ).
If the level of antiinnatia is much higher than normal it
suppresses even advantageous characteristics, thus causing the
various features of the autistic syndrome. Most notably, the innate
programming for communicating with and relating to other humans
tends to be reduced. The autistic brain thus tends to approximate to
the notional “blank slate”. But there is a twist.
Some human characteristics merely suppress more long-
standing characteristics shared by our pre-human ancestors. High
antiinnatia suppresses those suppressors with the result that some
pre-human characteristics re-emerge in autism (technically known
as atavisms). By this means are easily explained such peculiar
characteristics as the hand-flapping and toe-walking, and the
sometimes occurrence of webbed feet and wide-spaced eyes.
In the 1993 presentation of this paper I pre-introduced the
concept of antiinnatia with a soundbite-brief description as “general
impairment of gene-expression”. For reasons explained on a prev-
ious page, I have now changed that to “evolution-biased reduction of
gene-expression”.
Autism is not a condition of the brain but rather of the whole
body and beyond. A person can only be autistic in relation to a
particular environment (i.e. when their behavior is disadvantageous
in relation to that environment such as a highly intolerant
community), and cannot be autistic per se. And there can never be
any diagnostic test because it is not a disorder anyway.
Finally, it is important to note that this 1993 paper is
considerably strengthened now by the major evidential updates in
chapters 3 and 16.
Even more finally - the antiinnatia concept is not the slightest
bit “controversial”. Infinitely more controversial is the utterly
crackpot-wacko notion that antiinnatia would not exist or manifest
as autism, as is explained at pages 325-56 here.

How would one account for the folks with autism who have to wear helmets in order for them not to hit their heads on walls?

What sort of environment would be conducive to preventing this manifestation from happening?

I have to agree that you should "break it down" for the "laymen" (like me).

Define the rather esoteric term "antiinnatia," for example

There's an article about this published in 1993. I wish there were some reviews of it. I haven't seen any.

Science is all about collaboration and peer-review.

So it has to do with "epigenetics". How the environment can effect how genes are expressed.

There are evidences supporting that: http://pseudoexpertise.com/about.php