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7
The peer-reviewed publication
of a still-unfaulted theory
“Robin P Clarke is one of those rare souls with the ability to
assimilate and synthesise large amounts of information and generate
new and interesting ideas.” – Bernard Rimland, founder of Autism
Research Institute, founder of Autism Society of America, debunker
of Bettleheim’s theory, and originator of the modern bio/genetic
concept of autism.
“Well worth publishing”
– Hans J Eysenck, most-cited-ever scientist.
“Well-written, well-argued, well-documented”
– journal’s peer-reviewer comment.
“Get your autism puzzle-pieces here!”
– Autism research fundraisers.
(You may find this chapter hard to read. I found it hard to write.)
In a preceding chapter I cleared up some serious muddle about
what autism is in conceptual terms. In this chapter I will set out an
understanding of why autism is, in terms of causal processes.
A page or two below here I shall paste-in the text of my years-
ago-published paper which I re-typed into an Amstrad PCW quite a
few years ago, then incorporate some updates and enhancements of
presentation. (Puzzle-pieces had no association with autism back
then.)
I accidentally came to this theory via some vague impressions I
had, that I seemed to have more in common with some historically
famous creative people (“geniuses”) than with those I met in real
life. I did obviously differ from the geniuses in not actually having
produced any recognised outstanding works of genius myself. Then
my curiosity was increased further on reading that autism was
Copyright 2020
Robin P Clarke and Best Books Press
www.pseudoexpertise.com
The peer-reviewed publication 201
associated with parental high IQ. I wondered what could be the
cause of that. I encountered the 1971 theory of Moore and Shiek
that autism was caused by “prenatal imprinting”. It seemed to
resolve the question. But when I showed it to Mike Hunter at Aston
University he said he had already read the abstract and dismissed it
as no good. I had limited capability of engaging in conversation in
those years so I failed to ask him for any further explanation.
But some days or weeks later, when I was as usual still out of
bed at a very hushed 3 am. (which I now know is a symptom of
mercury poisoning), I wondered to myself what seemed a rhetorical
question. The imprinting theory must surely be correct because
what other explanation could there be of those links of autism and
IQ (and genius)? No sooner had I asked that question than I
thought of an answer to it: all three involved reduction of “innate
prejudices” (which concept I will clarify shortly). By the next day I
had refined that to the idea that they all involved suppression of
what I later called “innatons” (meaning innate predispositions,
innate preprogramming or tendencies). Let me explain. Autism
involved a higher level of this suppression, suppressing valuable
innate predispositions relating to communicating and relating (as I
knew only three things about autism at that time!). Genius resulted
from a more marginal suppression, liberating a person from
intellectually-prejudicing innate tendencies such as conformity, self-
conformity, pretentiousness, superficialness, wiahful thinking, and
presentmindedness (by which I mean the opposite of absentminded-
ness). And high IQ was caused by a lesser degree of suppression,
only suppressing rubbishy innate junk tendencies (“genetic noise”,
producing random errors and slowing in the brain – which my first
day’s terminology would have considered to be random junk
“prejudices” (like innately “knowing” that “2 plus 2 equals 5”).
The idea was that autism was effectively like a relatively
“blank slate” brain lacking some innate human nature tendencies
such as recognising other humans as one’s own species and
interacting with them in conventional ways. I thereafter went off to
the libraries to find out more facts about autism, IQ, and genius, to
relate to this conception and to test it against. And the more I
studied the more I found which fell happily into support of the
theory, with nothing undermining it instead.
This eventually resulted in the first version of a paper I sent to
journals, which included not only autism and IQ and genius but also
various other matters. There followed some further years of self-
educated struggling against unknown forces of resistance, during
which I concluded it might be easier to get it published if I first
separated out the autism part from the rest, and also cut out all
202 Experts Catastrophe
mention of the genius part in the hope of avoiding the academic
hostility to that concept. Thus resulted a substantial document
which was eventually published in the peer-reviewed journal
Personality and Individual Differences.
This person so contemptuous of theories thus unwittingly
became a theorist in defiance of his own intentions.
You need to bear in mind that this paper was originally written
for a very different audience some years ago since when a great deal
has changed both in autism research and in the wider world. A
whole new movement of Neurodiversity pride has arisen, along with
some people becoming extremely sensitive to seeming offensiveness
of terminology. And I have become much more experienced in
writing than back then. And paper-printed journals were very
hostile to “excessive” length such that a paragraph about errors and
slowing got more squashed than I am happy to see it now.
So for these reasons I am making some very minor changes to
the writing, which do not change the actual content or meaning but
which make for a better reading experience – it is merely a
“translation” to improved language rather than any revision. For
the convenience of cynics I will list all those changes near the end of
this chapter. In addition I am adding in some update notes in the
text, indicated thus: [2014 Update: blah blah...]
Not least I have changed “impairment” to “reduction”, and
“excessive” to “extreme”. This is because some readers would
mistakenly assume an implication that the person or their mental
functioning is what I mean is impaired or inferior. Also the word
“general” is obviously misleading and would be better changed, as
explained further on.
I shall also add an introductory outline of the theory here. That
is because (strange as it may seem) the original paper never actually
gave a summary of the theory itself but only the case for/against it.
Instead, after some introductory remarks, it presented a logical
argument (guided by some factual pointers), and then followed on
with a review of how the evidence stacked up, followed by some
concluding remarks. The resulting theory is stated there in the
paper but not all in one place or in very explanatory language.
I shall also add an appendix to this chapter relating to the
evidence of gene-expression differences in autism.
Finally, just as the paper in Chapter 3 began with an abstract,
so does this one here though in this case titled “Summary” instead.
Again, you should not let yourself get bogged down by it as you can
here just skip to the full article itself. Plus this hopefully
enlightening outline which now follows, well, follows after the next
bit.
The peer-reviewed publication 203
The difficulty of presenting a new concept
Explaining something new to people is often difficult. But it
gets much harder when a radically-new concept is involved, and one
that is not outrightly simple. The problem is that the terminology
does not yet exist for referring to the new concept, and one has to
find a way to use the pre-existing set of concept-labels (words) to
attempt to describe the new one.
Central to this theory is the concept which I labelled as
“antiinnatia” (and antiinnatia factors), and which is the essential
thing underlying the autistic syndrome and more. Being a newly
invented word, the inclusion of that word in the title and
introduction to my paper would have been rather unhelpful, as it
would read as meaningless nonsense to all except myself. So I tried
to avoid that problem by substituting an expanded wording in the
title and introduction, in place of “antiinnatia”. Namely “general
impairment of gene-expression”. I’ve already told you of my decision
to now change “impairment” to “reduction”, not due to its being
wrong but simply in the context of some people who would start
complaining emotionally about my supposedly describing autistics
as having “impairments” — such that this theory must be a work of
“hate speech” or worse.
But there’s a bigger problem, in my use of the word “general”
there. It could cause the reader to suppose that I had in mind that
all gene-expression is equally affected by antiinnatia, such that
autistics would have notable reductions of for instance hemoglobin
in blood cells, myosin in muscle cells, collagen in their skin, and so
on. Anyone who reads past the first few pages can see that I go on
to explain that the reduction is much less general anyway, and
instead tends to suppress disadvantageous expressions while
leaving advantageous ones unaffected. This theory paper was
praised as being well-written, by some very notable readers
including HJ Eysenck, Bernard Rimland, David Horrobin, and some
anonymous peer reviewers, so clearly this presentational bungle
cannot have been too seriously impeding of proper understanding.
But never-theless I now consider that that “general” word is less
than optimal there, and it appears that the presentation would be
improved by replacing it with “evolution-biased”. And so in this
updated presentation I am also changing the title and introductory
sections to remove that problematic “general” word. Meanwhile, the
intended meanings are entirely unchanged from the original version.
I should also point out that my meaning of the term “gene-
expression” was not confined to the modern narrow sense of
generating RNA or proteins from genes (as was already stated in my
original). And indeed the picture is now getting even more
204 Experts Catastrophe
complicated as it is now clear that the non-”gene” parts of the
genome (the “non-coding DNA”) are where the main species (and
individual?) differences originate anyway. As I see it, the genes are
merely the catalog of bricks and tiles supplied by the builders
merchants, while the “non-coding DNA” is the construction team
and the instructions to them (though somewhat mixed up).
Outline of the antiinnatia theory of autism (and IQ and
genius)
(This outline presents only the conclusions without the
evidence or reasoning that leads to them. It also does not include
any later extensions of the theory.)
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 indi-
vidual 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 charact-
eristics. 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 character-
istics 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 tend-
ency 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 regul-
atory 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
The peer-reviewed publication 205
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 original publication 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 initial paper is
considerably strengthened now by major evidential updates such as
those 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 325-26 here.
206 Experts Catastrophe
Author’s [nearly-]unrevised reprint of:
Personality and Individual Differences Vol.14, pp. 465-482
(Copyright Pergamon Press)
A theory of evolution-biased reduction of gene-expression
manifesting as autism
Robin P Clarke, Birmingham, England,
Summary--This is the first part of a combined theory of autism and
general intelligence (IQ). It is argued that “evolution-biased
reduction of gene-expression”, produced by a diversity of environ-
mental and genetic causes, is in moderation advantageous in
reducing genetic idiosyncracies. But in extreme it will produce a
condition involving atypicalities of appearance and behaviour, with
a particular relationship to high parental social class and IQ and
with particular sex distributions. Characteristics and findings
relating to schizophrenia, manic-depressive illness, or neuroses
indicate that they cannot reasonably be considered manifestations of
extreme evolution-biased reduction of gene-expression. By contrast,
characteristics and findings relating to autism accord very well with
this conception. The suggestion is that autism involves primary
atypicalities in diverse parts of the brain and in diverse
psychological functions. Random binding to DNA may be a
substantial mechanism of evolution-biased reduction of gene-
expression. [2014 Update to the preceding sentence: i.e., would
definitely cause reduction of gene-expression, and hence cause
autism, but only may be substantially involved (see para. 15)].
