What is the point of autism?

Andrew Walker

1998, Sunderland, Autism Research Unit, Durham conference papers; Edgar Schneider (1999) Discovering My Autism : Apologia Pro Vita Sua (With Apologies to Cardinal Newman) by Edgar Schneider; Jessica Kingsley Pub; ISBN: 1853027243


Three hypotheses are presented by an autistic person. Some observed association dynamics of autistic cognitive phenotype groups with each other, and with a defined non-autistic phenotype, are discussed. The origin of the autistic phenotype is considered in evolutionary terms and a two-ancestor explanation proposed; it is suggested that autism may be a genetic trait with a racial basis rather than a metabolic disorder. The inability of the autistic to perceive and communicate memes as units of social and cultural information is suggested as a definition of the autistic condition.


Introduction: Autism is not...

To be able to answer the question posed by the title of this essay, one must begin by considering and thus agreeing upon what autism is not. There is a general consensus among the non-autistic community of researchers that autism can be defined as a social inter-communication disorder which is expressed and described by a spectrum of related conditions of relative apparent severit linked and defined by a common triad of impairments (Wing, 1988, 1996). The author has previously suggested that the fundamental difference between the autistic and non-autistic condition is at the cognitive level; that non-autistic cognition is a social multi-channel communication system whilst autistic people use only a single channel of communication at any one time (Walker, 1997). When confronted with the many concurrent facets of communication inherent in the non-autistic social world, without learned coping strategies the single autistic channel is typically and characteristically overwhelmed.

The root 'cause' of autism is apparently less clear. Study of the possible causes of autism can be divided into four broad overlapping areas. The obvious drawback with disease as a cause of autism is revealed by asking why, historically, it affects only some families and not others; what is it's nature; how is it transmitted; and how does it cause damage? Though autism has been known for at least a century, there is still no categorical supporting empirical evidence, of any description, to suggest autism is caused by an external transmissible agent or disease. The second causal hypothesis is fundamentally flawed as it requires one to accept that an unspecified cranial injury specifically afflicts succeeding generations of some unbroken family lineage's, but not others. This explanation also asks one to ignore variables due to temporal and regional variations in medical care. There is apparent evidence which may suggest that certain environmental agents may exacerbate a pre-existing autistic condition. However, there is no categorical evidence, namely proof, to suggest autism is caused by an environmental factor (e.g. Shattock and Savery, 1997).

It is not just by a process of elimination that the cause of autism appears to be linked to that of a genetic origin. There is specific evidence to support heredity (e.g. Bailey et al., 1995). In view of this, an impartial observer may justifiably wonder why the other lines of research attempting to find a 'cause' of autism should continue when considering the supporting evidence, or lack of it, presented to date. A paper on a possible cause of autism (Wakefield et al., 1998) celebrated in the popular press recently suggests that research apparently based more on faith than reason may be more than simply an example of the sunk-cost fallacy or the prospect theory (Ayton and Arkes, 1998). The efficacy and otherwise of the findings of this research have been appraised elsewhere (Chen and DeStefano, 1998; Nicholl et al., 1998).

It may be that the reasons behind the quest for the cause of the autistic 'disorder' are governed by cultural considerations. In order that the parents of a 'disordered'-labelled autistic child can reconcile the perceived losses of their emotional and material balance sheet, an explanation is required in order to attach 'meaning', and thus blame, to their unfortunate circumstance. A simple cause-and-effect explanation is the most readily understood and accepted. An anthropomorphic search for explanation in terms of meaning is as inevitable as it is endemic in the non-autistic, as the social filtering process in the Allegorical model clearly predicts (Walker, 1997). The prevailing and pervasive quasi-religious belief structures in contemporary culture adapts evolutionary theory to make itself the ultimate expression of that process. It follows then that to be different is to be struggling, but aspiring, somewhere on the slopes below their self-declared position at the summit; like Australian Aborigines, autistic people are different and therefore exist to be cured.

Observations of autistic 'associations'

As expected, an informal study of the ancestry of the author has identified individuals who, by their observed or reported behaviour, appear to be non-diagnosed autistic individuals. Most are male and there is an unbroken autistic lineage and there is one individual with formally diagnosed coeliacs disease. In addition to the apparently autistic, there are two other significant groups associated with the family. Firstly, there is an apparent attraction to and 'clustering' of non-biologically related autistic people to the family. These are friends or individuals marrying in to the family who, though not biologically related, show non-diagnosed pre-existing autistic traits.

The second 'other' group are those who show no autistic traits, indeed they are highly 'non-autistic', are mostly female and are notable for the apparently chaotic effect they have had upon the otherwise socially pragmatic semi-autistic prevailing family culture. However, these individuals also import high degrees of social organisation and a rich complimentary culture to the otherwise socially apathetic family core. This 'socialite' phenotype may be defined as being exclusively anthropomorphically perceptive and receptive individuals, belonging to a broader non-autistic group characterised by a rich and all-pervasive culture of socialisation, whose individual utterances and actions are determined overwhelmingly by calculations of interpersonal loss and gain.

