Eye-contact and complex dynamic systems: an hypothesis on autism’s direct cause and a clinical study addressing prevention
Maxson J McDowell
Maxson J. McDowell PhD, LMSW, LP is a Jungian Analyst in private practice in New York City. He is past president of the C.G. Jung Foundation in New York. Formerly he was a molecular biologist at Duke University, M.I.T., and the MRC Laboratory in Cambridge, England.
Estimates of autism’s incidence increased 5-10 fold in ten years, an increase which cannot be genetic. Though many mutations are associated with autism, no mutation seems directly to cause autism. We need to find the direct cause. Complexity science provides a new paradigm - confirmed in biology by extensive hard data. Both the body and the personality are complex dynamic systems which spontaneously self-organize from simple dynamic systems. Autism may therefore be caused by the failure of a simple dynamic system.
We know that infants who cannot track their mother’s face often become autistic, that eye-contact initiates intersubjectivity which is blocked in autism, and that the infant-mother pair seems designed to promote eye-contact, as does the eye’s appearance. This author earlier proposed that failure of eye-contact might directly cause autism and that early non-maternal childcare, including television/video, would therefore be statistically linked to autism.
Waldman et al. (2008; 2006) recently proved that autism is strongly linked to precipitation (indoor activity) and to the introduction of cable. The most plausible explanation? Early exposure to television/video is linked to autism. Furthermore a normal developmental cascade (blocked in autism) has been deciphered: (a) Infant-mother eye-contact triggers increased maternal attention. (b) Early maternal attention permanently increases not only baseline vasopressin but also that oxytocin release which is triggered by subsequent maternal attention. (c) Vasopressin and oxytocin promote face recognition, gazing-at-the-eyes, emotion recognition, and social bonding.
The eye-contact hypothesis suggests a clinical study addressing prevention: recruit prospective parents who agree to curtail television/video/computer/wi-fi in their families; measure autism’s incidence in their children.
This paper attempts to show why an experimental hypothesis is plausible and merits testing. In brief the hypothesis is that autism begins with a failure in early learning and that changing the environment of early learning would dramatically change the incidence of the syndrome. Strong statistical evidence which supports this hypothesis has already been published by Waldman et al. (2008) but to date that evidence has largely been ignored, perhaps because it challenges prevalent beliefs about autism.
This paper also suggests that the current epidemic of autism is serious enough, and intellectually mysterious enough, to merit attention from a wider community of cognitive scientists: new ideas are needed. A confirmation of this paper’s hypothesis would have interesting implications for cognitive science.
Most clinicians and researchers in the field of autism (Hobson 2002; Klin and Jones 2007; Johnson and Morton 2009; Baron-Cohen 1994) agree that autism is a pervasive developmental disorder, that is, that a primary deficit in the fetus or infant begins (to a greater or lesser degree) a cascade of secondary developmental failures which constitute the autistic syndrome. After decades of research, however, the primary deficit has not been identified (Ungerer 1989; Muratori & Maestro 2007). This paper departs from the work of the researchers listed above only in arguing that the primary deficit which begins the cascade of developmental failures is not a genetic defect but is instead a failure in early learning.
Autism calls for an interdisciplinary approach; such an approach is difficult because insights from unfamiliar disciplines may not be well understood. Geneticists have found that autism is strongly associated with a large variety of genetic lesions. Understandably, geneticists emphasize the relevance of their own results for research in autism. Researchers who are not themselves geneticists have tended to overlook the important distinction between a genetic association and a genetic cause. This has led to the widespread assumption that autism is initiated/caused by a genetic defect.
But experts in autism genetics (Abrahams & Geschwind 2008) have shown, as I detail below, that none of the genetic lesions associated with autism seems to cause it directly: Abrahams and Geschwind say that each genetic lesion seems to disrupt brain development at a more general level, leading to a variety of developmental disorders including mental retardation; for each lesion, autism is sometimes - but not always - one of the resultant disorders. This means that each genetic lesion seems to disrupt brain development in such a way that the individual has an increased vulnerability for developing autism and other syndromes. There are diseases, sickle-cell anemia and Huntington’s disease are examples, for which a genetic lesion is the direct cause, but the genetic footprint of such diseases is quite different from that of autism. Though this may seem surprising, the available genetic evidence suggests that the direct cause of autism is not genetic. We need to identify autism’s direct cause, both to understand its mechanism and to prevent it.
To this end we need to consider all pertinent information. This paper explains some theory for readers for whom it may be unfamiliar.
1.1 Current research on the first causes of autism
Working with infants (or older children), several teams of researchers have recently described anatomical or behavioral traits which are correlated with autism. These researchers tend to assume that such traits are genetically determined. In no case, however, have they eliminated the possibility that the trait might be acquired by experience in the first days, months, or years after birth.
In their discussion of ‘embodied psychoanalysis’ Klin and Jones (2007) elaborate Hobson’s (2002) view that autism needs to be understood in the context of an ‘enactive mind’, that is, a mind which emerges as a result of the interactions an infant almost inevitably has with his/her environment. When these interactions are disrupted, autism may be the result. However Ami Klin and his associates (Kaiser et al. 2010) assume that such disruptions are initially caused by ‘strongly genetic neurodevelopmental’ defects. Kaiser et al. used functional magnetic resonance imaging with 4 to 17-year-old children and detected neural signatures which characterize ‘the disruption in brain circuitry’ associated with autism spectrum disorders.
Working with 30-month-old children Chawarsaki et al. (2010) showed that children with autism show atyptical ease of disengagement from attending to faces. In a 15-month-old infant with autism Klin and Jones (2008) observed altered face scanning and impaired recognition of biological motion. In two-year-olds with autism, Klin et al. (2009) identified abnormalities eye-tracking behavior and abnormalities in tracking of point-light displays of biological motion. Drawing upon an earlier claim by Simion et al. (2008) that ‘newborns have a predisposition for biological motion’, Klin et al. suggested that autism may result from ‘neurobiological anomalies that predispose’ an infant not to attend preferentially to biological motion.
Simion et al. (2008) claimed that two-day-old infants show spontaneous preferences for biological vs. nonbiological point-light animations. A viewing of Simion et al.’s point-light animations (available online, ibid), however, suggests that their results may be an artifact of experimental design. What they term ‘biological motion’ may be any motion in which the movement of points of light is coordinated to create contrasts of direction and speed, that is, in which visual stimuli reinforce each other: the authors may simply be detecting a newborn’s stronger response to stronger stimuli. These authors also observed a (smaller) preference for upright vs upside-down ‘biological motion’, but this observation might also be an artifact: a newborn might, for example, respond more strongly to stimuli in the lower half of its visual field.