~~~~~
[The main concept of this theory is antiinnatia, which could be
briefly stated to be “evolution-biased reduction of gene-expression”.
A more precise explanation of what this means will be given further
on here.]
It will be argued that the most prominent effect of varying
levels of “evolution-biased reduction of gene-expression” is the
production of individual differences in innate general intellectual
ability, by variable degrees of suppression of certain characteristics
that tend to produce slowing and errors in intellectual processing.
But that in extreme it causes the autistic syndrome. The full
application of the theory to intelligence and its correlates will be
presented in a separate paper.
The peer-reviewed publication 207
There have been many theories of autism. But there appear to
be no other theories of how evolution-biased reduction of gene-
expression would manifest itself.
The present theory differs from other theories of autism in
having the following combination of characteristics.
It is founded on an argument from well-established biological
principles, providing it with a basis in the context of evolution by
natural selection. Indeed, several conceptions that emerged in the
course of development of the theory turned out to be already well-
established findings, namely the association of reliability of
expression with advantageousness, the re-emergence of long-
suppressed characteristics, and the conservatism and resistance to
change of characteristics other than of appearance and behaviour.
It provides an explanation of why such a severely biologically
disadvantageous condition is not eliminated by natural selection,
and of why it is a relatively common mode of failure of the brain.
It addresses an exceptionally broad range of findings about
autism (and IQ). These include the wide diversity of behavioural
atypicalities (listed in table 2), including some particularly odd ones,
such as the distinctive hand-flapping and posturing, and also the
physical stigmata, attractiveness of appearance, special skills,
above-average parental IQ and differentially elevated parental
social class, the fourfold preponderance of males among the severely
autistic, and the tenfold preponderance among the mildly autistic.
Numerous specialist readers have found not one finding to cast
doubt on the theory, nor any flaw in the arguments presented here.
This was not for want of hostility.
And yet the theory cannot validly be dismissed as untestable,
or as equally compatible with any conceivable findings. Were such a
criticism justified, it would be possible to provide some substant-
iation by substituting, in place of findings about autism, the findings
about other conditions such as schizophrenia, manic-depressive
illness, or the like, and then rewriting the pages that follow so as to
explain all those findings instead. It will become clear that any such
explanations would be not merely speculative but absurd and
incredible. For example, why should evolution-biased reduction of
gene-expression manifest as alternating mania and depression?
Why should it first appear in adolescence, as does schizophrenia,
and why involve remissions and relapses? Why should relapses be
specifically triggered by hostility from others? Why should it be ten
times more prevalent among Afro-Caribbeans born in Britain than
among those migrating there, as is schizophrenia? Clearly the
charge of untestable explain-all is unwarranted.
208 Experts Catastrophe
The above combination of characteristics is very exceptional in
a scientific theory. Publication of the theory should not be further
suppressed by facile empty innuendos of “speculativeness” or
“untestability”, but only by substantiated arguments and evidence
that prove able to stand up to rejoinder.
Subsequent to the above words, referees and editors of the
British Journal of Psychology, recognising the untenability of all
other objections, concurred in the view that the theory made no
unforseen predictions (and was thus unworthy of publication even as
an article). This is simply not true. For example page [220] predicts
sequences of changes of SES and IQ distribution in response to
certain environmental factors; page [233] predicts certain EEG
findings; pages [227 and 233] predict that rigorous investigation will
confirm subjective impressions of tendency to intelligent-looking and
attractive appearance. But anyway, note that Darwin’s theory of
natural selection made no unforseen predictions whatsoever. Why is
this “criticism” so damning in this case but not at all in Darwin’s
case?
The scope of the present theory is the whole of the syndrome
that includes Kanner’s (1943, 1973) syndrome, Asperger’s (1944)
syndrome, early infantile autism, pervasive developmental disorder,
autistic-like individuals, and others who have one or two autistic
characteristics. Wing (1988) and Wing and Gould (1979) describe a
broad syndrome, the autistic continuum, involving variation in both
number and intensity of atypicalities. The present theory is a
general theory of that broad phenomenon; it accords with the
evidence of diversity of causes and effects, but is not here extended
to consideration of details of causal processes in specific cases,
because that would be excessively speculative at present.
Evolution-biased reduction of gene-expression
There now follows a presentation of an argument to the effect
that evolution-biased reduction of gene-expression would, in
extreme, be expected to give the characteristics of autism.
Thereafter the theory is related to empirical findings and to other
theories and ideas.
[2014 Update: “Phenotype” in the next paragraph is roughly-
speaking a posh word meaning the likes of me, you, or some other
living thing. In any case don’t let this word bother you.]
Gene-expression in its most narrow conception is the trans-
cription of genetic material into proteins. In this paper the term is
used more broadly to denote all or most of the processes through
which genes affect the characteristics of phenotypes. It hardly needs
arguing that these gene-expression processes are affected by envir-
The peer-reviewed publication 209
onmental factors (otherwise, variation, physical or psychological,
would be totally genetically determined). And it is equally well-
established that gene-expression is affected by other genes, such as
in interactive effects (epistasis) and that some genetic material, such
as regulatory genes, and DNA sequences for initiation and
termination of transcription, has effect mainly in enabling or
disabling the expression of other (structural) genes. There is
evidence that regulatory genes are involved in mammalian brain
development (He et al, 1989).
It is here proposed that some of these factors, both
environmental and genetic, produce an effect of [relatively]
substantially general and [sort-of] indiscriminate reduction of gene-
expression. It appears that this is an idea which has not previously
been postulated let alone investigated, yet it seems very unlikely
that such general-acting factors do not exist. Gene-expression
depends on processes that have many possibilities for malfunction,
with many common factors underlying (for example) all
transcription from DNA, all being dependent on, for example, supply
of nutrients and oxygen, and freedom from interference by viruses.
As for the idea that evolution-biased reduction of gene-
expression can be produced by genes, it will be argued further on
that such genes would necessarily be highly advantageous. This
makes their prominent existence virtually inevitable when set in the
context of a second consideration, namely that the random
generation of a mechanism that rather non-specifically reduces
gene-expression is very much more probable than the random
generation of (say) innate tendencies required for eating or drinking.
One such mechanism of genetically-produced reduction of gene-
expression is described by Watson, Hopkins, Roberts, Steitz, and
Weiner (1987). This relates to the fact that regulatory proteins (the
products of regulatory genes) not only have a strong affinity for their
specific binding sites on DNA, but also have a general though much
lower affinity for non-specific (random) DNA sequences; thus there
is “part-time” binding to “irrelevant” stretches of the genome. The
effect of such random binding is to prevent access by activator
molecules and RNA polymerases, thus preventing transcription and
gene-expression. Obviously, then, a surplus of regulatory proteins
(or pseudo regulatory proteins) would give the postulated non-
specific, quazi-indiscriminate reduction of gene-expression, but
whether this is the principal or even a major process is not clear at
present.
For convenience of presentation, processes and factors which
produce this relatively general, sort-of indiscriminate reduction/
suppression of gene-expression will hereinafter be referred to as
210 Experts Catastrophe
antiinnatia. Note that it involves both genetic and environmental
factors.
The argument that follows proves that antiinnatia must have a
quality-controlling effect, eliminating/ suppressing relatively dis-
advantageous characteristics and tending to leave those that have a
history of advantageousness.
(It is contended that the following two statements are self-
evidently true.)
In respect of genes producing advantageous effects those
producing them reliably will be more consistently selected in by
natural selection. By contrast, in respect of genes producing
disadvantageous effects those producing them reliably will be more
consistently selected out. Hence in respect of advantageous effects
reliability will become relatively preponderant whereas in respect of
disadvantageous effects reliability will become relatively rare. That
is, there will be a positive correlation between advantageousness
and reliability of expression. But this is hardly a radical conclusion;
it is well known that dominant characteristics tend to be
advantageous and recessives disadvantageous (though biologists
have failed to discover the reason just presented (Futuyma, 1986,
p 211)).
Thus, characteristics having more evolutionary history of
advantageousness will tend to be more reliably expressed, or in
other words, less reliably suppressed, that is, will tend to be less
affected by antiinnatia.
The implication of this is that antiinnatia has a quality-control-
ling effect, tending to suppress recently acquired idiosyncracies
(which tend to be disadvantageous) and leaving those characteristics
which have a relatively substantial evolutionary history of advant-
ageousness.
It should be noted that the idiosyncracies involved can be both
(1) idiosyncracies within a species, i.e., characteristics uncommon in
the species in question; and (2) idiosyncracies between species, i.e.,
characteristics of a species that are uncommon among related
species (e.g., language among mammals). Furthermore, antiinnatia
has no magic means of discerning advantageousness, present or
past, but rather there is the tendency, for the reasons just given, for
a history of advantageousness to correlate with reliability of
expression, and hence resistance to antiinnatia.
This quality-controlling effect implies that at different levels of
intensity antiinnatia affects different characteristics, and con-
sequently it enables not only the explanation of the features of
autism but also of general intelligence and its correlates.
Given the tendency of antiinnatia to suppress disadvantageous
The peer-reviewed publication 211
characteristics and leave advantageous ones, genes for antiinnatia
would be highly and persistently advantageous. Furthermore,
because of these advantageous effects, the more antiinnatia genes
an individual has, the more healthy they will tend to be, and the
more effective at getting on in life and in society (i.e., rising in social
class, of which more further on).
But beyond a certain level of intensity antiinnatia would be
disadvantageous, as considered in the next section.
Extreme antiinnatia
Extreme antiinnatia would eliminate or suppress not only
disadvantageous or neutral characteristics but also significantly
advantageous, even vital ones. And some of those characteristics
could be psychological ones.
