Worlds of Autism: Across the Spectrum of Neurological Difference

5. Autism and Genetics: Profit, Risk, and Bare Life

117 5 Autism and Genetics Profit, Risk, and Bare Life Majia Holmer Nadesan In 2007, the U.S. Centers for Disease Control reported that autismspectrum disorders affect 1 in 150 children. Parents, educators, medical professionals, and social-service providers demand that autism’s causes be identified and its social and economic risks be addressed and managed, despite considerable controversy over what autism actually is (see Nadesan 2005). Some autism advocates see autism as an inborn or environmentally caused medical condition that requires treatment and cure, whereas others see autism as a difference that requires accommodation. This chapter considers competing causal explanations and discusses the politics inherent within and informing these competing frameworks for interpreting and treating autism. The chapter critiques the politics of the inborn and genetic-based dominant frame governing autism research and public funding for autism in the United States by focusing on the allocation of funding for autism, the prioritization of pharmaceuticals, and expanding efforts to create autism-susceptibility tests. The chapter addresses the marginalization of environmental explanations for genetic changes that arguably derives from the research emphasis on finding susceptibility genes. The emphasis on inborn susceptibility has implications for people with autism and their families, as the search for genes may be prioritized over research and spending related to support, therapy, and accommodation in an economic context of public-spending cuts. People with autism and their families should consider carefully this formulation of autism as a heritable, genetic deficiency , because they will shoulder a growing share of the economic costs of accommodation and treatment as the austerity state cuts services. Some autism advocates reject altogether the idea of “deficiency”; thus, the construct of autism as a heritable, genetic-based disorder may be troubling as autism-susceptibility testing expands. The heritable model 118 MAJIA HOLMER NADESAN of genetic deficiency could legitimize a new prenatal eugenics as families seek to limit the economic and social impacts of having a child with autism. Autism becomes in this dystopic vision a marker of a devalued life form, or bare life. Autism Research Priorities: Genes, Dollars, and Susceptibility Tests Expert discourses have carved out a definition of autism operationalized through behavioral criteria. The DSM-IV stipulates that a diagnosis of autism (299.00 Autistic Disorder) requires that the patient exhibit symptoms (a total of six or more items) from a triad of behavioral or communication impairments, including: (1) impairments in social interaction, including impairments in nonverbal behaviors (“eye contact ,” “facial expressions,” “body postures,” and “gestures to regulate social interaction”), impairments in the ability to develop appropriate peer relationships, and impairments in emotional reciprocity (such as pleasure in other people’s happiness); (2) impairments in communication , including delays in expressive language, impairments in conversational competence, use of stereotypic or repetitive language, and lack of spontaneous make-believe play; and (3) “restricted repetitive and stereotyped patterns of behavior, interests, and activities.” Onset of delays and/or impairments must occur before the age of three for a diagnosis of autistic disorder (American Psychiatric Association 1994, 70–71). With few substantive differences, the diagnostic criteria stipulated in the ICD-10 by the World Health Organization (2009) basically mirror these criteria. Neither system specifies that mental retardation be an essential diagnostic feature of autism. Because of the heterogeneity of autistic expressions, both the ICD-10 and the DSM-IV include a diagnostic category for atypical expression: “Atypical Autism” in the ICD-10 requires that the patient meet fewer of the diagnostic criteria stipulated for autism, as does “Pervasive Developmental Disorder: Not Otherwise Specified” (299.80 PDD-NOS) in the DSM-IV. In the DSM-IV, late age of onset requires a diagnosis of PDD-NOS in the absence of other diagnostic possibilities (such as schizophrenia). Most medical and popular accounts of autism represent the disorder as involving brain damage, usually perceived as caused by genetic mutations or alleles (see Herbert 2005). The brain damage is believed to AUTISM AND GENETICS 119 manifest in the triad of impairments that constitute the disorder’s diagnostic criteria. Today, functional magnetic resonance imaging (fMRI) and other brain-scanning technologies can identify precise areas of the brain believed to be affected. Brain-imaging technologies can be employed to create “neural phenotypes” (Ramus 2006, 247), which are seen as necessary for establishing clear relationships between (1) brain and mind and (2) brain and gene, as researchers seek to map cognitive symptoms of...