Baron-Cohen et al. (2005) suggest that some aspects of autistic neuroanatomy may be extremes of typical male neuroanatomy. This extends Baron-Cohen’s (2003) argument that impaired empathizing and enhanced systematizing, both of which are characteristic of autism, are extremes of normal male characteristics. Chakrabarti et al. (2009) showed that sex steroid-related gene variations are associated with autistic traits in adults. As I explain later in this paper, such associations, if confirmed, would say nothing about direct causes: they would prove only that there is an indirect link.
Auyeung et al. (2010), associates of Simon Baron-Cohen, have shown that elevated foetal testosterone levels are positively correlated with psychological autistic traits in 18 to 24-month toddlers. They conclude that ‘given that sex steroid-related gene variations are associated with autistic traits in adults, this new finding suggests that the brain basis of autistic traits may reflect individual differences in prenatal androgens and androgen-related genes.’ It has not been proven, however, that autism originates in brain anatomy: differences in brain anatomy may be secondary to an early disruption in learning. Furthermore this research does not give evidence of direct causation. Prenatal androgen levels might promote autism indirectly by affecting post-natal learning processes.
Farroni et al. (2002), associates of Mark Johnson, found that when a human newborn is presented two photographs of the same face, one gazing directly at the infant, the other with eyes averted, the newborn looks preferentially at the direct gaze. These authors argue that their results support theories of an innate ‘eye-direction detector’ or of a sub-cortical face-detection mechanism in newborns (Johnson & Morton 1991; Baron-Cohen 1994). The mean age, however, of their subjects was three days while infants begin learning at birth from their intense exposure to human gaze. Furthermore, in Farroni et al.’s photographs of direct-gaze and averted-gaze (available online, ibid), it is vividly apparent that the former provides more visual edges. Their results are therefore fully consistent with the possibility, which I explain later in this paper, that a newborn detects an image of the eyes simply via the newborn’s preference for visual edges.
Faroni et al. (2005) found a preference in newborns for a visual stimulus in which a dark area is surrounded by a lighter surface (the contrast polarity characteristic of the human eye). Again their subjects had already been exposed to learning from human gaze because they were aged between 0.5 and 7 days. Faroni et al. (2007) showed that several-day-old infants exhibited a visual preference for smiling faces, but acknowledged that this preference might have been learned since newborns are intensely stimulated, from birth onwards, by exposure to smiling faces.
Elsabbagh et al. (2009), associates of Mark Johnson and Baron-Cohen, found abnormal neural correlates of eye gaze processing in 10-month-old infants who were siblings of children with autism spectrum disorders. Grossman and Johnson (2010) showed that five-month-old infants, like adults, recruit a specific brain region in the left dorsal prefrontal cortex when engaged in joint attention. This, they argue, ‘suggests that the human infant is [normally] neurobiologically prepared for sharing attention with other humans.’ These authors note that ‘impairments in joint attention are one of the earliest signs of autism,’ thus implying that a biological impairment of shared attention might cause autism.
Bergman (1985) documented the healing of an autistic child through psychoanalytic treatment. Deborah Fien (Poitras 2010) recently documented that at least 10%, and perhaps 20% of children who have clearly satisfied the criteria for a diagnosis of autism or autism spectrum disorder are able, given intensive behavioral therapy before age 4 or 5, to ‘move off the autism spectrum’. These results are not consistent with genetic causation because a genetic deficit is unlikely to be reversed by psychoanalytic or behavioral therapy.
1.2 A new hypothesis
I begin by noting that autism does not necessarily affect intelligence. Then I discuss a recent review of genetics research on autism. Then I describe the evidence which led to my hypothesis that the direct cause of autism is a failure of infant-mother1 eye contact.
Why is it plausible that a failure of eye-contact may cause autism? To answer this I discuss the new paradigm of complexity: a complex dynamic system self-organizes from the spontaneous interactions of simple dynamic systems, together with selection from the environment; in biology, genes are a precondition for anatomical and psychological structure but genes do not themselves predetermine structure (Elman et al. 1996 pp. 319, 350-2). The validity of this new paradigm is not in question (Holland 1995, 1998; Elman et al. 1996 pp. 322). It has been confirmed in economics and computer science and, in biology, by much hard evidence from biochemistry, molecular biology, entomology, and ecology. Nevertheless the new paradigm needs to be discussed because we have not fully absorbed its implications: we are still inclined to think of ourselves linearly as genetically-predetermined structures - like an automobile that is linearly predetermined by its blueprint.
I argue that, because the personality is a psychological complex dynamic system, it must self-organize out of psychological simple dynamic systems. The failure of one of these would have pervasive effects. Infant-mother eye-contact is a simple dynamic system which begins at six weeks.
2. Autism spectrum disorders and intelligence
The autistic syndrome varies greatly in severity. A child with Asperger’s syndrome (mild or high-functioning autism) has normal intelligence and language but has a social deficit and a narrow range of interests and activities (Rapin 1997). A child with classic autism may sometimes have high intelligence, but has more severe social symptoms including:
marked impairment ... of nonverbal behavior such as eye-to-eye gaze, facial expression, body postures, and gestures to regulate social interactions; failure to develop peer relationships; ... lack of showing, bringing, or pointing out objects of interest; lack of social or emotional reciprocity; failure to distinguish among persons; language that is not used for ... interpersonal communication, but is characterized by echolalia and references to the self in third person (ibid).
Hans Asperger (1944; Frith 1991) found that Asperger’s individuals could be highly successful in intellectual pursuits:
To our own amazement, we have seen that autistic individuals, as long as they are intellectually intact, can almost always achieve professional success, usually in highly specialized academic professions, often in very high positions, with a preference for abstract content. We found a large number of people whose mathematical ability determines their professions; mathematicians, technologists, industrial chemists and high-ranking civil servants.
It is common for scientists and mathematicians to show some degree of Asperger’s traits (Baron-Cohen et al. 2001). According to standard criteria it seems very likely that Newton, Einstein, and Cavendish had Asperger’s syndrome (James 2003). Because autism is sometimes associated with high intelligence its immediate cause does not necessarily affect intelligence: it’s immediate cause must specifically target social abilities.
3. The incidence of autism is increasing rapidly
The California Department of Developmental Services (2007) reported that:
From 1987 to 2007, the number of people with autism spectrum disorders grew 1,148 %. [This increase is] significant when compared to increases of 73 % for cerebral palsy, 66 % for epilepsy, and 95 % for mental retardation. During this same period, California’s general population grew 27 %.
In 1999 it was estimated that between 0.1 and 0.2 percent of all children are autistic (Gillberg & Wing 1999). In 2007 the Center for Disease control estimated that the incidence in the united states was 0.75 percent. In 2009 their estimate increased to 1 percent (Kogan et al. 2009). Ganz (2006; 2007) estimated that, due to the high costs of treating and caring for a typical autistic individual over his or her lifetime, the annual cost of autism to US society is thirty-five billion dollars.