Some readers may be sceptical of a notion that humans have in-
nate tendencies or genetically ‘hardwired’ predispositions. However,
such a view does not stand up well to examination. There is general
agreement that animals, including primates, have innate predis-
positions. And it is not very controversial to suppose that
heartbeats, breathing, and blushing inter alia are manifestations of
central nervous system innate predispositions. Some persons
nevertheless would appear to advocate that in respect of just one
species, namely humans, certain aspects of the nervous system do
not involve innate predispositions, namely those aspects that have
to do with ‘behaviour’ as distinct from heartbeats, breathing,
blushing, etc. Arguments and evidence against this peculiar
exclusion have been extensively presented elsewhere (e.g., Wilson,
1978).
Let us make this one very modest and reasonable assumption
that humans do have innate behavioural tendencies. For conven-
ience of presentation innate behavioural tendencies and the neural
mechanisms producing them will be hereinafter referred to as
innatons. Thus antiinnatia is here conceived of as producing
loss/impairment/suppression of a diversity of innatons. Some
suggestions of what particular innatons could be lost in autism will
be presented later in the consideration of particular symptoms.
It will now be argued that the effects of antiinnatia would be
particularly concentrated on psychological characteristics and
appearance.
Most significant physiological characteristics are of necessity
‘specified’ within narrow margins; for example blood pressure and
temperature. Reasons for this are (a) that the organism’s physiology
must work together as an integrated whole and this is only possible
if the diverse elements are somewhat standardised; (b) fairly small
212 Experts Catastrophe
variations, e.g., of blood pressure or temperature, can produce highly
significant reductions of functioning with consequent elimination in
natural selection.
By contrast, moderate idiosyncracies of innate behavioural
tendencies would be advantageous rather than disadvantageous.
This is because (a) uniformity of innate tendencies would tend to
produce predictability, with consequent vulnerability to competitors
and predators; (b) the diversity would tend to make individuals
complement one another rather than compete to occupy the same
narrow social roles or ecological niches.
Furthermore, moderate idiosyncracies of appearance, particul-
arly of physiognomy, would likewise be advantageous because
thereby biologically dominant individuals could mark their identity,
and because families of indistinguishable individuals would be beset
by problems.
It is well known that the conspicuous diversity (between and
within species) of external appearance and behaviour conceals very
great standardisation at the levels of physiology, cell types, and
biochemistry (Futuyma, 1986). Thus characteristics other than
morphology and behaviour tend to be highly longstanding.
It has already been argued that it is idiosyncracies that tend to
be relatively affected by antiinnatia. Thus given these concentr-
ations of idiosyncracies in behaviour and appearance we can expect
to find extreme antiinnatia manifested as atypicality of behaviour
combined with certain peculiarities of physical appearance. And
given the highly conservative unidiosyncratic nature of the other
aspects, extreme antiinnatia would not manifest as physical illness
except perhaps in the severest cases.
Causes and correlates of autism
This section starts with a number of arguments leading to a
particular conception of the relationship of autism to certain causes
and correlates, then continues with consideration of empirical
evidence relating to that conception.
It will not be proposed here that social class and IQ are causal
factors in autism; but some explanation of their nature is necessary
here for understanding of findings relating to them.
[[2016 Update: There is much scope for the reader getting
confused in the next few paragraphs. Partly we are here again up
against the problem of novel concepts never presented before, and
somewhat outstripping the writing skill I had at the time. The
theory posits that autism is characterised by reduction of human-
specific characteristics such as language and walking on feet rather
than toes, and by emergence of atavisms reverting to pre-human
The peer-reviewed publication 213
characteristics (such as the hand-flapping and webbed toes). But
ironically in the following paragraphs I am also arguing that the
antiinnatia causes the person to be more “average” and “typical”,
with less random atypicalities away from the human average (such
as having an extra toe or one eye larger than the other). So
antiinnatia tends to make the person closer to the average of the
syndrome of “humanness”. And yet as the antiinnatia increases
further, the person tends to get “averaged” yet more, towards the
average mammal, and hence less “human”. None of this is intended
to have any moral or political significance; I am simply describing
the scientific “how it is” (as I see it at least).]]
There is nothing that uniquely and invariably characterises
human beings. They usually but not invariably have two eyes, ears,
arms, etc., can use language, solve IQ tests, and so forth. But a fair
proportion of humans’ offspring are born without a brain, or like
siamese twins do not have a whole body to themselves. And to
define a human as one having human parents poses the equivalent
question of what a ‘human’ parent is. Thus it is evident that
humanness is a syndrome. [2014 Update: Meanings of the word
“syndrome” are discussed in Chapter 2 here.]
Just as there are variations between persons in the extent to
which they have characteristics of schizophrenia or autism, so
persons vary in the extent to which they have characteristics of
humanness, in the extent to which random mutation and
combination and chance events have made them atypical.
Some persons will be relatively distant from the core of the
syndrome of humanness by reason of genetic atypicality of
appearance or physical or behavioural functioning. They may be
lacking in motivations, abilities, or physical capacities. It is obvious
that such persons will generally tend to become relatively low in
socioeconomic status (SES). This could well be the major reason
why SES is correlated with good health and with IQ, even if not the
only one.
[2016 Update: Political projects to ameliorate health inequal-
ities have had notoriously limited success since I wrote that. That’s
not to say we should not keep trying or that I am some sort of
Darwinist anti-socialist. This theory has nothing to do with any
political biases, it’s just neutral science written by a person
consigned by society to the lowest of classes as it happens.]
It will be apparent from earlier pages that [so-to-speak-] genes
for antiinnatia will tend, by reducing idiosyncracies, to increase
individuals’ closeness to the core of the syndrome of humanness, and
hence genes for antiinnatia will tend to be genes for high social
class, in the sense described above. We would thus expect any cases
214 Experts Catastrophe
of autism that are more hereditary than environmental to tend to
come from higher social classes. (The co-involvement of heredity
and environment will be considered more fully further on.)
There is much evidence that IQ (general intelligence, g) is a
factor of individual differences which has major importance both
personally and socially, and that in contemporary populations it is
in substantial part non-cultural and inherited genetically (see e.g.,
Eysenck, 1979, 1982; Eysenck & Kamin, 1981; Jensen, 1980). An
indication of the great importance of IQ is the fact that a large
number of persons differentiated solely by relatively low IQ are so
unable to cope with ordinary life that they have to live in
institutions for the mentally subnormal. [2014 Update: This appears
to be no longer the case, which could be due to the reality of the
Flynn Effect increasing of IQs discussed in a later chapter here.]
The processes of genetic mutation and genetic recombination
affect us all. They introduce a random aspect into our genes, a sort
of “genetic noise”, limiting the perfectability of our genomes. At this
point I remind you of the concept of innatons explained about
earlier. We would expect this “genetic noise” from mutations and
recombinations to also cause “noise” in the functioning at the level of
innatons. This could be thought of as random junk innatons tending
to produce errors or slowing in mental processing, or alternatively as
random junk modifications of non-junk innatons.
For convenience of presentation these unhelpful innatons will
be referred to as IQ impairers. Being disadvantageous, hence un-
reliable (as explained earlier), these IQ impairers would be very
liable to suppression by antiinnatia. Levels of antiinnatia too low to
produce autism would affect the degree of expression of the IQ
impairers and hence help to determine general intellectual
efficiency, i.e., general IQ. Thus increased antiinnatia would be
associated with increased IQ. We would thus expect any cases of
autism that are more hereditary than environmental to tend to have
parents with above average IQ.
The disadvantageous IQ impairers would not be eliminated by
natural selection because of the constraints on its perfecting power
such as pleiotropy, recombination, and new mutations.
It has been remarked above that antiinnatia would be caused
by both genetic and various environmental factors. Quite properly it
is commonly thought that phenotypes are a product of interaction of
genes and environment, and cannot be produced by one or other
alone; but where a rare condition such as autism occurs it could be
mainly due to one or other of two possibilities – a rare combination
of genes or a rare environmental occurrence – and findings
presented further on suggest that there is in fact something of a
The peer-reviewed publication 215
dichotomy within autism that corresponds to this.
The suggestion is that similar outcomes should result from the
different causes, but this would not be exactly so, for the reason now
illustrated with an analogy.
In this analogy machines correspond to people and corrosion
corresponds to antiinnatia. If you store a number of machines in a
damp room certain parts such as exposed iron and steel will rust,
while other parts such as rubber and paintwork will not corrode. In
other words there is a consistent syndrome of ‘corrosion’. But
supposing the machines are placed instead in a dry room, but there
happen to be leakages of water through the roof, then while there
will be something of the same pattern of corrosion as before, it will
be less consistent and less complete, as some parts will be missed by
the water while others will be particularly affected. Likewise the
antiinnatia syndrome as produced mainly by environmental events
could be less consistent than that produced mainly by genes for
antiinnatia. Furthermore environmental factors would give a less
‘pure’ syndrome since they could produce collateral atypicalities
peculiar to themselves (such as spots from an infection). [2014
Update: Incoming mercury, even though it is of course an
environmental factor, might in its practical effect resemble more the
dampness process than the leakage process, if it is pervasively
distributed in the trace levels sufficient to cause autism. At higher
levels sufficient to kill nerve-cells, it might resemble the leakage
process.]
The conception that emerges from all this is of:
1. A relatively consistent syndrome mainly due to genes, and
associated with high parental IQ and SES; and
2. Essentially the same syndrome but less consistently
manifested and with collateral complications, mainly due to
one of a diversity of environmental events, associated with
average or below-average parental IQ and SES;
and we shall see that this is exactly what investigations of autism
have found, as will now be explained.
