Pfeffer Lecture: “An integrative model of autism spectrum disorder: ASD as a neurobiological disorder of experienced environmental deprivation, early life stress and allostatic overload”, William M. Singletary, MD.

 

A number of recent convergences within neurobiology, and between neurobiology and psychoanalysis, allow us to view autism through a new lens. This perspective highlights biological risk factors that might operate through final common pathways to produce the ASD syndrome. The goal of this article is to integrate and elaborate upon this confluence of findings, and to develop a working model of ASD that could parsimoniously account for central aspects of ASD, promote greater collaboration in research, and lead to more effective treatment. Converging evidence suggests that ASD is a potentially reversible neurodevelopmental disorder in which neurobiological factors – not poor parenting – interfere with the child–caregiver interaction. The infant then experiences deprivation of growth-promoting parental input even though it is available. The model proposed here adds what seems to have been largely unrecognized in the field of autism: the child’s experience of social deprivation and isolation signals threat to the child and may result in overwhelming stress with significant psychological (traumatic or toxic stress) and biological (allostatic overload) components and consequences. Allostatic overload results when attempts to cope with threat impose too great a burden, resulting in a pathophysiological state or process that damages the body and predisposes one to the development of disease. Critically, this model proposes that allostatic overload plays a major role in the course of ASD by amplifying the neurobiological vulnerabilities generally considered to make primary contributions to the development of autism. Furthermore, through the process of allostatic overload, neurobiological and psychological factors interact in a nonlinear fashion and are both seen to underlie the symptoms of ASD which develop through maladaptive coping and neuroplasticity. Thus, this model might explain both the progression to, and the ongoing symptoms of, the ASD syndrome. In addition, the model could also account for successful intervention by promoting the reversal of this process via adaptive coping and neuroplasticity. Factors that may facilitate adaptive neuroplasticity include providing an enriched environment, increasing social and emotional connection, and decreasing anxiety, stress, and allostatic load. Personal descriptions of the experience of ASD, as well as psychoanalytic clinical work with children with ASD, are in accord with this model. Psychoanalysis may thus be considered a research tool that assist in uncovering the child’s inner world of feelings and meanings, an under-appreciated element in autism. Making sense of the child’s experience of isolation and threat helps the ASD child feel understood and less afraid. Clinical material will illustrate how, for some children on the higher end of the autism spectrum, recovery is made more likely by increasing the sense of connection and decreasing the experience of stress.

This event is free and open to the public. No RSVP required; first come, first seated. All welcome!