Byrd et al. (2002) have shown that the increase in California from 1987 to 1998 cannot be accounted for by changes in diagnostic criteria, by mis-classification, or by the immigration of autistic children. Hormatertz-Picciotto & Delwiche (2009) have shown in a rigorous statistical study that the increase in California cannot be explained by differential migration, diagnosis at earlier ages, changes in diagnostic criteria, and inclusion of milder cases. The incidence of autism rose 7- to 8-fold in California from the early 1990s to 2008. Changes in diagnostic criteria seemed to contribute a 2.2 fold increase, inclusion of milder cases a 1.56 fold increase, and earlier age at diagnosis a 1.24 fold increase. These increases total a 5 fold increase, which leaves a 2-to 3-fold (very large) increase unaccounted for. While other statistical artifacts have not yet been fully excluded (for example, wider awareness, greater motivation of parents to seek services as a result of expanding treatment options, and increased funding for treatment), the most plausible explanation for these figures is that there has been a sharp increase in the real incidence of autism.
Yazbak (2003) commented:
Suggesting that a sudden and exponential increase in autistic disorders is not real, and results only from better diagnosis, amounts to denial ... Similarly, though some affected children have Fragile-X Syndrome or a family history of autism, it does not seem reasonable to insist that the present autism outbreak is solely caused by hereditary factors. Genetic disorders have never presented as epidemics, and investing the scant available resources solely in genetic research diverts them from the scientific exploration of more plausible environmental etiological factors.
Genetic factors cannot account for a rapid increase in autism in many countries because the gene pool cannot change rapidly without extremely large migrations. The increase must, therefore, be triggered by a rapid change (in many countries) in one or more as-yet-unidentified environmental factor(s).
4. A biological deficit?
4.1. Biological deficits are neither necessary nor sufficient causes
Rodier (2000), who argued for a biological cause, said that:
In utero exposure to rubella (German measles) or to birth-defect-causing substances such as alcohol ... increases the chances that autism will develop. People with certain genetic diseases, such as phenylketonuria and tuberous sclerosis, also have a greater chance of developing autism. None of these factors, however, is present frequently enough to be responsible for many cases.
In identical twins, one twin may be autistic and the other not. A direct cause of autism should be both necessary (without it, no autism) and sufficient (when present, so is autism). Though a variety of biological factors are associated with autism, none of the biological factors is either necessary or sufficient.
4.2. A recent review of genetic research
In a review titled ‘Advances in autism genetics: on the threshold of a new neurobiology,’ Abrahams & Geschwind (2008) summarize the data as follows:
Thus, in contrast to the complete absence of any biological understanding of ASD (autism spectrum disorders) as recently as 30 years ago, we now know that defined mutations, genetic syndromes and de novo copy number variations account for about 10-20% of ASD cases. However, the striking finding that none of these known causes accounts for more than 1-2% of cases is reminiscent of mental retardation, an overlapping but distinct neurodevelopmental syndrome for which there is no single major genetic cause, but rather many relatively rare mutations.
New data on de novo copy number variations which are linked to autism was published this year by the Autism Genome Project (Scherer et al. 2010) but the new data does not change the above percentages nor their meaning. Scherer et al. confirmed Abrahams and Geschwind’s percentages by noting that, taken together, all known genetic variants could only account for 20% of cases of autism and that, of the genetic variants they had found, none were present in more than 1% of individuals with autism.
No one genetic factor accounts for more than 2% of cases, which means that no one genetic factor is a necessary cause since at least 98% of cases occur in its absence. Neither is any one genetic factor, with the possible exception of Potocki-Lupski syndrome, a sufficient cause. Elsewhere in this review the authors state that ‘there is a growing list of single genetic lesions, each of which seems to be largely sufficient to cause an ASD’. But their data shows that only 20-70% of the individuals who have a single lesion also have an ASD, which means, by definition, that the genetic lesions are not sufficient.
Abrahams & Geschwind themselves state that no genetic factor seems to be a direct cause of autism. They note:
Overall, none of the molecules or syndromes currently linked to the ASDs have been shown to selectively cause autism. Instead, each seems to result in an array of abnormal neurobehavioural phenotypes, including autism, Asperger syndrome, non-syndromic mental retardation and other neurodevelopmental abnormalities.
This indicates that genetic lesions ‘cause’ autism only in the indirect sense that genes are a precondition for all biological phenomena. A familiar example of indirect ‘causation’ is genetically-based blindness which, though it may be strongly associated with illiteracy, is neither necessary nor sufficient to cause it. Blindness blocks everything which depends upon vision and thus indirectly ‘causes’ illiteracy. Another example is genetically-based fair skin which, though strongly associated with skin cancer, is neither necessary nor sufficient to cause it and is not skin cancer’s direct cause. When a disease does have a direct genetic cause - familiar examples are Huntington’s disease and sickle-cell anemia - then the mutant allele is both necessary and sufficient: it has its effect by changing the building blocks which are available to self-organization.
In the first paragraph quoted above, the authors note that autism’s genetic footprint is like that of the ‘overlapping but distinct neurodevelopmental syndrome,’ mental retardation, ‘for which there is no single major genetic cause, but rather many relatively rare mutations.’ Mental retardation reflects the overall functioning of the cerebral cortex and thus is a frequent result of anything which interferes with brain development. The many not-necessary genetic lesions associated with mental retardation are therefore likely to be ‘causes’ only in the indirect sense. The same is true for the many neither-necessary-nor-sufficient genetic lesions associated with autism.
The authors describe autism as a ‘neurodevelopmental’ and ‘neurobehavioral’ syndrome. These adjectives imply that neurological abnormalities are causal but this has not been proven. Characteristic changes in neuroanatomy may be associated with autism (see, for example, Elsabbagh et al. 2009) but, since brain anatomy is plastic and extensively shaped by early learning, such changes may readily be a secondary consequence of autistic behavior.
Under the subheading ‘Autism has a strong genetic basis’ Abrahams & Geschwind summarize current evidence thus:
Several lines of evidence support genetic factors as a predominant cause of the ASDs. First is the growing body of literature demonstrating that mutations or structural variation in any of several genes can dramatically increase disease risk. Second, the relative risk of a child being diagnosed with autism is increased at least 25-fold over the population prevalence in families in which a sibling is affected. Third, siblings and parents of an affected child are more likely than controls to show subtle cognitive or behavioral features that are qualitatively similar to those observed in probands (the broader autism phenotype); this is consistent with the segregation of quantitative sub-threshold traits within these families. Fourth, independent twin studies, although small, indicate that concordance rates for monozygotic twins (70-90%) are several-fold higher than the corresponding values for dizygotic twins (0-10%) (refs). An important question for future work will be to clarify how environmental and genetic factors interact to influence risk and presentation.