A diversity of environmental adversities have been associated
with autism and appear to be causal (reviews include Prior, 1987,
and Gillberg, 1988). Besides prenatal and perinatal conditions such
as rubella and hypoxia, later developments can produce autism; for
example Gillberg (1986) reports a case of ‘typical autism’ produced
for 70 days in a 14 year old by herpes simplex encephalitis.
Folstein and Rutter (1988) and LeCouteur (1988) conclude that
evidence suggests that genetics has an important role in causation of
autism. The first three studies of table 1 add further support to this.
216 Experts Catastrophe
Smalley, Asarnov and Spence (1988) state that the data are not
compatible with monogenic, autosomal recessive or X-linked
recessive inheritance for all cases; but that there could be
multifactorial inheritance, as with IQ. This is further supported by
the existence of a continuum ranging from severe autism through
the much milder and more common Asperger’s syndrome (Gillberg &
Gillberg, 1989; Frith, 1991) to normality.
Comparison of autistic persons having neurological signs –
suggesting environmental causation – with those not having them
finds that they have essentially the same syndrome of behaviours
(Garreau, Barthelemy, Sauvage, Leddet, & Lelord, 1984).
But the most noteworthy findings are those relating to social
class and parental IQ.
Decades ago it was thought that findings indicated that parents of
autistic persons tend to be of above-average social class (SES) and
IQ. Subsequently Schopler, Andrews and Strupp (1979) proposed
that these results had been entirely due to various factors biasing
the sampling of the autistic population. Among other things it was
suggested that lower-class parents would have lacked access to the
information and expertise required for description and diagnosis of a
then obscure condition; and they suggested that later studies
avoiding these problems contradicted the earlier results. It will be
argued here that sampling bias does not provide a credible
explanation of the findings. And anyway, there need not be one
absolute yes/no conclusion in respect of all times, places, and
subtypes.
Schopler et al did not prove that sampling bias had occurred,
but only showed that some conceivable biasing factors were indeed
correlated with SES. And their interpretation is challenged by a
number of findings, including Lotter’s particularly thorough survey,
regarding which they could only suggest that Lotter’s unspecified
criterion of complex rituals may have been biased.
Sanua (1986, 1987) observed that (a) between earlier and later
studies there was a broadening of the definition of autism to include
individuals with evidence of organic causation or of brain damage;
and (b) all the studies that were claimed to show no upper-class bias
in fact showed bimodal distributions of SES. He proposed that the
bimodal distributions were due to combining of two separate
phenomena, ‘genuine’ autism and similar conditions with organic
(environmental) causes. The relationship of this distinction to the
theory herewith will be readily apparent.
The peer-reviewed publication 217
Anthony (1958)
III III IV V
0
10
20
30
40
50 Low Organic
Organic
Social Class
Percent
Treffert (1970)
III III
0
10
20
30
40
50 Non-organic
Complicated
Social Class
Percent
Kolvin et al. (1971)
I,II III,IV,V
0
20
40
60
80 Pure
Complicated
Social Class
Percent
Fig. 7.1. Graphs of social class derived from Table 1 on the next page.
(These graphs were not included in the original publication,
due to lack of computer graphics at that time.)
218 Experts Catastrophe
Table 1. Social class of parents of autistic persons as found in
certain studies [for graphs see previous page]
Author/year/group N SES % p
Anthony (1958)a I II III IV V
Low organic 100 43 23 20 14 0
<0.0005
Organic 100 9 20 40 19 12
Kolvin et al. (1971) I,II III,IV,V
Pure 21 57 43
=0.026
Complicated 24 21 79
Treffert (1970) I II III
Non-organic 69 44 33 22
<0.007
Complicated 53 20 35 45
Cox et al. (1975)
Autistic 19 74 11 16
<0.05
Dysphasic 23 35 9 57
Fifteen studiesb
Autistic (bimodal) 981 42 27 [31]c
<10
-20
Controls census 17 40 [43]c
a Values of N for this study are estimated/inferred from the
percentages; Anthony states only that nearly 100 psychotic children
were involved.
b Anthony, 1958; Cox, Rutter, Newman & Bartak, 1975; Creak &
Ini, 1960; Gillberg & Schaumann, 1982; Kolvin, Ounstead,
Richardson, & Garside, 1971; Lotter, 1967; Lowe, 1966; McDermott,
Harrison, Schrager, et al 1967; Pitfield & Oppenheim, 1964; Prior,
Gajzago, & Knox, 1976; Rutter & Lockyer, 1967; Schopler, Andrews,
& Strupp, 1979; Treffert, 1970; Tsai, Stewart, Faust, & Shook, 1982;
Wing, 1980; omissions include: Campbell, Hardesty, & Burdock,
1977; Kanner, 1943; Ritvo et al, 1971; Ward & Hoddinott, 1965.
c These numbers in brackets are affected by bimodal distribution
and excluded from the calculation of significance.
The peer-reviewed publication 219
Three studies of parental SES identify (and compare) groups of
organic vs non-organic or pure vs complicated. Their findings are
shown in table 1 [and the added graphs]. The probability of all three
being due to chance is substantially less than one in 5 million.
Cox, Rutter, Newman and Bartak (1975) did not use organicity
as a criterion but did use a comparison group who were dysphasic, a
condition they described as comparable in obscurity and severity to
autism. Their results are also shown in table 1, and the probability
of all four results being due to chance is substantially less than one
in 100 million.
The sampling bias explanations were intended to account for
the class distributions of autism in general; they were not intended
to account for these differential findings. Quite what sampling
biases would differentiate between organic/ complicated and non-
organic/pure, or autistic and dysphasic? If these differentials really
were due to some unknown sampling bias then it follows from the
markedness of their results that there must have been a very great
preponderance of autistic persons remaining undiscovered.
These results are in line with the general trend which is
indicated in table 1 by the aggregated results of 15 studies
(including some bimodal distributions); the preponderance of class I
over class II has a high level of statistical significance (p < 10-20).
This suggests that sampling bias has not been a major influence in
the generality of studies.
In summary, these findings cannot seriously be squared with a
sampling bias explanation, whereas they concur excellently with the
theory presented here. And they present the following challenge:
what else could be the cause of these differential distributions?
Could it be, perhaps, that something in caviar or champagne causes
autism and that for some mysterious reason it produces the pure
type rather than the complicated? And will this alternative
explanation get to grips with many other facts about autism? The
objective conclusion is surely that these differentials are powerful
support for the theory.
The theory also provides explanation of another characteristic
of the SES data, namely the discrepancies between studies at
different times and places. Geographical differences may be partly
accounted for by the differing distribution of differing persons; for
example a rough, noisy area such as Camberwell, London (the
location of Wing’s study) would attract some sorts of persons and
repel others, probably including those with characteristics of
Asperger’s syndrome.
But there is likely to be a more important process. During the
last century there have been considerable unprecedented changes in
220 Experts Catastrophe
the environment. These include changes in the chemicals in the air
we breathe and in food and drink, and changes in medical
technology, not least affecting the prenatal and perinatal environ-
ment. And not only is there the aforementioned evidence of
involvement of perinatal conditions in autistic etiology, but also the
finding of Wiedel and Coleman (1976) of a link with unspecified
chemicals.
Now let us consider the effect of such environmental changes on
the prevalence of the two categories of autistic persons, namely
hereditary and environmental (and note that because autistic
persons rarely become parents the autism phenotype is subject to
extreme natural deselection).
Suppose, firstly, a longstanding unchanging environment.
There would then be a constant ratio of the two categories (genetic
and environmental). Suppose that subsequently there is an increase
in some ubiquitous environmental antiinnatia factors, perhaps air
pollution. Thereupon certain genotypes that had previously been
just below the threshold for autism would become autistic, and they
would belong to the hereditary, SES-linked category (the
environmental factor being ubiquitous). In due course, this new
environment would reduce the frequency of high-antiinnatia
genotypes in the population, and so the level of hereditary autism
would fall again. Conversely, a reduction of the ubiquitous factors
would result for a while in the virtual disappearance of hereditary
autism, and so on. As regards non-ubiquitous antiinnatia factors,
such as obstetric adversities and infections, a different pattern
would occur. If a rare perinatal adversity were to become somewhat
more common, then obviously, autism of the environmental category
would become more prevalent. [2016 Update: This has now
happened, as shown by Hallmayer et al., (2011).]
Methodologically impressive epidemiological studies are
relatively easy to perform in certain countries, notably Japan and
Sweden, because of systematic medical data collection covering the
whole population. But that very fact attests to the atypicality of
those nations in respect of technological sophistication; It follows
that studies in contemporary Japan and Sweden could well show
only a part of the dynamic pattern presented above.
The only epidemiological survey of the IQ of parents (Lotter,
1967) found substantially above-average scores on the Mill Hill
Vocabulary Scale (p < 0.005) and the Standard Progressive Matrices
(χ2(2, N = 15) = 98.7, p < 10-20). The other studies of parental IQ
have given similar, though less marked results (Cantwell, Baker, &
Rutter, 1978). Members of Mensa (IQ > 148) have been found to
have three to six times the normal frequency of autistic siblings and
The peer-reviewed publication 221
children (Sofaer & Emery, 1981). though the significance of this is
somewhat limited by the small number of cases. Because there is a
substantial correlation between IQ and SES, and because this
theory proposes similar bimodal distributions for both, these
findings must be set in the context of the preceding discussion of
evidence concerning SES.
Sex differences in autism and in intelligence variance
Well established findings are that about four times as many
males as females are autistic, and that among the less disabled the
ratio is even higher, about ten times (Wing, 1976; Lord, Schopler, &
Revicki, 1982).
These observations link up with the finding that most
intelligence tests have greater variance for males than for females,
and that an evoked potential correlate of IQ also has greater
variance in males (standard deviation of 59 for males, 50 for
females) (Hendrickson, 1982). Hendrickson notes that such a
difference corresponds to a male/female ratio of 5.5:1 above IQ 145
and of 47:1 above IQ 175.
