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The trouble with neurodiversity : etiologies, normativity, and the autistic struggle for identity Garen, Josef 2014

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The Trouble with Neurodiversity:Etiologies, Normativity, and the Autistic Struggle for IdentitybyJosef GarenB.Sc., The University of British Columbia, 2011A THESIS SUBMITTED IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OFMASTER OF ARTSinThe Faculty of Graduate and Postdoctoral Studies(Science and Technology Studies)THE UNIVERSITY OF BRITISH COLUMBIA(Vancouver)October 2014© Josef Garen, 2014AbstractScientific research into the etiology of autism has lead to an explosion in proposed agentsimplicated in the development of autism over the past 70 years. Genetics, neurotoxins,vaccinations, viral infections, parenting practices, neurological abnormalities, among others,have been proposed to explain what increasingly appears to be a heterogeneous andoverdetermined condition. These proposed etiologies and the treatments they suggest pose apeculiar problem for the neurodiversity movement, an activist group of autistics and nonautisticswho hope to promote a positive understanding of autism. In broad terms, the neurodiversitymovement opposes cure-oriented research and activism typical of the scientific community andmainstream autism advocacy organizations. They hope to counter this trend by promoting autismas a positive identity – a normal human variation, rather than a pathology.The tension between these two modes of thought provides a rich terrain for exploring thepossibilities of identity formation even as human behaviour increasingly falls under the rubric ofmedical science. The scientific research discussed in this thesis simultaneously constructs and isconstructed by an understanding of autism as a pathology, and in so doing challenges the claimsof the neurodiversity movement both directly and indirectly: reproductive technologies andproposed treatments for autism force parents to make judgements about the worth of autisticpersons, for example. This thesis draws on literature from bioethics, philosophy of medicine, anddisability studies to situate both the neurodiversity movement and the scientific community indebates about normality, normativity, suffering, and the nature of disease. I argue that while theneurodiversity movement's emphasis on normality is ultimately misplaced, the movementnevertheless has much to teach us about rights, identity, authority, and self-determination.iiPrefaceThis document is the original, unpublished work of the author, Josef Garen.iiiTable of ContentsAbstract............................................................................................................................................iiPreface............................................................................................................................................iiiTable of Contents............................................................................................................................ivAcknowledgements..........................................................................................................................vDedication.......................................................................................................................................vi1. Neurodiversity and its discontents...............................................................................................11.1 Introduction...........................................................................................................................11.2 Neurodiversity.......................................................................................................................41.2.1 Natural human variation................................................................................................71.2.2 Identity...........................................................................................................................81.2.3 Anti-cure......................................................................................................................111.2.4 Rights and acceptance.................................................................................................131.2.5 Social model of disability............................................................................................141.3 Controversy and criticism...................................................................................................161.4 Etiologies of autism.............................................................................................................201.4.1 Neurological underpinnings........................................................................................221.4.2 Genetics.......................................................................................................................251.4.3 Heavy metals and other environmental pollutants......................................................271.4.4 Vaccines.......................................................................................................................291.4.5 Viral infections and immunology................................................................................311.4.6 Parenting practices and behavioural interventions......................................................322. (De)medicalizing autism............................................................................................................362.1 Genetics and reproductive technology construct autism as a disease.................................372.2 Environmental pollutants construct autism as a disease.....................................................432.3 Neurodiversity and “normality”..........................................................................................462.4 The “normal” function model.............................................................................................502.5 Three ways to be normal.....................................................................................................512.6 Identity revisited..................................................................................................................572.7 Conclusion...........................................................................................................................59Bibliography..................................................................................................................................64ivAcknowledgementsI'd like to extend my thanks to John Beatty and all the people involved in the Science andTechnology Studies Graduate Program at UBC for opening up this space of interdisciplinaryscholarship and providing a place for a curious, aimless child like myself to rest for a moment. Iespecially am grateful to Alan Richardson for his direction, guidance, and insightful criticismthroughout the writing of this thesis.I'd also like to thank Jeanne Keegan-Henry for her assistance and for her uniquelyinformed views on the world of mental health, Morag Keegan-Henry for her near-supernaturalability to understand even my most ill-formed thoughts, and my father for his eagerness to readanything I put in front of him, even though I always use too many commas. My family, ofcourse, deserves my unending gratitude for their love and support. Any success I've had in lifebelongs, ultimately, to them.Finally, I'd like to thank my colleagues and friends, Lee Nelson, Peggy Chiappetta, AlexisBeckett, Warren Bowen, and Shoshana Deutsh for the long summer days spent drinking PBR inthe alleyway and the many stimulating conversations we shared in our windowless basementoffice that always smelled faintly of wet dog.vDedicationfor M.vi1.  