Psychiatric diagnoses such as Autism Spectrum Disorder (ASD) are primarily attributed on the basis of behavioral criteria. The aim of most of the biomedical research on ASD is to uncover the underlying mechanisms that lead to or even cause pathological behavior. However, in the philosophical and sociological literature, it has been suggested that autism is also to some extent a 'social construct' that cannot merely be reduced to its biological explanation. We show that a one-sided adherence to either a biological or a social explanation leads to a moral dilemma, a Catch-22, for autistics and for those living with them. Such explanations close the space for self-identifying as autistic and at the same time being considered to be in good mental health. They foreclose the possibility of making sense of the lived experience of (and with) autistics. In this paper we argue that such lack of space for moral imagination inherently leads to scientific stalemate. We propose that one can only go beyond this stalemate by taking an ethical stance in theorizing, one that enables better intersubjective understanding. Only on such a view can behavior and biology be linked without either disconnecting them or reducing the one to the other.
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http://dx.doi.org/10.3389/fpsyg.2020.529193 | DOI Listing |
Am J Med Genet A
January 2022
Department of Neuropsychiatry, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Front Psychol
November 2020
NeuroEpigenEthics, Department of Philosophy, University of Antwerp, Antwerp, Belgium.
Psychiatric diagnoses such as Autism Spectrum Disorder (ASD) are primarily attributed on the basis of behavioral criteria. The aim of most of the biomedical research on ASD is to uncover the underlying mechanisms that lead to or even cause pathological behavior. However, in the philosophical and sociological literature, it has been suggested that autism is also to some extent a 'social construct' that cannot merely be reduced to its biological explanation.
View Article and Find Full Text PDFNeuroimage Clin
June 2021
The Cognitive Neurophysiology Laboratory, Department of Pediatrics, Albert Einstein College of Medicine, Bronx, NY, USA; Department of Neuroscience, Rose F. Kennedy Center, Albert Einstein College of Medicine, Bronx, NY, USA; The Cognitive Neurophysiology Laboratory, Department of Neuroscience, The Ernest J. Del Monde Institute for Neuroscience, School of Medicine and Dentistry, University of Rochester, Rochester, NY, USA. Electronic address:
22q11.2 deletion syndrome (also known as DiGeorge syndrome or velo-cardio-facial syndrome) is characterized by increased vulnerability to neuropsychiatric symptoms, with approximately 30% of individuals with the deletion going on to develop schizophrenia. Clinically, deficits in executive function have been noted in this population, but the underlying neural processes are not well understood.
View Article and Find Full Text PDFHerz
April 1994
Deutsches Herzzentrum München, Germany.
Congenital heart diseases are starting to benefit from the major advances provided by the advent of molecular biology methods. It is now possible to identify genes which are responsible for congenital heart diseases. The gene responsible for supravalvular aortic stenosis--an autosomal dominant trait--was cloned last year.
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