There are straightforward evolutionary explanations for
greater variance among males. An individual male can have many
more offspring than an an individual female, and so exceptionality
in a male can make more impact in natural selection. And in a
social system where an “alpha male” excludes others from breeding,
genes for reduced variance in males would be selected against.
[Meanwhile females have only a small number of possible children,
so evolution favours them being risk-averse “conservative” and
hence more average, hence with that lower variance.]
The relative frequency of different phenotypes depends in
substantial part on their probability of arising by random
combination of genes and other factors. But the relative frequency
of phenotypes also tends by definition to correlate with the relative
biological advantageousness of those genotypes that tend to produce
them. Hence arises the relative preponderance of exceptionality in
males, as indicated by the IQ variances. But the translation from
genotypes to phenotypes is, of course, not absolutely directly
determinate, but rather involves a spread of probability, through the
mediation of environment. Thus there will tend also to be a
preponderance of closely related phenotypes (closely related in terms
of cause rather than effect). And it will be appreciated that
according to the present theory the phenotype most closely related to
the highly exceptional individual is the mildly autistic, and
somewhat less closely related is the severely autistic. Thus there
would be a marked preponderance of mildly autistic males, and a
222 Experts Catastrophe
less marked preponderance of severely autistic males, as is found.
What other cause could there be for these observations?
[2014 Update: Some have claimed that the preponderance of males
is because males are more affected by mercury and or by fetal
testosterone. But that merely moves the question on to why males
are more affected by those factors. They explain only some of the
how, and not any of the ultimate why.]
Emergent characteristics
When this theory was being developed it became clear that
some features of the syndrome could not be credibly explained as
simple suppressions of innatons, most notably the distinctive rapid
hand-flapping alternating with posturing. This led to the idea of
“uncovering” (impairment of suppressors) of pre-human innatons,
and thence to the following thoughts.
Some differences between a species and its immediate ancestor
can be roughly categorised as gaining of a characteristic or losing of
a characteristic. A characteristic that has had a long (multi-species)
history of advantageousness is likely (as explained above) to be well-
established in the sense of being very reliable, i.e., difficult to lose,
and in that case losing of the characteristic may most readily result
from evolution of a new characteristic that suppresses it. But this
suppressing characteristic would tend to be less longstanding, less
well-established and hence (as explained above) more vulnerable to
antiinnatia. Hence the effect of antiinnatia would be to tend to
suppress the suppressor and make the more-established older
characteristic manifest again. Thus normal humans could feature
suppressed genetic traces of innatons and physical characteristics
common among humanity’s antecedents, and the autistic syndrome
could involve re-emergence of pre-human innatons and physical
features.
Lest at this point some readers should be overcome with
incredulity, the following should first be noted. Gould (1983) states
that “the biological literature is studded with examples of these
apparent reversions” (called atavisms) (p. 180). Indeed there is clear
experimental demonstration of re-emergence of a characteristic not
expressed for more than 80 million years (Kollar & Fischer, 1980;
Futuyma, 1986, p 434-6). And a model of DNA organisation
(Bodnar, 1988; Bodnar, Jones & Ellis, 1989), with extensive
empirical support, shows how information held in DNA “domains”
may be suppressed or released by mutations or by environmental
factors such as those causing cell differentiation; it also provides a
mechanism for atavisms.
There is at least one example of an atavism being produced by
The peer-reviewed publication 223
both genetic and environmental factors independently, namely the
tetraptera mutation in Drosophila. This mutation produces
reversion to the four-winged condition that is the norm in higher
insects. An identical effect – a phenocopy – can be produced by
subjecting normal Drosophila (which have the gene to suppress the
extra wings) to either heat shock or ether at a critical stage of
development.
However, these reminiscences from evolutionary history could
be far from perfect or comprehensive, because of the distortions
produced by more recent selection pressures.
Physical appearance in autism
It was argued above that extreme antiinnatia would affect
physical appearance, and particularly would reduce idiosyncracies
and perhaps also produce emergence of some pre-human physical
features. In addition, or alternatively there could be loss of human-
specific features (idiosyncracies common to the species), giving
tendency towards the average mammalian form.
It was demonstrated by Francis Galton that attractiveness of
appearance is largely a matter of averageness, of absence of
idiosyncracies. Such results have recently been found to be
independent of race and culture (Langlois & Roggman, 1990). Thus
because antiinnatia tends to suppress idiosyncracies it should be
expected to increase attractiveness of appearance. And in fact, there
have been recurrent observations to the effect of autistic persons
being of “intelligent-looking”, “attractive” appearance. And Walker
(1976) found significant occurrences of stigmata as follows: low
seating of ears: P < 0.001; wide spacing of eyes: P < .01; webbing of
toes: P < 0.01. These stigmata do seem to have a pre-human
character but we do not see what might seem more obviously
expected, for example fur and a tail. But surely there are other
relevant factors involved which account for this discrepancy, namely
the complexity and improbability of the genetic coding required for a
characteristic, the force of recent selection of the suppression, and
the greater importance (in natural selection) and hence reliability of
such things as lacks of tails and fur as opposed to slight deviations
of form.
Atypicalities of the brain in autism
It was argued earlier that extreme antiinnatia would produce
behavioural atyplicalities by preventing or impairing the expression
of a diversity of innatons. This could involve primary atypicalities in
numerous parts of the brain.
224 Experts Catastrophe
Investigations of brain “pathology” in autism have found a
diversity of atypicalities but none of them have been found to be
consistently present (reviewed by Prior, 1987, and Gillberg, 1988).
It is not at present possible to discern whether these observed
atypicalities are causal of autistic symptoms or are merely collateral
occurrences. And it has been argued by Ciaranello, Vandenberg, &
Anders (1982) that the causal atypicalities would be in fine details
such as elongation of dendrites and axons, synapse formation or
establishment of connections with surrounding neural elements.
They suggest that “lesions at this stage might be so morphologically
subtle as to escape detection with conventional techniques yet have
profound clinical consequences”.
Goodman (1989) noted that there is a conspicuous lack of
agreement about what is the primary neurological “abnormality”
(brainstem and reticular formation (Hutt, Hutt, Lee & Ounsted,
1965; Ornitz, 1985; Rimland, 1964), left hemisphere (McCann, 1981;
Prior, 1979), mesolimbic system (Damasio & Maurer, 1978; Peters,
1986), cerebellum (Courchesne et al, 1988)), and of what is the
primary psychological “abnormality” (social/affective (Fein,
Pennington, Markowitz, Braverman & Waterhouse, 1986; Hobson,
1989), recognition/memory (Boucher & Warrington, 1976; Rimland,
1964), handling of complex symbols (Ricks & Wing, 1975), theory of
mind (Leslie, 1987), lack of motivation to understand (Frith, 1989)).
This led Goodman to favour the idea of a shared vulnerability of
several neural systems, involving genetic and environmental factors.
Such multiple primary atypicalities had already been proposed by
Wing and Wing (1971). These proposals are obviously in agreement
with the present theory.
Atypicalities of behaviour in autism
All that remains to be accounted for by the theory is the most
significant set of facts about autism: the syndrome of behavioural
atypicalities.
Table 2 gives a list of characteristics of autistic persons, based
on the list in Wing (1976); I have made additions to Wing’s list
because it was concerned only with clinical features, and because
there have been subsequent developments.
It will be appreciated that with the current limited state of
understanding of the mechanisms by which neurons produce
behaviour it is not possible to specify the physical form of any of the
innaton mechanisms, nor of how they produce their presumed
effects. Nor is it practicable to provide conclusive arguments of
involvement of innatons in respect of all of the items. But it should
be possible to show that there are here a substantial number of
The peer-reviewed publication 225
atypicalities which can all be plausibly supposed to be caused by loss
of innatons, and in many cases strong grounds for suspecting innate
involvement.
Turning to Table 2, we come first to atypicalities of communic-
ation. A theory of innate predispositions in language has already
been proposed by Chomsky (1957) but it is difficult to see any
relationship of that theory to these symptoms; hence the present
theory and Chomsky’s do not seem to offer one another much
support at this point. But it seems quite conceivable that Chomsky’s
universal grammar would not be notably vulnerable to antiinnatia
because its mechanism would be relatively simple and hence
reliable.
And yet there are a number of facts that strongly point to the
conclusion that there is some innate predisposition in language
development: (a) language learning is easier for young children
than for adults, in striking contrast to the general trend of increase
in ability and skills throughout childhood and adolescence – it is
surely remarkable that the stupendous task of learning the
meanings of words and grammar without the aid of any dictionary
or translation can be achieved by children who are in other respects
very simple-minded, while intelligent adults take degree courses to
achieve a lesser task in non-native languages; (b) humans very
consistently develop language competence regardless of
environmental impediments and intellectual deficiencies, yet efforts
to teach non-humans have consistently failed to reach beyond a very
basic level; (c) damage to certain parts of the brain produces
impairments highly specific to language; (d) there is a great
difference between pidgins and creoles (Bickerton, 1984).
If a person hears utterances in a language unrelated to any he
already knows he will not be able to distinguish in what way the
various phonemes are grouped into words, since generally speaking
words flow into one another without a break, i.e., those spaces
between words as on this page do not have a counterpart in the
sounds of the language. Would you guess, for example, how to
divide up the following utterances in Cornish and Japanese
respectively?:
“Unscuberchymblssquythawrukentradhejapelhacusaynuogell.”
“Watasiwasukosimoikitakunakattanodesugatootooikaseraretesi
maimasita.”