Pinker (1991) and Karmiloff-Smith et al (1995) support an explanation of cognitive 'domains' as genetically determined computational modules. Following the trend towards universal phenotyping (Einfeld and Hall, 1994), delineation of the socialite sub-group allows for differentiation within the non-autistic group in social cognitive terms. The non-autistic group can therefore, as for autism, be expressed as a spectrum of phenotypes of relative social cognitive ability. As they are a measure of the same attribute, both spectra form part of a more extensive continuum with autism as one end member. Williams syndrome is characterised by individuals who have low IQ but paradoxically possess apparently unaffected and consummate social cognitive skills (Reilly et al. 1990; Udwin and Yule, 1991). Williams syndrome is therefore seen to be opposite to autism in terms of social cognitive ability and forms the other end member. Other sources of anecdotal evidence tend to suggest that this family may be typical of an autistic type; featuring autistic and socialite phenotypes as a common theme, usually appearing in voluntary association, often as typical parents of autistic children. Other studies appear to acknowledge the relevance of parental phenotype (Baron-Cohen and Hammer, 1997).

Accounting for the extremes of social cognitive phenotype: a two-ancestor hypothesis

The cognitive spectrum in terms of a histogram of frequency distribution may be expressed as a distribution curve. We would expect to find a normal curve which reflects the occurrence of diagnosed autistic and Williams' people at the tails, thereby constituting only a tiny proportion of the whole population. The curve represents and is the sum of all races and, as such, may hide racial or regional and environmental developmental differences. The obvious bimodal nature of an autism-Williams syndrome-only curve may be a reflection of an earlier racial distinction. To support a two ancestor hypothesis for cognition, two distinct sources of genetic material from two isolated ancestral populations in which cognition evolved differently are required. Both of these sources must, in turn, originate in an earlier common stock.

Neanderthals (H. sapiens neanderthalensis) and Cro-Magnons (H. sapiens sapiens and their respective forebears) apparently fulfil the criteria, namely that they are contemporary and interacted and probably interbred during a period of around seventy thousand years until thirty thousand years ago. These hominids are interpreted to be similar in overall inferred intellectual ability and shared a common ancestor. Their apparent differences are the result of divergent evolution caused by evolving at different latitudes (Stringer, 1996). Significant cognitive differences can be inferred from their respective environments. The harsher more northerly latitudes caused a greater dependency on technology and lower population density in Neanderthals, whilst the more favourable southerly climate favours a higher population density and an emphasis on higher social skills in Cro-Magnons. This may have caused a bimodal social cognitive curve in favour of Cro-Magnons, which may have been reversed in favour of the Neanderthals if technological cognition was the sole criterion.

At approximately the four thousandth filial generation, which corresponds to the present day, by applying the established principals of heredity we may reasonably expect the two ancestor bimodal curve to evolve to that resembling a normal curve. This hypothesis may therefore explain the current geographic and proportional distribution of autism and Williams syndrome in the population, the autistic and non-autistic and cognitive spectra, and respective social cognitive phenotypes.

Are autists immune to mind-viruses?

If it is accepted that there are at least two separate and distinct genetic origins for contemporary human cognition, then it may be reasonable to expect this expressed by their descendants as a 'bipolar' culture. Individuals and institutions in society apparently do identify and align themselves with, for example, either art or science, or else technology or religion. Each respective culture records for posterity its respective progress, its legacy, to future generations by established means. Technologists in science and engineering produce journals. Art, religious and popular culture is transmitted by two methods, one similar to that of technology by means of material works, and another which is less obvious.

Dawkins (1976) has defined the meme as 'a unit of cultural transmission, or a unit of imitation' which is transmitted from brain to brain as a 'mind-virus'. Socialite phenotypes, that is individuals who see and perceive their universe in allegorical cognitive terms, may communicate within their culture to like minded others by means of memes. The corollary is that autistic phenotypes do not because they perceive their universe in terms of the strictly physical and thus memes are cognitively 'invisible'. This may define the autistic phenotype and be the reason why each phenotype group has an apparently separate reality and share few common terms of reference.


Discussion: The implications, a cause for concern

Observations of associations: fashionable theory again?

A systematic investigation of extended family units would confirm the existence, or otherwise, of non-related autistic clusters. The socialite and autistic social cognitive phenotypes identified here appear broadly analogous to existing group models of folk psychologists and folk physicists respectively (Baron-Cohen et al., 1997a). The scorekeeping mentality, similar to that of the socialite phenotype, appears to have been reported on previous occasions. It may be characterised by 'fridge mothers' (e.g. Bettelheim, 1967) and quantified, for example, by the Exchange Orientation Scale (Murstein, 1978). Though the reasoning supporting the former was subsequently disproved (DeMyer et al., 1972), the original observations may still be illustrative of a real observed fundamental miscommunication occurring between the socialite phenotype mother and the autistic phenotype child.

