By Dr Giacomo Vivanti

Since its publication our paper “Intellectual Development in Autism” has been subject to debate and discussion. In the paper, we advance the thesis that symptoms of autism, by precluding children to fully take advantage of the social input from the environment during early critical periods, might negatively affect their intellectual development. Therefore, children who have severe symptoms of ASD may be at increased risk of developing intellectual disability, as a consequence of more severe “virtual deprivation” from environmental input.

This notion represents a significant departure from the conventional idea that intellectual disability is a comorbid condition causally unrelated to ASD, with relevant implications for research. For example, children with ASD and intellectual disability are often excluded from research studies, based on the idea that their intellectual disability is a confounding factor that does not provide information on the nature of ASD. By suggesting a relationship between severity of ASD and intellectual disability, however, we argue that the practice of excluding children with ID in ASD research is ill considered, and that rather, research should investigate why those children have an Intellectual Disability, with the ultimate goal of fostering positive outcomes for all individuals with ASD. While some observers and scholars highlighted the relevance of the research question and the proposed interpretations, a number of criticisms have been raised that we would like to address. For example, in this article recently published on the Simons Foundation website, Sir Michael Rutter and Professor Patricia Howlin express doubt on the conclusions of the paper, despite empirical confirmation of our thesis with two independent data sets.

Professor Rutter states that “abundant evidence shows that autism is associated with brain abnormalities” and “The association of intelligence with the severity of autism symptoms may not reflect the effect of symptoms as such, but rather the fact that the symptoms are themselves a reflection of brain pathology”.

We fully agree that brain abnormalities are the cause of the behavioural symptoms in ASD and ID, and want to highlight that this notion is not incompatible with the idea that brain abnormalities that affect social behaviour and social learning might ultimately impact on intellectual development. So, while it is certainly true that symptoms of ASD and ID reflect brain abnormalities, we also emphasise that these biologically-based symptoms preclude the developing brain from receiving important environmental inputs that are necessary for “normal” cognitive development. Of course, as Professor Rutter indicates, it is possible that the severity of cognitive impairment and severity of autism reflect the severity or the extension of underlying biological factors, rather than one being a risk factor for the other. However this notion does not have unequivocal empirical evidence. Our model is in line with recent developmental theory and empirical evidence suggesting an important role of participation is social exchanges and social learning opportunities for various aspects of intellectual development (Dawson, 2008; Kuhl, 2007; Petersson, Reis, Baltes, Reuter-Lorenz, & Rosler, 2006; Pluess & Belsky, 2013)

Professor Howlin’s argues that “There are some individuals with high IQ who are very severely affected by their autism and some individuals with low IQ who have autism but the impact isn’t as great”. Again, we do not disagree. In fact, in the paper, we state that a dissociation between severity of ID and severity of ASD is possible. Rather, we argue that severe symptoms of ASD is a possible “risk factor” for abnormal intellectual development, a statement that is not incompatible with the notion that at the individual level, there are will be some individuals that will not ‘fit’ the prediction of this model. The fact that some individuals with high hypertension or obesity do not have cardiovascular problems and some individuals have cardiovascular problems without having high hypertension or obesity does not deny the fact the hypertension and obesity are risk factors for cardiovascular events. Importantly, the notion that individuals with more severe autistic symptoms are more likely to also have lower IQ is not based on our data only, which, as observed by Professor Howlin, are based on a small sample (although our N of 83 subjects can be considered well above the average in autism research) but also from other, larger studies (e.g., Dykens & Lense, 2011; Gotham, Pickles, & Lord, 2012)

In sum, while it is important that interpretation of our data can and should be challenged, it is hard for us to find points in the observations of our authoritative colleagues that are conceptually inconsistent with the logic of our developmental model of autism. The relevance of initial brain abnormalities and the wide diversity in symptom presentations pointed out in their comments could not be overstated. We believe that brain abnormalities result in these heterogeneous presentations through interaction with the environment. The mechanisms through which such interactions affect cognitive development however are still poorly understood. The constructive questioning of our conclusions from authoritative colleagues enable us to reiterate that this research area is in its infancy, and more empirical work is needed to understand the complex interplay of biological constraints, social engagement and social learning and intellectual development in ASD.

Links

The original OTARC blog post – Why do many children with ASD also have an intellectual disability?

The online article quoting Professor Rutter on the website of the Simons Foundation, Autism Research Initiative (SFARI)(August 15, 2013) – Intelligence stable across life, says 40-year autism study

Frontiers in Neuroscience (July 5, 2013): Intellectual development in autism spectrum disorders: new insights from longitudinal studies

References

Dawson, G. (2008). Early behavioral intervention, brain plasticity, and the prevention of autism spectrum disorder. Development and Psychopathology, 20(3), 775-803.

Dykens, E. M., & Lense, M. (2011). “Intellectual disabilities and autism spectrum disorder: a cautionary note,” in Autism Spectrum Disorders, eds D. Amaral, G. Dawson, and D. Geschwind (New York: Oxford University Press), 261–269.

Gotham, K., Pickles, A., & Lord, C. (2012). Trajectories of autism severity in children using standardized ADOS scores. Pediatrics, 130(5), 1278-1284.

Kuhl, P. K. (2007). Is speech learning ‘gated’ by the social brain? Developmental Science, 10(1), 110-120.

Petersson, K., Reis, A., Baltes, P., Reuter-Lorenz, P., & Rosler, F. (2006). “Characteristics of illiterate and literate cognitive processing: Implications of brain-behavior co-constructivism,” in Lifespan development and the brain: The perspective of biocultural co-constructivism, eds. P. B. Baltes, P. Reuter-Lorenz, & F. Rösler (Cambridge: Cambridge University Press), 279-305.

Pluess, M., & Belsky, J. (2013). “Differential Susceptibility,” in The Infant Mind: Origins of the Social Brain, eds. M. Legerstee, D. Haley, M. Bornstein (New York: Guilford Prss), 77-96.