Eye-contact and complex dynamic systems: an hypothesis on the direct cause of autism and a clinical study which would address prevention


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Eye-contact and complex dynamic systems: an hypothesis on the direct cause of autism and a clinical study which would address prevention.
Maxson J. McDowell PhD, LMSW, LP.

622 West 114th Street, Suite 54, NY, NY 10025

maxmcdowell@jungny.com

www.jungny.com
Biography

Maxson J. McDowell is in private practice in New York City as a Jungian analyst. He is a former president of the C. G. Jung Foundation for Analytical Psychology. Earlier he was a molecular biologist at Duke University, M.I.T., and the M.R.C. Laboratory of Molecular Biology in Cambridge, England.


102-word abstract

Autism’s sudden increase contradicts genetic causation. The new paradigm of complexity (decisively confirmed by biological evidence) shows that both body and personality are complex dynamic systems which self-organize from simple dynamic systems. Autism’s immediate cause may be failure of a simple dynamic system, failure of infant-mother eye-contact. This hypothesis has recently been supported not only by statistical evidence but also by the discovery of a developmental sequence, operating at the level of oxytocin and vasopressin and initiated in part by eye-contact, which is disrupted in autism. The eye-contact hypothesis suggests a clinical trial which would address prevention.
277-word abstract

Estimates of autism’s incidence have increased 5-10 fold in ten years, an increase which cannot be genetic. Though many mutations are associated with autism, no direct genetic cause has been found. Complexity science provides a new paradigm (confirmed in biology by extensive hard data) whose implications we have not yet absorbed. 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. subsequently 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 baseline vasopressin and the 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 which addresses prevention: recruit prospective parents who will greatly reduce usage of television/video/computer/wi-fi in their families; measure the incidence of autism in their children.

1. Introduction
Many factors have inhibited research on autism. Ethical considerations limit researchers’ access to data from subjects with autism. Since the ‘refrigerator mother’ theory was challenged by Rimland (1964), parents have resisted being blamed for their child’s autism. Vaccines are still being blamed for autism though this has been disproven. The pharmaceutical and insurance industries promote drug treatment for psychological problems. Geneticists promote genetic causes, for example in the Autism Genome Project. Belief in a genetic cause has led many to deny the overwhelming evidence that autism’s incidence is increasing (as a paradigm becomes outdated, evidence it cannot accommodate may be denied.)
Autism research needs an interdisciplinary approach; such an approach is difficult because insights from unfamiliar disciplines may not translate or may not be taken seriously. But, for genuine rigor, pertinent information needs to be considered. This paper draws upon information from the following disciplines: biology, primatology, evolution, morphogenesis, genetics, molecular biology, biochemistry, neuroscience, cognitive science, logic, statistics, complexity science, psychoanalysis, infant-mother observation, clinical work with autistic children, public health.
I begin by arguing that autism is a disability specifically in social functioning. Then I show that geneticists studying autism themselves agree that the genetic lesions which are associated with autism do not directly cause it; instead these lesions seem to disrupt brain function more generally, with autism being one of a range of consequences. Then I describe the evidence which led to my hypothesis that the direct, immediate cause of autism is failure of infant-mother eye contact.
The intention of this paper is to show that the eye-contact hypothesis merits further research. Autism has become an epidemic for which new ideas are urgently needed. A confirmation of the eye-contact hypothesis would also have interesting implications for brain science.
How could failure of eye-contact could cause autism? 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. This new paradigm has been confirmed in biology by much hard evidence from biochemistry, molecular biology, entomology, and ecology. Nevertheless the 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.
I show that the eye-contact hypothesis is supported (a) by statistical evidence linking precipitation and cable television to autism and (b) by the discovery of a developmental sequence, initiated in part by infant-mother eye-contact and operating at the level of oxytocin and vasopressin, which is disrupted in autism. Finally I propose a clinical study which would test the hypothesis and address prevention.

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 (ref Baron-Cohen). 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) 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 only 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 the 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. A developmental cascade

Clinicians and researchers 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. After decades of research, however, the primary deficit has not been identified (Ungerer 1989, pp. 85-8; Muratori & Maestro 2007).
4.2. Children may recover from 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 contradict biological causation because a biological deficit would not be healed by behavioral therapy.

4.3. 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.
4.4. A recent review of genetic research

In a review titled ‘Advances in autism genetics: on the threshold of a new neurobiology,’ Abrahams and 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 and 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 suggests 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’ the authors 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 all 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.
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