Author’s
[nearly-]unrevised reprint of:
Personality and Individual Differences
Vol.14, pp. 465-482, 1993
(Copyright Pergamon Press)
(Copyright Pergamon Press)
A Theory of General Reduction of Gene-Expression
Manifesting as Autism (1993 with 2014 revisions of presentation)
Manifesting as Autism (1993 with 2014 revisions of presentation)
Robin P Clarke rpclarke[at]autismcauses.info
THIS IS NOT FORMATTED CORRECTLY (NO PARAGRAPHS) SO PLEASE DOWNLOAD FROM LINK AT RIGHT INSTEAD. Also some silly web controllers are blocking due to assuming this is a pedo porn site because it includes certain words beginning with s and ch, so I will try to delete them all from below here!
Preface about the presentational revisions
This paper was originally written for a very different
audience around 25 years ago, since when a great deal has changed both in
autism research and in the wider world.
Thus there was no mention of mercury (of which I knew almost nothing at
the time) or of the autism increase (of which no-one else knew much either back
then). And also I have become much more
experienced in writing than back then.
And paper-printed journals were very hostile to “excessive” length such
that at least one paragraph got rather more squashed than I am happy to see it
now.
So for these reasons I am making some minor changes to the
writing, which do not change the actual content or meaning but which make for a
better reading experience. For the
convenience of cynics I will list all those changes at the end. 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 may mistakenly assume an implication that the person or
their mental functioning is what I mean is impaired or inferior.
I shall also add an introductory outline of the theory
here. That is because (strange as it
may seem) the 1993 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.
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 individual differences. Exactly the same factors which generally
cause high IQ also cause autism at higher levels, and enable potential creative
genius in a narrow intermediate range of levels. I have named these factors antiinnatia factors, because
they suppress or reduce the gene-expression of innate tendencies or
characteristics. Hence
anti-innate.
Humans (and animals in general) have many innate
characteristics such as a nose in the middle of their face, eating, breathing,
blushing, learning to walk and talk and relate to their own species more than
to others. All these innate
characteristics depend on gene-expression of information in the genes.
Certain factors both genetic and environmental have a
tendency to reduce gene-expression not just in respect of isolated genes but
generally. The gene-expression
processes can be generally reduced by many common factors such as deficiency of
energy supply or nutrients, interfering
pathogens, gene-expression-controlling regulatory genes, molecules part-time
binding to DNA, and also standard epigenetic factors such as methylation of
DNA.
Disadvantageous
characteristics are less reliably expressed than advantageous ones. So they are more liable to be suppressed by
antiinnatia. These antiinnatia factors consequently have the effect of a
quality-controlling filter, preferentially suppressing disadvantageous
characteristics while leaving advantageous characteristics unaffected.
Furthermore, antiinnatia particularly affects behaviour and
appearance.
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 antiinnatia causes raised IQ).
Higher-than-normal levels of antiinnatia suppress 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 longstanding
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.
Autism is not a condition of the brain but rather of the
whole body and beyond. A person can
only be autistic in relation to a particular environment (i.e. when their
behavior is disadvantageous in relation to that environment such as a highly
intolerant community), and cannot be autistic per se. And there can never be any diagnostic test because it is not a
disorder anyway.
Finally, it is important to note that this 1993 paper is
considerably strengthened now by the major evidential updates elsewhere (but to
date still prevented from publication).
Author’s [nearly-]unrevised reprint of:
Personality and Individual Differences
Vol.14,
pp. 465-482, 1993 (Copyright Pergamon Press)
pp. 465-482, 1993 (Copyright Pergamon Press)
A Theory of General
Reduction of Gene-Expression Manifesting as Autism (1993 with 2014 revisions of
presentation)
Robin P [M] Clarke,
Birmingham, England,
(Received 20
September 1991; received for publication 14 July 1992)
Summary--This is the first
part of a combined theory of autism and general intelligence (IQ). It is argued that general reduction of
gene-expression, produced by a diversity of environmental and genetic causes,
is in moderation advantageous in reducing genetic idiosyncracies. But in excess it will produce a condition
involving abnormalities of appearance and behaviour, with a particular
relationship to high parental social class and IQ and with particular [gender]
distributions. Characteristics and
findings relating to schizophrenia, manic-depressive illness, or neuroses
indicate that they cannot reasonably be considered manifestations of excessive
general 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 abnormalities in diverse parts of
the brain and in diverse psychological functions. Random binding to DNA may be a substantial mechanism of general
reduction of gene-expression. [2014
Update: i.e., would definitely cause reduction, and hence cause autism,
but only may be substantially involved (see para. 15)].
It will be argued that the most prominent effect of general
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 excess it
causes the autistic syndrome. The full
application of the theory to intelligence and its correlates will be presented
in a separate paper.
There have been many theories of autism. But there appear to be no other theories of
how general 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 abnormalities (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 substantiation 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 general impairment 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-Carribeans born in Britain than among those migrating
there, as is schizophrenia? Clearly the
charge of untestable explain-all is unwarranted.
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 [6] predicts sequences of
changes of SES and IQ distribution in reponse to certain environmental factors;
page [12] predicts certain EEG findings; pages [8 and 9] 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 abnormalities.