Even when forewarned that utterances contain separately
meaningful words it must be difficult to discover them, but in the
absence of an innate predisposition to search for such words certain
characteristics of autistic persons seem inevitable: complete failure
of comprehension, and the perfect reproduction of utterances in their
226 Experts Catastrophe
Table 2. Characteristics of autistic persons
(a rearrangement of the table of Wing, 1976, with additions)
A. Effects of nonfunctioning of innatons
1. Disorders of communication:
*Problems in comprehension of speech.
*Complete absence of speech (mutism) or, in those children who
do speak:
* -Immediate echolalia (parrot-like copying).
* -Delayed echolalia.
* -Repetitive, stereotyped, inflexible use of words and phrases.
* -Confusion over the use of pronouns.
* -Immaturity of grammatical structures in spontaneous (not
echoed) speech.
*Poor control of pitch, volume and intonation of the voice.
Problems of pronunciation.
*Poor comprehension of the information conveyed by gestures,
miming, facial expression, bodily posture, vocal intonation, etc.
*Lack of use of gesture, miming, facial expression, bodily posture
and vocal intonation to convey information.
‘Pragmatic’ deficiencies of verbal communication (see text).
2. Problems of motor imitation: difficulty in copying movements;
muddling right-left, up-down, and back-front.
3. Erratic patterns of eating and drinking, including consumption
of large quantities of fluid [also category C].
4. Lack of dizziness after spinning round.
5.*Apparent aloofness and indifference to other people, especially
other children.
6.*Lack of imaginative play or creative activities.
7.*Attending to minor or trivial aspects of people or objects instead
of attending to the whole.
8. Socially immature and difficult behaviour.
9. Failure to use gaze, facial expression, posture and gesture to
regulate social interaction. (a)
10. Rarely seeking others for comfort or affection. (a)
11. Rarely offering comfort or responding to others’ distress or
happiness. (a)
12. Rarely initiating interactive play with others. (a)
13. Rarely greeting others. (a)
14. No peer friendships in terms of mutual sharing of interests,
activities and emotions – despite ample opportunities. (a)
15. Lack of reciprocal eye-contact and social smile in first months.(a)
16. Normal attachments not present when expected. (b)
17. Rarely imitating, even when motivated. (c)
The peer-reviewed publication 227
18. Deficit of joint attention behaviours (i.e., showing an object or
pointing). (c)
B. Less direct effects of nonfunctioning of innatons
19. Abnormal responses to sensory experiences (indifference,
fascination).
20. Spontaneous large movements, or fine skilled movements, or
both may be clumsy in some children though others appear to
be graceful and nimble.
21. *An unusual form of memory: the ability to store items for
prolonged periods in the exact form they were first experienced.
22. *Intense resistance to change, attachment to objects and
routines or a repetitive, uncreative interest in certain
subjects.
23. *Absorption in repetitive activities, stereotyped movements,
self-injury, etc.
C. Emergences of long-established innatons
24. Abnormal responses to sensory experiences (distress).
25. Abnormal responses to pain and cold.
26. The use of peripheral rather than central visual fields [and or
category A].
27. Looking at people and things with brief flashing glances rather
than a steady gaze [and or category A].
28. Jumping, flapping limbs (i.e. alternate handflapping and
posturing (d)), rocking, and grimacing.
29. A springy tip-toe walk without appropriate swinging of the
arms.
30. An odd posture when standing, with head bowed, arms flexed at
the elbow and hands drooping at the wrist.
31. Erratic patterns of sleeping and resistance to the effects of
sedatives and hypnotics [and or category A].
32. *Inappropriate emotional reactions [and or category A].
D. Other suppressions of relatively idiosyncratic characteristics
33. Immaturity of general appearance and unusual symmetry of
face. (Attractive appearance, and intelligent appearance, and or
stigmata such as low seating of ears, wide spacing of eyes, and
partial webbing of toes. (e) )
34. *Skills that do not involve language, including music, arithmetic,
dismantling and assembling mechanical or electrical objects,
fitting together jigsaw or constructional toys. (Some very
retarded can read words out loud. (f) )
228 Experts Catastrophe
* Items essential for diagnosis of autism as described by Kanner (1943).
(a) Rutter & Schopler (1987). (b) Volkmar (1987). (c) Sigman,
Ungerer, Mundy & Sherman (1987). (d) Walker & Coleman (1976).
(e) Walker (1976). (f) Silberberg & Silberberg, (1967); Snowling &
Frith, (1986); Welsh, Pennington, & Rogers, (1987).
entirety as semantic units. And it is remarkable that some autistic
persons can read in the sense of translating from printed letters to
speech (which 14% of the population of the USA cannot currently
do), yet completely lack comprehension (Silberberg & Silberberg,
1967; Snowling & Frith, 1986).
Probably there is also a predisposition towards forming of a
conception of and monitoring of the mental state of others, of their
intentions, information, assumptions and points of view (this has
been conveniently labelled a “theory of mind”) [2014 Update: though
only some years after I had started mentioning that concept myself
in earlier versions of this paper sent to journals and others.]
Its absence could manifest not only in the mixing up of ‘you’
and ‘I’, but also in certain ‘pragmatic’ failures of communication
(pragmatics being defined by Bates (1976) as use of speech and
gesture in a communicative way, appropriate to the social context).
Pragmatic deficiencies identified by Paul (1987) and Volkmar
(1987) are:
1. Lack of use of non-linguistic knowledge in interpreting sentences
(e.g., “Colour this circle blue” is only understood if preceded by
“I’m going to tell you to do some things”).
2. Difficulty in judging how much and what pieces of information
are relevant in response to enquiries. (e.g., “Did you do anything
at the weekend besides raking leaves?” “No”.)
3. Difficulty in identifying the topic initiated by the other.
4. Failure to establish joint frame of reference, e.g., beginning
discussion without providing adequate background information.
5. Failure to take social norms or listeners’ feelings into account
(e,g., “You’re very fat”).
6. Reliance on limited conventional stratagems of conversation or
stereotyped expressions (e.g., “Do you know about Cambodia”).
The notion of “theory of mind” is also supported by experiment-
al evidence of inability to attribute false beliefs to others (Baron-
Cohen, Leslie, & Frith, 1985; deGelder, 1987; Leslie & Frith, 1987);
and quite how does the “theory of mind” come about anyway except
The peer-reviewed publication 229
innately?
Leslie (1987) has proposed innate mechanisms (an expression
raiser, a manipulator, and an interpreter) to account for pretend
play and the manifestations of “theory of mind”. This scheme seems
unnecessarily complex – all that is required is innate concepts (or
preparedness for concepts) of others having beliefs and attitudes,
coupled with the awareness, possibly innate, that such beliefs do not
have to be true or logical.
Baron-Cohen (1988) observes that Leslie’s innateness theory
accounts well for some findings about autism, while others are
better explained by Hobson’s (1989) theory of innate mechanisms for
expression of emotions and their recognition in others. But the
theory presented here accounts not only for all these findings but
also for the many others indicated in this paper.
It seems likely that the development of language and non-
verbal communication depends on not only the abilities of compre-
hension and expression but also on motivation. Probably a motivat-
ion to influence others (to get them to help, etc.) would be an
inadequate basis for the learning of communication skills if not
accompanied by a motivation towards informing and expressing for
its own sake. Only a small proportion of human communication
consists of appeals, requests, or inducements to perform desired
actions; informing and expressing predominate. Deficiency of such a
motivation is suggested by the lack of joint attention behaviours
(item 18), the tendency to communicate only to request some favour,
and the complete absence of expressive gestures even though
instrumental gestures are used (Attwood, Frith, & Hermelin, 1988).
Deficits of joint attention gestural behaviours (pointing, showing)
are found to predict subsequent language development in autism
(Mundy, Sigman & Kasari, 1990). Such motivation and behaviour
would presumably either be innate or a consequence of innate
reward contingencies.
It also seems parsimonious to assume that nonverbal commun-
ication involves in humans as in animals, innatons for its generation
and reception.
Certain other characteristics of autism appear to relate to
processes that must have an innate element, as will now be
considered.
As with the other sensory organs, there must be some innate
neural mechanism for detecting and interpreting movement of the
fluid in the balance-sensing labyrinths of the inner ear, and
deficiency of that mechanism would prevent dizziness caused by the
inertial flow of the fluid after spinning (item 4).
230 Experts Catastrophe
A number of the features listed in table 2 could be explained in
terms of deficiency of imitating, namely poor control of pitch,
volume, intonation and pronunciation, deficiency of non-verbal com-
munication, problems of motor imitation, erratic eating and
drinking, lack of pretend play, and the various atypicalities of social
functioning (items 2, 3, 6, 8-16, 18, and parts of 1), though it seems
more likely that most of these involve loss of specific innatons. But
surely, the normal tendency to imitate must itself be innate, and
hence all the abovementioned must be dependent one way or
another on innatons. It might be objected that imitation could be
learned by operant conditioning, but this would still depend on
something (namely innatons) providing specifications of what
constitutes ‘reward’, ‘punishment’, and ‘imitation’.
Indifference to some sensory experiences could occur if innatons
for interpreting or reacting were impaired. And how else could the
orienting response arise other than innately?
The clumsiness of some autistic persons could be due to
dysfunction of innatons either directly involved in controlling or
coordinating movements, or involved in providing the feedback
required for appropriateness of the movements. The alternative
gracefulness and nimbleness will be considered further on.
The unusually accurate memory (item 21) can be understood in
terms of a lack of innatons that normally produce categorisation,
coding, grouping, compartmentalising, or other processing of data.
For example, normals remember sentences not as strings of letters
or sounds but as strings of words. Hermelin and O’Connor (1970)
found that unlike normals, autistic persons do not find meaningful
sentences easier to remember than meaningless ones. And the
intense resistance to small changes in the environment (as opposed
to a complete change of environment) could well be a result of the
difficulty the unprocessed memory has in adapting to such partial
change – the need to start the memorising all over again. Perhaps
there are innatons in normal memory processes for the avoidance of
such problems.