The statement made above in the subheading, ‘autism has a strong genetic basis’, is justified only in the indirect sense by the evidence given. First, some mutations dramatically increase the risk: these mutations may be ‘causes’ only in the indirect sense. Second, siblings are 25-fold more likely to develop autism: again the genetic similarities may be ‘causes’ only in the indirect sense; moreover, sibling data does not distinguish between genetic and environmental factors since siblings share physical, chemical, biological, psychological, and social environments. Third, siblings and parents are more likely to show subtle autism-like symptoms: the same two qualifications apply. Fourth, independent twin studies of monozygotic twins compared with dizygotic twins show a several-fold increase in concordance: again these studies do not distinguish between a genetic association and a genetic cause.
Since this paper is authoritative and summarizes all current evidence, we must conclude that autism is sometimes associated with genetic defects but that such defects are likely to be ‘causes’ only in the indirect sense that genes are a precondition for all biological phenomena. Though sophisticated tools exist for studying genetic lesions, this may not be a promising direction for research in autism. Our understanding of autism would be greatly advanced if we could identify a defect which is autism’s direct, immediate cause.
5. Tracking the mother’s face
The correlation between autism and congenital infant blindness (Brown et al. 1997; Hobson et al. 1999; Bower 2009) is very high. If the mother of a blind baby relates to it actively by means of touch and sound then her baby’s development may be close to normal; if the mother does not do so then her baby is very likely to develop autism (Als et al. 1980). These autistic children do not have higher-than-normal rates of any other biological factor. What they have in common is blindness and a consequent failure to relate to the mother in infancy.
There is also a high incidence of autism in children who were institutionalized at birth (Fraiberg 1977, pp. 185-7). There was a high incidence, for example, in children who were adopted in the U.K. from orphanages in Romania (Rutter et al. 2001). These children are normally sighted but were neglected in cribs during infancy. The Romanian children do not have higher-than-normal rates of any biological factor. Infants who have cranial nerve palsy with consequent paralysis of eye muscles are also liable to develop autism (Stromland 2000).
These three different groups, congenitally blind children, children institutionalized at birth, and children with cranial nerve palsy, share one common deficit: they are all unable to track a care-giver’s face. It seems that early deprivation in visual stimulus by a care-giver’s face often leads to autism.
6. A deficit in psychosocial development with secondary brain differences
An autistic child seems not to know that his or her mother has a subjective self. Hobson et al. (1999, p. 55) suggested that the ‘final common pathway’ (primary deficit) is a failure to develop a theory of mind. A theory of mind (or the lack thereof) may be inferred from a child’s visual behavior. An autistic child makes little eye-contact, pays little attention to the mother’s face, and ignores the mother’s facial expressions. Consequently the child lacks social referencing: it cannot evaluate an ambiguous situation by checking the mother’s expression. The child also lacks shared attention: it cannot follow the mother’s eyes see what she is seeing, nor point to share feelings about something with the mother. Such deficits have recently been demonstrated at less than six months. These studies used home movies of infants who were later diagnosed as autistic (Maestro et al. 2001). Amongst infants later diagnosed to be autistic, some appear never to achieve eye-contact while others achieve some eye-contact, then lose it in subsequent months (Muratori & Maestro 2007). Since a limited degree of eye-contact normally begins at birth (Farroni et al., 2002), a deficit in eye-contact may also begin at birth.
From evidence of this kind, Trepagnier (1998, p. 158) proposed that brain differences are secondary in autism. She suggested that a failure in face-processing (due to very-early-onset anxiety/affective disorder) is the key. Klin et al. (2002) showed that an autistic person looks preferentially at the mouth rather than the eyes in another’s face. A normal person does the opposite. Klin et al. suggested that this preference may represent a core social deficit in autism.
7. The eye-contact hypothesis
Both Hobson and Trepagnier proposed that psychological deficits cause autism. I have proposed that the primary deficit in autism is the failure of the infant-mother pair to achieve or retain eye-contact (McDowell 2002; 2004a, b)2. I further proposed that, (a) provided a blind infant is actively mothered, the infant-mother pair may achieve an equivalent contact through the other senses, (b) a sighted infant who is neglected may fail to achieve or retain eye-contact, (c) each of the biological factors associated with autism increases the risk that the infant-mother pair will not achieve or retain the eye-contact, and (d) the attainment or functioning of eye-contact may be disturbed to varying degree.
To understand how an early failure of eye-contact could lead to autism, we must first discuss complexity.
8.1. Human complexity
A human being, body and personality, represents an astronomically high degree of complexity which is not commensurate with the relatively small amount of information stored in genes. One estimate is that human body contains about 5x1028 bits of information in its molecular arrangement, while the human genome contains only about 105 bits of information (Elman et al. 1996, p. 319.) It is known that a gene functions by predetermining the sequence of bases in a ribonucleic acid and the sequence of amino acids in a polypeptide. The three-dimensional structure of an enzyme or regulatory protein then emerges from the polypeptide’s spontaneous folding (self-organization) under the chemical constraints of the intracellular environment (Alberts et al. 2007 pp. 134-7, 387-8)3. An enzyme then catalyzes a chemical reaction while a regulatory protein modifies gene expression. The other structures within the cell - for example the DNA double helix, chromosomes (Wood and Crowther 1983; Alberts et al. 2007, pp. 195-245), transfer RNA molecules, ribosomes (ibid pp. 378-9), membranes (ibid p. 9) and mitochondria - all self-organize spontaneously. Since genes do not predetermine structure even at the level of the folded form of enzymes and regulatory proteins, they certainly do not predetermine multicellular structure.
Furthermore the total number of different genes in our chromosomes is very small. We have only about five times as many genes (20,500) as a bacterium (3-5,000) (Broad Institute of MIT and Harvard 2008; Alberts et al. 2007, p. 31). A microscopic nematode, one of the simplest animals, has about 19,000 genes. But our structure is astronomically more complex than that of a bacterium or nematode. Moreover, we evolved from a species of ape - the common ancestor of humans and chimpanzees - within the last six million years.
The rate at which genes mutate is unchanging: six million years is only long enough to permit a small number of mutations. Current estimates are that humans and chimps differ by perhaps 2,000 significant mutations (Chimpanzee Sequencing and Analysis Consortium 2005; Lovgren 2005). The genetic difference between humans and chimps is no more than that between two species of mice. In humans these genetic differences achieve their dramatic effects mainly by changing the timing of the process by which a fertilized egg develops into an adult (McKinney & McNamara 1991; for a recent example of the role of mutations in development see Saenko et al. 2010). For example, one genetically-determined difference between a human and an ape is that, in human development, the cerebral cortex continues to grow in volume for a longer period of time. The result is that we have a bigger cortex. The greater complexity of our cortex cannot be predetermined by mutations because, by astronomically large orders of magnitude, there are not enough mutations to do so. Its greater complexity must be achieved by other means.