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.
General Reduction of Gene-Expression
There now follows a presentation of an argument to the
effect that general reduction of gene-expression would, in excess, be expected
to give the characteristics of autism.
Thereafter the theory is related to empirical findings and to other
theories and ideas.
Gene-expression in its most narrow conception is the
transcription 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 environmental 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 substantially general and
indiscriminate reduction of gene-expression.
It appears that this is an idea that 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 general 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 con-sideration, namely that the random generation of a
mechanism that generally impairs 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 general reduction
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 general, indiscriminate reduction of
gene-expression, but whether this is the principal or even a major process is
not clear at present.
For convenience of exposition, processes and factors that
produce general, indiscriminate reduction/suppression of gene-expression will
hereinafter be referred to as 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
disadvantageous 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 a 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-controlling
effect, tending to suppress recently acquired idiosyncracies (which tend to be
disadvantageous) and leaving those characteristics which have a relatively
substantial history of advantageousness.
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 character-istics, and
consequently it enables not only the explanation of the characteristics of
autism but also of general intelligence and its correlates.
Given the tendency of antiinnatia to suppress
disadvantageous 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
innate 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 predispositions. 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 predis-positions, 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 convenience 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 character-istics 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 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,
particularly 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 concentrations of idiosyncracies in behaviour and
appearance we can expect to find excessive antiinnatia manifested as abnormality
of behaviour combined with certain peculiarities of physical appearance. And given the highly conservative
unidiosyncratic nature of the other aspects, excessive 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.
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:
“Syndrome” here meaning a clustering of characteristics, not necessarily
pathological.]
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 abnormality of appearance or
physical or behavioural functioning.
They may be deficient 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.
It will be apparent from earlier pages that 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
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 as
discussed by me elsewhere.]
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 unreliable (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.
[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.]
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 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 abnormalities
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.
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).
Table 1.
Social class of parents of autistic persons as found in certain studies
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 chiren 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.
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 (a) that 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) that
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.
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. 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
nonorganic/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 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 environment. 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.
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 (c2(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
chiren (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.
[Gender] 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 all others from breeding, genes for reduced variance in males would be
selected against.
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, 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 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 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 excessive 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.
Abnormalities of the Brain in Autism
It was argued earlier that extreme antiinnatia would produce
behavioural abnormalities by preventing or impairing the expression of a
diversity of innatons. This could
involve primary abnormalities in numerous parts of the brain.
Investigations of brain pathology in autism have found a
diversity of abnormalities 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 abnormalities are causal of autistic symptoms or are merely collateral
occurrences. And it has been argued by
Ciaranello, Vandenberg, & Anders (1982) that the causal abnormalities 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 abnorm-alities had
already been proposed by Wing and Wing (1971).
These proposals are obviously in agreement with the present theory.
Abnormalities 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 abnormalities.
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 abnormalities that 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 disorders of
communication. 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 chiren than for adults, in striking contrast to the general
trend of increase in ability and skills throughout chihood 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 chiren 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."
"Watasiwasukosimoikitakunakattanodesugatootooikaseraretesimaimasita."
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 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 experimental 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 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 comprehension and
expression but also on motivation.
Probably a motivation 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
communication 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).
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 communication,
problems of motor imitation, erratic eating and drinking, lack of pretend play,
and the various abnormalities 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. 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, compart-mentalising, 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. 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, predictable 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, & Schreibman, 1986).
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
reinforcement'. 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: Video of Purgatorius, a rat-like
ancestor of humans for 160 million years xx. Video of 8-yr-old Anthony
mentioning that hand-
Table 2. Characteristics of autistic persons
(a rearrangement of the table of Wing, 1976,
with additions)
(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 chiren 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 chiren.
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
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 chiren
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)
* 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).
c Sigman, Ungerer, Mundy & Sherman (1987). d Walker & Coleman (1976). e Walker (1976). f Silberberg & Silberberg, (1967); Snowling & Frith, (1986); Welsh, Pennington, & Rogers, (1987).
flapping
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).
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 explanations 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 abnormality; 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 abnormalities 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 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 chiren 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 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 excessive 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
exaggerated 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 excessive general impairment of gene expression can be expected
to manifest as abnormality of behaviour and appearance, with certain
relationships to high parental SES and IQ and environmental factors, and a
peculiar [gender] 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 abnormality 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
psychological forms of therapy, such as holding therapy, special learning
programs, or specially modified environ-ments 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 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.
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List of changes made from the 1993-published
version.
{In addition to a number of notes indicated
thus [2014 Update:....]
Impairment > Reduction
impairment > reduction
hypotheses > conceptions
hypothesis >
interpretation
impairment > reduction
impairment > reduction
(etc)
impairments >
suppressions
excessive > extreme
that > which
Excessive > Extreme
Excessive > Extreme
exposition > presentation
that > which
|
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.)
exposition > presentation
these > these unhelpful
innatons
highly sensitive to > very
liable to suppression by
Thus ... high > Thus
increased ... increased
that is > [none]
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]
come about > come about
anyway
some readers > one of
this journal’s reviewers
hypothesis > theory
that > which
discredited (so it seemed)
> seemingly discredited
hypotheses and > [none]
hypotheses > postulates
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