It seems reasonable to suppose that a person having many or
all of the characteristics of items 1 to 18 and 24 to 32 would find life
confusing and unpredictable in many ways. This would result in
stress and distress that could be alleviated by reassuring, predict-
able data, and items 19, 22, and 23 are probably in part a
manifestation of this seeking of predictable, reassuring data
(perhaps in item 19 “fascination” may be a slight misinterpretation).
This accords with the finding that these behaviours are more
frequent in unfamiliar circumstances (Runco, Charlop, & Schreib-
man, 1986).
The peer-reviewed publication 231
It has been proposed (Lovaas, Newsom, & Hickman, 1987) that
a number of autistic behaviours including these latter involve self-
stimulation, and result from the resulting “perceptual reinforce-
ment”. This is consonant with the above but fails to explain why
certain peculiar behaviours have this self-reinforcing quality
exclusively in autism (e.g., the distinctive handflapping, of which
more below), or why the behaviours are characteristically repetitive
and predictable. Surely, the repetitiveness/ predictability is because
the reassurance is rewarding hence reinforcing; and surely the
particular repertoire of behaviours available for reinforcement
depends on what innatons the individual has – which ties in with
the idea that autistic persons have emergences of pre-human
innatons.
A number of autistic characteristics seem strongly suggestive of
emergences of pre-human innatons; indeed that is how the idea
originated. There now follows a presentation of specific instances,
then a consideration of the general merits of these explanations.
Autistic persons’ short periods of rapid hand-flapping and
posturing are suggestive of the bursts of running alternating with
rigidity that are seen in birds, squirrels and rats in certain wild
contexts.
We do not see foot-flapping such as would produce running,
presumably because it has been substantially suppressed by natural
selection. However, the mean periodicity of the hand-flapping rate
(0.26 seconds) and its mean duration (1.76 seconds) and the mean
duration of posturing (1.85 seconds) (Walker & Coleman, 1976) all
correspond well to the characteristics of the squirrel and rat
behaviours (though these same measurements are re-reported as
0.25, 3.51, and 3.67 seconds by Coleman, 1978).
[2014 Update: Online video of Purgatorius, a rat-like ancestor
of humans for 160 million years. Online video of 8-yr-old Anthony
mentioning that hand-flapping (“stimming”) is often accompanied by
equally-uncontrolled moving forward. Both observations are
remarkably in line with the explanation given above.]
Item 29 suggests the walking manner of a nonhuman primate,
in addition to which walking on toes rather than heels is the norm in
mammals.
A species idiosyncracy of humans is their upright posture.
Most animals stand on four legs, and when such animals stand on
rear legs alone they characteristically position their front legs ready
to meet the ground when they fall down to it, and they position their
heads drooping downwards since otherwise their eyes, ears, mouth,
and nose would be pointing upwards. It seems that these same
predispositions can be seen in autistic persons (item 30).
232 Experts Catastrophe
Innatons are probably also involved in ensuring that eating and
drinking are regulated to the requirements of the digestive system.
Innatons more appropriate to animals of different size and with
different digestive systems could cause the abnormalities of eating
and drinking.
Regarding item 24, a case has been reported of extreme distress
induced by the presence of a silver teapot (Wing, 1976), and a
similar case involved a silvery spoon with an ornate end. It is well-
known that phobias are usually evoked by evolutionarily long-
standing stimuli rather than by guns, electric wires, etc. It is
notable that in both the present cases a silvery object with one plane
of symmetry and of complicated shape was involved. In the pre-
human world there would have been no teapots or spoons, and such
a shape would usually be indicative of an animal, and if a silvery
one, perhaps a reptilian predator just emerged from water.
The jumping, rocking and grimacing of some autistic persons
may be a reappearance of non-verbal communications/expressions of
pre-human primates.
These notions of emergent innatons are not very testable at
present but at least they provide explanation of a number of very
peculiar phenomena in terms of a few well-established biological
principles, as indicated earlier. The alternative to these explan-
ations is to suppose that by some freak of improbability “it just so
happens” that abnormal brain functioning produces this particular
pattern of hand-flapping and posturing resembling a common
animal behaviour, and “it just so happens” that it also produces this
particular standing posture resembling that of four-legged animals,
and “it just so happens” that it also produces the manner of walking
of most mammals, and “it just so happens” that it also makes infants
scared of teapots and spoons that resemble animals in their plane of
symmetry, . . . (not to mention all the other facts about autism here
integrated together by antiinnatia). In the past fifty years no other
alternatives to these “just so” non-explanations have emerged.
[2014 Update: Nor in the subsequent 20 years either!]
It might be casually supposed that emergence of innatons could
just as credibly account for any conceivable atypicality; but, then,
supposing that autistic persons walk on their heels, adopt the
postures of ballet dancers, and flap their tongues rather than their
hands, what are the equally credible explanations?
It is not necessary to suppose that all the behavioural
atypicalities are primary manifestations of lacks of innatons or
emergences of pre-human ones. The suggestion of Carr and Durand
(1987) that autistic persons’ aggression and tantrums occur because
of lack of any more appropriate means of expression is fully
The peer-reviewed publication 233
compatible with this theory.
Two remaining characteristics in table 1, namely gracefulness
and nimbleness, and special skills, seem rather unlikely
concomitants of a severe pervasive disabling “disorder”, but they are
quite in harmony with the theory presented above. They may be
simply accounted for as further manifestations of the “quality-
controlling” effect of antiinnatia, as already exemplified by the
attractive appearance of autistic persons and the link with high
parental IQ and SES. This may also be the cause of the finding that
many (though not all) autistic children show relatively great
imagination and productivity in drawing (Boldyreva, 1974).
An important fact about autism is that while a significant
minority of autistic persons are of average to high IQ, the majority
are markedly subnormal with IQ below 70. According to the present
theory all these autistic persons have the characteristic that
normally produces high IQ, namely high suppression of IQ
impairers, as explained earlier. But if the extreme antiinnatia also
suppresses certain other innatons necessary for effective mental
functioning, such as innatons for language skill, then low IQ will
nevertheless result. Unequal impairment of different IQ-aiding
innatons would account for the notoriously uneven scores on
intelligence sub-tests (Lockyer & Rutter, 1970), which is exag-
gerated in some individuals (idiots savants), probably by constant
selective practice and social reinforcement of their single
competence.
Certain EEG waveforms have been found to show marked
correlations with IQ (e.g., Ertl, 1968; Ertl & Schafer, 1969; Shucard
& Horn, 1972; Hendrickson, 1982). The theory of IQ associated with
this theory of autism includes a mechanism which in computer
simulation reproduces the shape of these waveforms; in this
mechanism interindividual differences in the waveforms are
determined by the degree of suppression of the IQ impairers. Thus
it is to be expected that idiots savants and autistics would have
waveforms such as are usually associated with high IQ despite being
of low or unmeasureable test-measured IQ. This could be a useful
aid to diagnosis.
Concluding discussion
Numerous other theories of autism have been proposed, but
none of them address more than a fraction of the findings presented
here, and few attempt any explanation of why such a severe disorder
exists and is not extremely rare. So with good reason there has
continued to be a widespread view that the syndrome constitutes an
unresolved mystery. The present paper has argued that extreme
234 Experts Catastrophe
evolution-biased reduction of gene expression can be expected to
manifest as atypicality of behaviour and appearance, with certain
relationships to high parental SES and IQ and environmental
factors, and a peculiar sex distribution. The autistic syndrome is
shown to accord fully with the requirements, whereas other
psychiatric syndromes cannot be credibly conceived as doing so. A
remarkable diversity of facts about autism challenge the theory, but
they all prove consonant with it. Thus, though no scientific theory
can be absolutely proved correct, the reasonable conclusion is surely
that the autistic syndrome no longer presents a mystery, except in
respect of many important details yet to be fully elucidated.
An obvious shortcoming of the theory as presented here is that
it provides little or no description, physical or chemical, of the
mechanisms of the innatons and antiinnatia. This is unavoidable at
present because so much remains unknown about, on the one hand,
the precise brain mechanisms that produce behaviour, and on the
other hand, the processes controlling gene-expression. If such
detailed information becomes available then according to this theory
it may be possible to develop drugs to adjust gene-expression such as
to prevent or cure autism. Research to date in neuroscience and
gene-expression does not seem to indicate any obvious starting
points for investigation, other than the possibility of drugs to reduce
the prevalence of proteins that tend to bind randomly to DNA.
Perhaps other fruitful starting points could be provided by the
etiological factors associated with autism. For example, information
emerging about the molecular-biological effects of rubella and herpes
virus, or of atypicality of the genome associated with autism, could
be interpreted in the light of the theory.
The theory does not imply that there is no value in psycho-
logical forms of therapy, such as holding therapy, special learning
programs, or specially modified environments or routines.
It has been suggested by one of the this journal’s reviewers that
the present paper has to a substantial extent unwittingly retrodden
the same ground as Rimland’s 1964 book, and arrived at mostly the
same conclusions.
At a time when autism was widely thought to be caused by
inappropriate behaviour of parents, Rimland argued against that
theory in favour of the conception, which accords with the present
theory, of autism resulting from genetic and non-psychological
environmental factors.
He also argued that the findings of above-average parental IQ
and SES were not attributable to sampling bias. However, his
conclusion was subsequently seemingly discredited by the
accumulation of subsequent studies that showed no relationship
The peer-reviewed publication 235
anyway (Schopler et al, 1979, and subsequent). Rimland further
proposed that an excess of genes for high IQ tended to produce a
vulnerability to autism. The theory presented here concurs with
this, but goes further by presenting an explanation of why this
would be so, in terms of antiinnatia and IQ-impairing innatons.