The brain’s complexity is much informed by its environment (Karmiloff-Smith 2009). For example, when a child learns to speak the language centers in the human cortex expand relative to adjacent cortical areas. If the child does not learn to speak those areas do not expand. Thus the information required for the formation of language centers in the brain is mostly acquired by learning to speak. Experiments with ferrets have confirmed this (Sharma et al. 2000). Visual information from the eyes was surgically redirected to the auditory region of the newborn ferrets’ developing cortex; the auditory region became a visual region.
8.2. A new paradigm
To understand complexity Holland (1998, see pp. 8-9, 229-31: the parallel evolution of eyes in vertebrates and cephalopods; also the evolution of cells), Gell-Man, Kauffman and others have elucidated a new paradigm: complexity emerges (self-organizes) when a small number of simple components interact spontaneously according to simple rules and the environment provides simple selection criteria.
This can best be understood by means of an example. In chess (Holland 1998, p. 23) there are only six different pieces - 32 pieces in all - set up in a simple pattern on a board of 64 squares. Each of the six pieces moves according to its own simple rules. When all the pieces interact, however, there emerges an astronomically large number of possible sequences of moves. This complexity is nowhere specified in the game’s rules but is an emergent consequence of those rules. Most sequences are nonsensical. By applying a few simple selection criteria, however, we can easily select serviceable games. Examples of selection criteria are: only sequences ending in checkmate or stalemate; only sequences shorter than 20 moves. The pieces and their simple rules generate possibilities while simple selection criteria ensure that only serviceable games emerge. Because each selection criterion has a dramatic, pervasive effect on the outcome, a small increase in the number of selection criteria can make the outcome highly predictable. Thus complex, functional, predictable organization can be achieved from minimal information: this is what is needed to account for human complexity.
8.3. Dynamic systems
Live phenomena are not static, like a finished chess game, but dynamic. A dynamic system is a spontaneous organization which requires a continual flow of energy. An example is the whirlpool in your sink: it forms only while the kinetic energy of moving water flows through it. If you block the drain, the kinetic energy subsides and the whirlpool ceases to exist.
Dynamic systems share the following properties:
Dynamic systems also exist in living cells: the Krebs cycle, for example, burns fuel molecules to produce heat and carbon dioxide (plus energy-storing molecules which transfer energy to other dynamic systems throughout the cell).
8.4. Complex dynamic systems
The whirlpool, the fire, and the Krebs cycle are each simple dynamic systems. A collection of several simple dynamic systems may spontaneously interact with each other according to simple rules, thereby forming a complex dynamic system. These rules are not imposed from an external blueprint, but arise spontaneously from the intrinsic properties of the component systems.
In the living cell, for example, the Krebs cycle is one of many cycles/pathways, each a simple dynamic system. (Each ‘structure’ within a cell also behaves like a cycle/pathway and can also be understood as a simple dynamic system.) Each cycle produces molecules which are consumed by other cycles. Each cycle is homeostatic. The activity of each cycle is regulated by the supply of its input molecules and the demand for its output. Thus ‘supply and demand’ is one of the simple rules by which cycles interact (Alberts et al. 2007 pp. 88-102; Mitchel 2009). All these component simple systems, interacting together, form a homeostatic network which is the cell. In this (schematic)4 description, a cell is a ‘first-order’ complex dynamic system.
Many cells interact spontaneously to form a kidney. Each cell creates products which are used by other cells. Each cell is regulated by other cells according to simple rules. Together the cells form a homeostatic network. In this (schematic) description, an organ is a ‘second-order’ complex dynamic system (Holland 1998, pp. 225-31). Organs interact spontaneously in a homeostatic network to form an individual plant or animal, a ‘third-order’ complex dynamic system. For bees, ants, and termites (Bonabeau et al. 1997), individuals interact spontaneously to form a colony, a ‘fourth-order’ complex dynamic system. Plants, animals, and micro-organisms interact spontaneously according to simple rules to form an ecosystem (Levin 1998; Scheffer 2009; Loeuille 2009), a ‘fourth- or fifth-order’ complex dynamic system. An ecosystem integrates myriad interactions to form a flexible but intensively-ordered whole. And yet there are no genes to order an ecosystem.
8.5. Complex adaptive systems
Because it adapts spontaneously to its environment, a higher-order complex dynamic system is sometimes termed a complex adaptive system. An ecosystem, for example, adapts to climate changes to maximize biomass. A market-based economy (Arthur 1999) is a complex adaptive system whose component systems are individual businesses. It adapts spontaneously to its environment to maximize productivity.
Some complex adaptive systems have the capacity not only to adapt, but also to learn an adaptation, that is, the adaptation includes persistant internal changes which influence the system’s future behavior. Such systems can then move progressively through a series of further adaptations. In biological evolution learning occurs at the level of population: the population evolves over many generations. An ecosystem not only adapts to environmental changes but also evolves in the direction of greater diversity and greater biomass.
8.6. The human personality:
Carver and Scheier (2000) defined the personality as ‘a dynamic organisation, inside the person, of psychophysical systems that create a person’s characteristic patterns of behavior, thoughts, and feelings.’ My definition5 expands theirs to include the interpersonal: the personality is a person’s system of desires, affects, feelings, bonds, ambitions, ideals, expectations, sensations, images, memories, dreams, intuitions, ideas, habits, skills and activities, conscious and unconscious, interior and interpersonal.
8.6.1. Is software and dynamic
Computer software is composed of programming instructions; it is different in kind from computer hardware. Hardware and software affect each other’s functioning but the difference between them is clear. In a similar way the human personality, as defined, uses the brain and body as a vehicle but is psychological, different in kind from the brain and body (the human systems may overlap more than the computer’s).
Unlike computer software, the personality is a dynamic system which can only exist while psychological energy flows through it, that is, while it receives psychological stimulation and expresses itself (Stolorow 1997; Beebe et al. 1997).
8.6.2. Self-organizes from elemental systems
A system is termed ‘living’ if it fulfills the following criteria: reacts to its environment; adapts to its environment; reproduces; grows; obtains and uses energy; is composed of cells; is capable of evolving. The personality fulfills all these criteria: it reacts and adapts to its environment, it reproduces itself in the next generation, it grows, it is nourished by ‘input’ psychological energy (love, companionship, play, stimulation, challenge, education, experience), it generates ‘output’ psychological energy (aggression, hurt, grief, excitement, love, joy, creativity), and it evolves. For the personality an individual person is the equivalent of a cell.
In the realm of psychology, therefore, the personality must be considered alive. But we know that all living things are complex adaptive systems which emerge from the self-organization of simpler systems. It follows that the same must be true for the personality. Given the evolutionary and genetic constraints discussed above (8.1), the human personality must necessarily organize itself by means of the spontaneous interactions, according to simple rules, of a small number of psychological simple dynamic systems. It should therefore be possible to identify some of these elemental systems.