This recurring 'attraction of opposites' theme, observed between the extreme socialite and autistic phenotypes in the context of adult relationships, though apparently incongruous at first sight, appears to be superficially mutually beneficial and conformable with existing relationship theory such as sperm competition (Baker and Bellis, 1995). There is evidence which supports the proposition that Williams syndrome is 'opposite' to autism in the folk domains of cognition (Baron-Cohen et al., 1997a), in terms of relative abilities and deficits (e.g. Bellugi et al., 1988; Gillberg and Rasmussen, 1994; Karmiloff-Smith et al, 1995; Vicari et al., 1996; Baron-Cohen et al., 1997b), and possible physiological similarities and dissimilarities (e.g. August and Realmuto, 1989; Power et al., 1997). Whilst Williams syndrome may be, unlike autism, associated with metabolic disorder, Williams syndrome may nevertheless serve to illustrate a model in extremis for the opposite end member to autism, on the theoretical social cognitive spectrum, of the observed effects of deficits in all of the cognitive domains except social skills (non learned language skills).

An excess of sociobiological reductionism or when less is more?

The cognitive phenotypes described above may indicate that there is a range of variation in the whole population in social cognitive terms which is too wide to explain without a two-ancestor theory. Successful mountaineers, explorers and certain survivors of disasters show natural adaptation to tasks in apparently hostile environments by using 'single-minded' decision processes. A simple instinct to run away is an obviously better strategy when confronted with an avalanche than wasting time consciously initiating a decision making process which may involve assessing subjective variables. It could thus be argued that an individual who perceives his or her world in the latter allegorical terms, a socialite phenotype, would be at a relative evolutionary disadvantage in such an environment. Lesser and Murray (1998) have suggested that single-minded 'monotrophism', or attention tunnelling, may be a 'hunter' adaptation analogous to the autistic phenotype. A broad and shallow, rather than narrow and deep, attention pattern characterises the non-autistic condition. Pinker (1998) has suggested that there may be an argument to support the 'savannah-brain' theory; that some forms of mental dysfunction are due to a mismatch between the environment in which we now live and the environment in which we evolved.

It is an apparent paradox that the search for evidence to support hypotheses of biochemical response of autism to environmental variables (e.g. Shattock et al. 1990), namely autism as a metabolic disorder due to biochemical cause, may in fact be due to a historical adaptation or otherwise to the relative geographical availability of components of certain food staples during an ancestral racial separation.

Memes are not us; do autistic dream electric sheep?

The origin, transmission and interpretation of implicit social and interpersonal behaviour including essentially verbal and non-verbal communication is described by Social Learning Theory (SLT) (e.g. Bandura, 1977). In simple terms, SLT, whilst accepting aspects of conditioning theory, focuses on observational learning by offspring to explain the origins of normal social behaviours as principally a function of environment as opposed to heredity. It is possible that the processes inherent in SLT are synonymous with the transmission of memes. It may follow that an apparent fundamental lack of meme processing and transmission in autistic phenotypes may exclude them from the normal interpersonal interactions with other cognitive phenotypes.

Classical psychological interpretations of human interaction such as those described Brown (1986) give a general account of human relationships in Equity Theory, which in turn encompass Exchange Theory (e.g. Thibaut and Kelley, 1959; Blau, 1964; Homans, 1974). These key papers essentially describe certain facets of human social interaction in terms of crude elementary economics; a bleak perspective, the terms of reference of which may be foreign and thus morally incompatible to the 'idealised' culture inherent in autistic interaction. Williams (1998) suggests that autistic are 'stuck' at an early sensing developmental stage, an apparently pre-cynical condition prior to the acquisition of meme communication, whilst the non-autistic continue to an interpretation stage.

Not 'the wrong trousers'

At the conference presentation of this paper, an experiment was performed where the non-autistic phenotypes comprising the audience were asked the question 'what is the point of the patches on my jeans (trousers)?' All of the respondents suggested that they were 'designed' to present a social statement of one sort or another, thus implying that they were acting as memes. When autistic people were asked the same question they suggested that the patches are there simply to cover holes. Although the jeans had in fact blindly evolved patches to cover holes, both answers to the question are correct and they are not mutually exclusive; the answer depends wholly upon the cognitive cultural perspective of the observer's own phenotype. To conclude otherwise would be to place oneself at the evolutionary summit of Mount Ignorance.

Conclusion: waving, not drowning!

The point, or singular purpose, of the autistic condition is that it may have been evolved separately as a response to specific environmental conditions. If this sociobiological hypothesis were to be substantiated by empirical anthropological and genetic evidence, it follows that there would be significant implications for the status of the autistic within society. There would no longer be a case for the inclusion of the autistic in the classifications of those who are disordered and in need of a cure; they would be regarded more properly as 'differently functioning'. The corollary would be that we, the autistic, suffer not from a disorder, but merely from numerical inferiority in social cognitive cultural terms. Proof and acceptance of such a hypothesis would, of course, have considerable repercussions not just for the autistic and their families but also for the future of the burgeoning commercial autism 'care' industry.


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Published in: Psychobiology of Autism: current research and practice. Sunderland, England: Autism Research Unit (1998). ISBN 0 95284898 0 4

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