The present theory also differs from Rimland (1964) in his
positing a single primary disability (inability to relate new stimuli to
remembered experience). The fable of the blind men and the
elephant comes to mind (they described it in turn as like a tree
trunk, a snake, a leaf). Over the years a number of suggestions have
been made of what might be a primary psychological or neurological
‘abnormality’ in autism (listed earlier). Quite possibly most of these
are correct as partial accounts of aspects of autism. And their
authors were not unreasonable in doubting the validity of other
aspects of the then uncertain syndrome. But the suggestion of the
present paper is that more or less the whole of the “elephant” has
been genuine all along.
Finally, a few words about criteria for evaluation of theories.
There has recently become widespread a view that to be worthy
of publication a theory must present precise and readily testable
predictions. I agree that these are worthy qualities in a theory, and
regret that that presented here is still at some points deficient in
this respect. But it seems to me that there is a more important
quality that a theory can have, against which precision and ease of
refutation are only secondary. This is what we might call its degree
of harmony with the totality of facts, its explaining power, the
degree to which it encompasses a whole spread of observations
within a scheme of a few basic postulates, and integrates them with
the canon of existing understanding. Should any reader think this
to be an easy quality to obtain, I commend to their consideration the
numerous previous theories of autism, of which only a few have been
cited here.
There is no reason to presume that reality has been specially
designed for the convenience of investigators conducting empirical
tests, and those who effectively make that presumption censor
themselves from any understanding that does not conform to their
preconception.
References
The references cited in this paper were in the original
publication listed at the end here as usual in a scientific paper, but
as this is incorporated in a book chapter they have here been merged
with the list at the end of the book instead.
236 Experts Catastrophe
List of changes made from the originally-published version.
{In addition to a number of notes indicated thus: [2014 Update:....]
general > evolution-biased [in numerous instances]
impairment > reduction [in numerous instances]
excess > extreme [in numerous instances]
abnormalities > atypicalities [in numerous instances]
hypotheses > conceptions
hypothesis > interpretation
impairments > suppressions
excessive > extreme [in numerous instances]
that > which [in numerous instances]
exposition > presentation [in numerous instances]
Given the existence of innatons and genetic diversity (from
mutations and recombination), we would expect to find various odd
innatons which interfere with effective mental functioning by
producing idiosyncratic errors or slowings. >
The processes of genetic mutation and genetic recombination affect
us all. They introduce a random aspect into our genes, a sort of
“genetic noise”, limiting the perfectability of our genomes. At this
point I remind you of the concept of innatons explained about
earlier. We would expect this “genetic noise” from mutations and
recombinations to also introduce “noise” in the functioning at the
level of innatons. This could be thought of as random junk innatons
tending to produce errors or slowing in mental processing. (Or
alternatively characterised as random junk modifications of other
innatons.)
these > these unhelpful innatons
highly sensitive to > very liable to suppression by
Thus ... high > Thus increased ... increased
that is > [none]
[none] > as will now be explained
hypotheses > explanations
hypothesis of sampling bias > sampling bias explanation
Now > Now let us
(note > (and note
environment: there > environment. There
[none] > (genetic and environmental)
; there are additions to Wing’s (1976) table > based on the list of
Wing (1976); I have made additions to Wing’s list
hypotheses > notions
hypothesising > suspecting
is > being
hypothesised > [none]
The peer-reviewed publication 237
come about > come about anyway
some readers > one of this journal’s reviewers
hypothesis > theory
discredited (so it seemed) > seemingly discredited
hypotheses and > [none]
hypotheses > postulates
Appendix: Modern hi-tech studies of autism causation
Since the original publication of the theory, technology has
developed to the extent that changes of expression of specific genes
in autism can now be studied. A meta-analysis of such studies was
given in a 2013 dissertation by Carolyn Lin Wei Ch’ng. At first
thought you might suppose that this should conspicuously confirm
the reductions of gene-expression which this theory has as its main
premises. And yet an unclear picture emerges instead.
What you need to bear in mind is that the overall amount of
reduction by antiinnatia would be very small even in autism. A 50%
overall reduction of gene-expression would just about certainly
result in gross non-viability rather than (“mere”) autism. A more
likely level of reduction in autism could be something like 0.1% or
even much less, as per the first graph of the last chapter here. And
the autism atypicalities would not be caused by body-wide
reductions of major protein outputs such as hemoglobin, collagen,
and so on. Instead they would be caused by very specific tweaks of
special factors in a small minority of neurons or associated glial
cells, such as to no longer pre-program those neurons to connect in
specific ways to manifest as innate predispositions (innatons).
Researchers would only find these atypicalities if they were
analysing the correct very few neurons and targetting the correct
small minority of RNA transcripts involved therein.
But there is already considerable difficulty in the relatively
rough and off-targetted analyses they are doing. The brain is an
extraordinarily complicated and little-understood thing very inconv-
eniently enclosed within a solid skull and not at all suitable for
prodding around inside until after death anyway. And so these
more challenging studies could be analogous to searching for plastic
needles in live haystacks encased in blood-filled “skulls” of concrete.
I would like to think that my ideas could someday be triumphantly
confirmed with such observations, but it looks like it may be forever
impractical. And indeed likely that the entire quest to identify the
precise cellular-molecular details of what has “gone wrong” (or more
properly “gone different”) in autistic brains may never succeed.
And meanwhile there could be better directions for autism
research to concentrate on, as can be inferred from Chapter 3 here.
238 Experts Catastrophe
But before I “sign off” this chapter, another line of molecular
analysis needs to be discussed. A reader might think as follows.
Surely if the theory were correct, then it should be possible to
identify the “antiinnatia genes” which it claims to be causing higher
risk of autism and high IQ. And yet this doesn’t seem to be
happening. Instead, there has been at best limited success in
identifying any genes clearly and majorly causal of either autism or
high IQ, let alone being “antiinnatia genes”.
I suspect a first part of the problem is that (as indicated in my
original publication) there would be not merely a handful of
“antiinnatia genes”, but many, something like thousands or more
(including variations in the non-coding DNA, hence not strictly
“genes”). A minority of those variants might have effect mainly in
increasing or decreasing the antiinnatia. But many might be
primarily contributing to some other xyz, such as basic cell
structure, while meanwhile also affecting the antiinnatia to some
extent.
A second complication is what we might call “pseudo autism
genes” (and again also including the non-coding DNA). As follows.
Let us suppose there is a genetic variation which specifically causes
increased shyness (or muteness, or mental incapacity), even though
it is not an antiinnatia gene and does not tend towards causing the
autism syndrome more generally. Nevertheless, the only thing that
autism researchers will be able to see is that that genetic variation
is associated with the “diagnosis” of autism. And they would not
know that that association is only because a person being more shy
(or mute or mentally incapacitated) is more likely to be “diagnosed”
as autistic as a result of their shyness (/etc.) and hence “diagnosed”
as a result of that gene, even though it is not at all associated with
increased antiinnatia or causing actual autism (per se rather than
“diagnosis” as autistic).
And a third and most important part of the problem relates to a
point I made in the opening pages of this chapter. Namely that the
main differences are likely to not be mainly in the genes (i.e. those
lengths of DNA which are code from which proteins are produced),
but in other parts of the genome, namely the “non-coding DNA”.
This relates to another major mistake in the history of DNA
science (alongside the misunderstanding of mutation discussed in
Chapter 2). The mistaken wisdom supposed that the information for
production of a human or other living entity was contained mainly
in its genes, that is the parts of the genome which consist of code
which gets “translated” into proteins. The newer understanding, not
least since the major ENCODE study, is substantially otherwise (as
discussed by for instance Mattick 2013; Parrington 2015; Carey
The peer-reviewed publication 239
2015; Maimon 2013). And in fact in retrospect (or in my own case
“meanwhile-spect”, as I didn’t think much about the subject until
writing this book!), it is rather obvious that the genes are more like
equivalent to just the catalog of components available from the
builders merchant, sizes of bricks and tiles available, rather than
any instructions from the architect (blind or otherwise). Or more
accurately, more like equivalent to a collection of moulds for
producing those bricks and so on. And the pattern of “expression” of
the genes would also not determine the design, just as merely
“expressing” 900,000 bricks, 80,000 tiles, and 40 glass panes would
leave much uncertainty about the building that could result from
such “expression”. Rather, in this newest understanding, it is the
“non-coding DNA” which contains most of the information on the
“design” or instructions for construction of the organism. It is
notable that the differences between species are far more in that
non-coding DNA than in the coding “genes”. This also answers the
mystery of why autism has such a strong “genetic” component (about
1/3 even in Hallmayer et al. 2011) and yet the genomics studies
struggle to find the relevant “genes”.
(The whole terminology here has got in an even worse muddle
than the autism “disorder” nonsense.)
The problem for researchers is that they have even less under-
standing of the functional significance of most bits of the “non-
coding-ome”, than they do of the genes. In respect of the actual
genes they can at least relate them to the corresponding proteins
and then delude themselves that they thereby understand what that
gene “does” for the organism.
Meanwhile I should mention that Rett syndrome, which has
often been mistaken for autism (or maybe is a sort of autism?) was
in 1999 shown to be due to defect of the MeCP2 gene, and “In fact,
the majority of genes that are regulated by MeCP2 appear to be
activated rather than repressed.” (Chahrour et al. 2008). Hence the
disability involves de-activating of lots of gene expressions. Which
was and is of course the central concept of the antiinnatia theory.
Oh well, I’m writing this as the very last bit of this book (gasp!),
and I can now latest-update that Casanova et al. (2016) have just
now reported that:
“we find that the majority of genes that confer high risk for
autism are located within the nucleus and function as nuclear
epigenetic regulators.”
and
“it is clear that the majority.... are tightly linked with general
dysregulation of gene expression, “
Well, what a surprise. (~~~~~~~)
Copyright 2020
Robin P Clarke and Best Books Press
www.pseudoexpertise.com