8.6.3. Is a system of interactions
A crucial difference between humans and other mammals is socialization. Many human attributes have evolved in whole or in part for social signaling:
The cerebral cortex seems to have evolved to its modern size mainly to enable social interactions (Dunbar 1992). The writing of literature shows that intelligence is essential for understanding social interactions. Music, song, dance, theater, movies, television, advertising, poetry, literature, architecture, visual art, and programs of training, education, and research all revolve around socialization, as does much of technology. Thus anatomical, behavioral, evolutionary, and cultural evidence all shows that, for humans, socialization is key.
The personality emerges mostly in interactions with other people6 first in the infant-mother interaction. The personality does not exist like the brain or the heart, as a complex dynamic system inside of a single person. It is more like an on-going conversation, a system of interaction which can only exist between two or more people (Stolorow 1997; Lachman 2000). Beebe et al. (1997) reviewed how the infant’s personality evolves as the infant-mother pair interact. For stability and vitality, the adult personality also needs continued interaction. The elemental psychological systems from which the personality self-organizes, therefore, are likely to be simple dynamic systems of interaction.
8.6.4. Failure of an elemental dynamic system of interaction
If one of the personality’s elemental systems failed to initiate, the effects upon the personality’s development would be pervasive. If an elemental system operated for some months and then ceased to operate, the effects would also be pervasive. (A complex adaptive system requires the continual functioning of its component systems.) If an elemental system operated at a lower-than-normal level, the effects would be pervasive but less severe.
The above is consistent with the pattern of effects in autism: autism is a pervasive cascade of disordered development which often begins very early; some infants achieve a degree of interactive functioning in the first year but subsequently become autistic; amongst individuals the severity of symptoms varies greatly. Here is the paradigm shift. Old paradigm: autism is caused by a genetic defect; new paradigm: autism is caused by the failure of a simple dynamic system of interaction.
Eye-contact is an elemental dynamic system of interaction. It has a profound affect on both participants, alerting each, making each more aware of the other’s subjectivity, and forming at least a momentary bond between the two.
Among mammals, a human infant is unique in that a human infant is biologically designed to establish eye-contact. When a mother breast- or bottle-feeds her infant the distance between her infant’s eyes and her own eyes corresponds exactly to the distance at which a new-born’s eyes can focus (at birth the range of focus is narrow). While breast feeding, a human mother spends about 70% of her time gazing at her infant’s eyes (Stern 1977, p. 35-6). At about six weeks the infant learns to make eye-contact with the mother. Eye-contact stimulates the mother to play more with the infant. The mother plays with facial expression, with voice, with face presentations, with head movements, and with proximity games (ibid, p. 37). Such a positive feedback loop must inevitably reinforce the subsequent progression of stimulating and comforting interactions (see below; also Beebe et al. 1997). As I discuss later, these ‘socially pleasant sensory experiences’ have a permanent effect on the infant’s oxytocin and vasopressin levels ( Fries et al. 2005) and these, in turn, enhance subsequent interactions.
The foregoing vividly illustrates self-organization in infant development. Eye-contact itself begins so early that it is likely to be one of the original simple dynamic systems of interaction from which the personality self-organizes.
10. The evolution of social gaze
For many species of birds, an image of the eyes is a potent signal warning of the danger of predators (Janzen et al. 2010). We can deduce an evolutionary sequence by comparing modern primates because humans evolved from ancestral primates very like modern primates. Within that evolutionary sequence, social gaze became increasingly important.
In most primates the visible eye consists mainly of dark iris with only a very small proportion of sclera. The sclera is almost always brown or light brown rather than white. But in humans the visible eye has a large expanse of white sclera which provides a sharp contrast to the dark iris (Emery 2000, pp. 583, 585). This helps an observer to determine the precise direction of a human’s gaze.
When viewing faces, a monkey shows an extreme bias for looking at the eyes and the small region surrounding the eyes. The eyes play a central role in a primate’s facial expression and thus in emotional communication (ibid., pp. 585-6). Staring and frequency of eye-contact are key social signals. The direction of one monkey’s attention, coupled with its facial expression, conveys crucial information to a second monkey about the object of attention (joint attention). It may inform the second monkey about the social status of a third, or about food or about danger.
Apes, but not monkeys, appear to use the direction of another’s gaze as a clue to the other’s intended behavior. This is more complex than joint attention because it requires an awareness of the other as a repository of potential behavior. It seems that only humans, however, practice shared attention (ibid., pp. 588, 594), in which two individuals are each aware of the direction of the other’s gaze (I know that she sees it and she knows that I see it). Shared attention is a component of theory of mind. In psychological terms its equivalent is intersubjectivity. These observations are direct evidence that, as the primate’s eye has evolved in appearance (towards more visual contrast between iris and sclera and hence towards a better signal of gaze direction), so it has evolved in psychological function (towards enabling intersubjectivity).
This is supported by experiments with human subjects (Baron-Cohen et al. 1997, pp. 323-5). Subjects were asked to identify complex emotional states (scheme, admire, interest, thoughtful, arrogant) from photographs of the whole face, from cropped photographs showing only the mouth, and from cropped photographs showing only the eyes and eyebrows. When the whole face or the eyes alone were seen, accuracy of identification was equally high. When the mouth alone was seen, accuracy was low. Thus the other’s complex subjective state is conveyed by the appearance of the eyes. This last conclusion is confirmed by the work of Klin et al. (2002, p. 809).
11. The development of intersubjectivity
11.1. Intersubjectivity is emergent
Trevarthen & Aitken (2001) proposed that there is an innate brain structure, defective in autism, which promotes intersubjectivity. I argue that intersubjectivity cannot be innate because, as earlier stated, there are too few genes and because genes are incapable of predetermining detailed neuroanatomy.
Bion (1962/77, p. 36) described the breast-feeding mother’s ‘reverie . . . [which is] imparted to the channels of communication’. Winnicott (1971/86, p. 112) said: when [the baby] looks at the mother’s face . . .what the baby sees is himself or herself . . . the mother is looking at the baby and what she looks like is related to what she sees there.
Stern (1985, p. 139) described how the infant develops a sense of self within the infant-mother interaction. At what he termed the intersubjective phase, beginning around eight months, the infant senses that infant and mother each have inner mental states which they can share (I am excited and I know that she feels my feeling.) Just as the infant’s body develops in relationship with the mother’s body and her actions, so the infant’s sense of self develops in relationship to the mother’s awareness of and inner response to the infant. This is particularly the case for the intersubjective sense of self (I see that my mother sees me as lovable, so I see myself that way too). In the words of Stern et al. (1998, pp. 907-8):
. . . the intersubjective goal . . . [is] a mutual recognition of each other’s motives, desires, and implicit aims that direct actions, and the feelings that accompany this process . . . [This] also implies a signaling or ratifying to one another of this sharing . . . The work is asymmetrical, with the caregiver . . . doing the lion’s share.
11.2. Achieving eye-contact
Stern’s model of development shows why eye-contact is important. The mother senses the presence of the infant’s inner life in part through the infant’s eyes. Likewise, the infant senses the mother’s inner life in part through the mother’s eyes.
Infant and mother also engage each other through smell, taste, touch and sound. An infant has remarkable cross-modal perception. Infants recognize the smell of their own mother’s milk (Stern 1985, pp. 39-40). Beebe, Lachman and co-workers have shown that by four months the infant-and-mother pair have developed vocal-rhythm coordination, the degree of which predicts both attachment and cognition at twelve months (Jaffe et al. 2001; for a review see Beebe et al. 1997; for examples of mother and five-week-old infant interactions which show the centrality of eye-contact, ibid, pp. 153-4; Gergely & Watson 1996; Beebe 2005).
If the baby is born blind then it must detect the mother’s inner life through the other senses. Infant-observation studies by Fraiberg (1977, pp. 3-9) and Als et al. (1980) compared groups of blind and sighted infants (all mothers were sighted):
For the blind infant, containment is more difficult. The visual focus is missing. Closer tactile contact, nuzzling, and more continuous enveloping with the mother’s voice make up for it . . .The sighted infant’s interaction with the mother is similarly structured, yet not as explicit, nor are the cycles repeated as often, as containment and goal attainment are facilitated by visual feedback . . . the process of implementation is much more conscious for the mother of the blind infant (ibid., pp. 198, 201).
The studies by Fraiberg and Als et al. show that, for sighted infants (the vast majority), eye-contact with the mother is central to establishing an infant-mother bond.
One might object that the infant interacts visually with the mother’s whole face, not just the eyes. Visually, however, the eyes are highlighted in the face by virtue of their duplication, intense color, extreme light-dark contrasts, sharpness of edge, regular shape (which is echoed by moving curved lashes and brows), and rapid movements. That the movements of the mother’s eyes follow (are contingent with) the infant’s movements must make the eyes the more compelling. Gergely (2001, p. 411) notes that ‘young infants are very sensitive to the contingent relationships between their motor responses and consequent stimulus events’. The mother also follows her infant with ears and nose, but these are visually undistinguished and they give no evidence of following. Even to an adult the eyes are visually compelling; as an infant first learns to distinguish forms, the eyes are likely to be the first image the infant masters.
In order for the infant to achieve eye-contact, the infant must learn to visually recognize the mother’s eyes. Visual recognition requires that, in some sense, the recognizer has stored a visual ‘image’ (an ‘image’ could be no more than a list of visual criteria) of that which is to be recognized. This stored image is then compared with incoming images until a match is found.
11.3. How the infant learns to recognize the mother’s eye
11.3.1. Visual edges in the image of the eye
A reflex is not peculiar to humans but is intrinsic to the function of an organ. Blinking and coughing are examples. When the eyelid evolved in reptiles it necessarily had a movement reflex (Gans and Parsons 1973). A reflex is a simple element of behavior which involves only a few muscles. It behaves as though it were hard-wired into the nervous system. I will show that such reflexes help a newborn to recognize the mother’s eye.
In a newborn infant some behaviors seem to precede learning. For example, Spitz and Wolf (1946) found that an infant gazed preferentially at a human face or at a schematic drawing of a face. A line drawing of two eyes, a nose, and a mouth was sufficient. They suggested that the infant inherits a schematic image of the human face and seeks a match for that image in its immediate environment.
Friedman (1964) and Haaf and Bell (1967) proved, however, that the infant gazed preferentially only at some elements of the face. It made no difference if the elements were scrambled in the drawing. The infant gazed preferentially at moving edges. The most attractive moving edges within the mother’s face were the sharp angles at the corner of the eyes (two edges intersecting), the light/dark contrasts between the pupil and the white sclera of the eye (an edge), and the contrast between eyebrow and skin (an edge) (Stern 1977, p. 37). There are also edges around the lips and around the outer rim of the head.
Haith (1966) and Salapatek (1975) proved that, from birth to about one month, an infant seeks out any visual stimuli which includes both movement and ‘edge density’, that is, the concentration of edges in a given space. By two months the infant’s vision is beginning to mature: the infant begins to recognize when facial features are scrambled and shows a preference for naturally-ordered features.
11.3.2. Visual edges and the cortex
Research on the vision of adult vertebrates (fish, frogs, cats, and monkeys) helps to explain the human infant’s preference for visual edges (Michael 1969). All vertebrates analyze visual input primarily into a series of moving edges. The analysis is done by neurons in the retina of the eye and by neurons in areas of the visual cortex which are adjacent (closely connected) to the retina. This means that the brain does not initially ‘see’ a whole image. Rather it initially ‘sees’ a series of moving edges.
A computer analyzes an image into a stream of digits, zeros and ones, which it records. The stream of digits contains the information needed to recreate the image but is not itself a spatial analog of the image. In a similar fashion the retina and the adjacent visual cortex analyze the image into multiple streams of moving edges. Elsewhere within the brain, this data must be ‘synthesized’ in some way to form an ‘internal image’ which permits later recognition of the same visual input. I imply nothing about the mechanism by which this is accomplished, nor about the nature of the internal image. These are not known. It is logically necessary, however, that an internal image is not achieved whole, like a photograph, but by synthesis.
The experiments of Friedman and Haaf and Bell (v.s.) distinguished a stage through which the infant must pass before it learns to see like an adult. Since the newborn recognizes moving edges, we know that the neurons in the newborn’s retina and adjacent cortex are pre-wired (or very quickly wired) to analyze visual input into edges. The newborn also has functioning muscle reflexes which enable it to focus its eyes, to fix upon an object, and to track an object (Stern 1977, p. 34; 1985, p. 40). All this very early wiring provides for the visual reflexes by which the newborn tracks the visual edges in its mother’s face.
Cortical neurons have been identified which only fire when the infant recognizes a face (Elman et al. 1998, p. 116). Only after the infant has learned to ‘synthesize’ an internal image of the face could the infant discriminate between naturally-ordered and scrambled images of the face. This explains what Salapatek ( v.s.) observed experimentally, that at two months infants begin to distinguish between scrambled and ordered features.
During breast feeding, as noted earlier, the mother’s eyes are within the newborn’s (limited) focal range and the mother spends 70% of her time gazing at her infant’s face. The infant-mother pair is thus designed to ensure that the newborn will stare at the sharp, high-contrast, moving edges of its mother’s eyes. Thus the infant will construct a cortical image of the mother’s eyes and associate that image with breast (or bottle) feeding.
It is perhaps a human’s sense of self which most distinguishes him or her from other mammals. It is remarkable, therefore, that the human sense of self is initiated by the geometry of breast feeding. A cat’s eyes are equally sensitive to moving edges. Because of the way a kitten feeds, however, it does not begin life gazing at its mother’s eyes.
12. Two lines of current research which support the eye-contact hypothesis
12.1. Oxytocin, vasopressin, and a developmental cascade
Children who were institutionalized at birth show secondary brain differences which interfere with face recognition and bonding.
In infants, the level of the neuropeptides oxytocin and vasopressin is normally increased by socially pleasant sensory experiences (Fries et al. 2005). In turn these neuropeptides promote social bonding, the display of selective infant-parent attachments and the formation of memories of these interactions. Fries et al. showed that, in adopted children who had previously been raised in orphanages, there were very large reductions in the baseline level of vasopressin. They also showed that there were very large reductions in that elevation of oxytocin which, in normal controls, is triggered by close contact with the mother.
Rimmele et al. (2009) showed that, when administered to normal adults, oxytocin specifically improves recognition memory for faces but not for nonsocial stimuli. Andari et al. (2010) found that when adult subjects with autism inhaled oxytocin, they interacted preferentially with more social partners, felt more trust and preference and, when looking at faces, spent more time gazing at the eyes. Guastella et al. (2010) found that inhaled oxytocin improved emotion recognition in young adults with autism spectrum disorders.
Thus a developmental cascade, which is triggered in part by early infant-mother eye-contact and which is disrupted in autism, is being deciphered at the molecular level:
12.2 Precipitation levels and autism incidence are strongly linked
When I first proposed that failure of early eye-contact was the immediate cause of autism (McDowell 2002, 2004a,b), I pointed out that this hypothesis led to a testable prediction: autism would be statistically linked to early non-maternal child care which includes time spent watching television/video screens.
There are a number of reasons to suspect that television watching might trigger autism. Because the recent increase in autism is world-wide, its environmental trigger must also have recently increased worldwide: television/video/computer exposure meets that criterion. Due to the growth of cable television, of VCRs, and of DVDs, television watching by very young children has grown dramatically over the last few decades (Kaiser Family Foundation 2003; 2006), as has the incidence of autism. There is evidence that early childhood television viewing hurts language, cognitive, and attentional development (Anderson and Pempek 2005). For example Christakis et al. (2004) found a statistical link between early childhood television watching and later diagnosis of ADHD (see also Christakis et al. 2009). In light of such evidence the American Academy of Pediatricians Committee on Public Education (2001) recommends no television viewing for children below the age of two and no more than one to two hours per day for older children. Olmsted (2005a,b) found that the incidence of autism amongst the Amish, who watch no television, is extremely low.
It is self-evident that children’s time spent indoors now involves much use of television/video/computer/wi-fi screens. Waldman et al. (2006) used data from Bureau of Labor Statistics’ American Time Use Survey to confirm that young childhood television watching is statistically linked to precipitation.
Waldman et al. (2008) then published rigorous, statistical data demonstrating a strong link between the incidence of autism in the US and precipitation rates. Precipitation levels appear to account for 40% of autism diagnoses and are therefore very significant in the causation of autism. Waldman et al. (2006) also showed that, in Pennsylvania and California from 1972 to 1989, increased autism incidence correlated strongly with county-by-county introduction of cable television. Cable also increases the time spent watching television.
The statistical associations proved by Waldman et al. could conceivably be due to the effects of indoor air pollution or to vitamin D deficiency, both of which might increase with time spent indoors. Although indoor air pollution and vitamin D deficiency must be tested, they are both implausible as causes of the autism epidemic. If either were to have a neurological effect it would be non-specific; it is very unlikely that either would specifically target the development of brain structures required for social interaction. We know that intelligence, which indicates healthy overall neurological development, is normal and sometimes superior in individuals with Asperger’s syndrome.
The most plausible explanation for Waldman et al.’s results is that television/video/computer/wi-fi use interferes (by distracting either the mother or the infant or both) with an early, critical stage of infant-mother bonding. We know that infant-mother eye-contact is central to early bonding. It is likely that eye-contact would be the component of early bonding most directly affected by competition with the glowing screens to which we have become addicted (Christakis 2010).
13. Conclusion and a clinical study which would address prevention
I have presented theory and evidence to suggest that autism may be directly caused by a failure in early infant-mother eye-contact, a failure which becomes more frequent with the increasing use of television/video/computer/wi-fi screens in the home. More generally, it may be possible to identify some of the early simple dynamic systems of interaction from which the personality self-organizes: if this were confirmed it would have interesting implications for brain science.
Those invested in other theories of autism may tend to dismiss the eye-contact hypothesis. Parents of autistic children, for example, are sensitive to being ‘blamed’ for their children’s condition. Early breast feeding may offer a helpful analogy here. For a few hours after birth an infant has spontaneous mouth movements by which it seeks to suck the mother’s nipple. If the newborn is promptly applied to the nipple, breast feeding tends to begin easily. If breast feeding is delayed then it is more difficult to establish; sometimes bottle feeding is then favored. Parents might be be comforted by understanding that failure to establish a behavior during a very-early critical period does not reflect upon the overall quality of their parenting.
The forgoing suggests a clinical study which would address prevention. It would be possible to recruit a select group of parents who undertake (a) to greatly reduce, from birth for the first few years, their whole family’s exposure to television, video, computer, and wi-fi screens, and (b) to keep records of such exposure which may occur. It would not be necessary or desirable to ask these parents to forgo other strategies for preventing or treating autism. Waldman’s research suggests that, compared with the general population, the children in this study might show a large reduction in the incidence of autism. Such a result, in an initial study, would encourage more parents to take part in a larger study.
2. Earlier I proposed that the failure was to acquire or retain the image of the mother’s eye. Eye-contact itself is a more measurable phenomenon. Eye-contact requires recognition which requires that the infant acquire an image, in some sense, of the mother’s eye. Return
3. Molecular biologists have described in fine detail the mechanisms by which macromolecules self organize. In their writing, however, molecular biologists do not always distinguish between the invariance of primary structure (invariant because it is directly specified by genes) and the invariance of secondary, tertiary, and quaternary structure (invariant because, in the normal intracellular environment, the outcome of macromolecular self-organization is predictable). Return
5. This inclusive definition is compatible with most theories of personality, for example with trait, type, psychoanalytic, behaviorist, social cognitive, and humanistic theories. It also recognizes that psychological life is in large part interpersonal, that is, residing in the exchange between people as they relate to each other. I give objective evidence for the centrality of the interpersonal in section 8.6.3. Return
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AcknowledgementsI am very grateful to my wife, Joenine E. Roberts, L.M.S.W., L.P., for invaluable advice and support.
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