Neurodiversity and its discontents1.1 IntroductionAutism spectrum disorders (ASD), as defined by the Diagnostic and Statistical Manual of MentalDisorders (DSM-5), are highly heritable neurodevelopmental disorders characterized by“Persistent deficits in social communication and social interaction” and “Restricted, repetitivepatterns of behavior, interests, or activities.”1 In severe cases, autistic persons may have deficitsin language use, intellectual impairment, and difficulties with sensorimotor skills. With as manyas 1 in 88 children in North America diagnosed at some point on the autism spectrum andprevalence continuing to rise,2 ASD is often characterized as an “epidemic”3 and an “urgentglobal public health concern.”4 The number of diagnoses has increased dramatically since thecondition was first described in the 1940s by Leo Kanner and Hans Asperg, but this increase hasnot been uniform. Reported rates of autism prevalence vary widely across the globe,5 andpopular media has focused particular attention on purported autism “hotspots” in technologymeccas such as Silicon Valley.61 American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (Arlington, VA: American Psychiatric Association, 2013).2 Centers for Disease Control and Prevention, “Prevalence of Autism Spectrum Disorders: Autism and Developmental Disabilities Monitoring Network, 14 Sites, United States, 2008,” Surveillance Summaries 61, no. 3 (2012), 1.3 Cf. Wazana, Ashley, Michaeline Bresnahan, and Jennie Kline, “The Autism Epidemic: Fact or Artifact?” Journal of the American Academy of Child & Adolescent Psychiatry 46, no. 6 (2007).  A quick web search reveals how commonly the descriptor “epidemic” is used when referring to the increase in autism prevalence.4 Tomljenovic, Lucija, and Christopher A. Shaw, “Do Aluminum Vaccine Adjuvants Contribute to the Rising Prevalence of Autism?” Journal of Inorganic Biochemistry 105, no. 11 (2011), 1489.5 This may be largely due to the extreme difficulty in carrying out cross-cultural studies of illness prevalence.  SeeElsabbagh, Mayada, et al., "Global Prevalence of Autism and Other Pervasive Developmental Disorders.” Autism Research 5, no. 3 (2012).6 Cf. Blume, Harvey,“Neurodiversity: On the Neurological Underpinnings of Geekdom,” The Atlantic September 30, 1998, and Silberman, Steve, “The geek syndrome.” Wired 9, no. 12. (2001), geographical and temporal variability in the prevalence of the condition has manyproposed explanations, from social factors such as increasing public familiarity with autism andbroadening diagnostic boundaries, to physiological explanations including genetics,vaccinations, and environmental pollutants. Hundreds of millions of research dollars are devotedannually to this question, coming from governmental organizations such as the NationalInstitutes of Health as well as various non-governmental organizations and charitable societiessuch as Autism Speaks/Cure Autism Now, the Organization for Autism Research, and Talk AboutCuring Autism.7 Much of this research, especially that funded by the latter organizations, isexplicitly aimed at finding a cure – some method of ameliorating the symptoms of existingautistic persons or preventing new cases of autism from occurring.In response to this dominant pattern of cure-oriented autism advocacy led by parents andfamily members of autistic children and the concomitant media portrayal of autism as a“tragedy,” a loose association of autistic bloggers, authors, and activists have come together tocombat what they perceived to be an oppressive hegemonic framework of pathologization. TheNeurodiversity Movement, as it is called, began in the late 1990s and grew through onlinemessage boards, chatrooms, and newsgroups, attempting to promote a different vision of autism.They saw autism not as a “tragedy” to be suffered through, nor as a disease or disability, butrather as a positive identity – a neurologically different way to be a person, and a difference thatought to be respected and cherished, just as we respect the differences between men and women,gay and straight people, and so forth. Neurodiversity advocates reject the dominant medical,scientific, and popular positions that autism ought to be cured, treated, or prevented when7 The NIH alone spent $186 million on autism research in the 2013 fiscal year. See National Institutes of Health, “Estimates of Funding for Various Research, Condition, and Disease Categories (RCDC),” March 7, 2014,, promoting instead the acceptance and self-determination of autistic persons above all.There is tension between these two different ways of characterizing autism as, mostobviously, the “neurodiverse” and the “popular” differ on the question of whether autism oughtto be cured. But there are subtler ways in which scientific research, especially etiologicalresearch, and the neurodiversity movement are at cross purposes. The goal of this thesis is toexamine the ways in which scientific developments in autism etiology complement, contradict,and problematize the neurodiversity position, and vice versa. Knowing the origin of a conditionnot only changes how we think and talk about the condition, but it also suggests treatments forthe condition, and in some cases can even change the nature of the condition itself.8 In thisChapter, I attempt to draw the battle lines in the debate between the scientific and neurodiverseconcepts of autism. I begins in Section 1.2 by drawing on a variety of neurodiversity publicationsin an attempt to describe the core beliefs of the neurodiversity movement. These include thebelief that autism is not a pathology and ought not be cured, that autism is a natural humanvariation, and that autism is an identity, as well as endorsements of nondiscrimination and thesocial model of disability. My hope is to provide an accurate and representative picture of what isultimately a somewhat heterogenous and disunified movement, without aiming for completegenerality.In Section 1.3, I attempt to communicate the flavour and diversity of current scientificinvestigations into the etiology of autism. As whole volumes have been written on this topic, Ican only briefly discuss the various factors that have been implicated in the production of autism,focusing primarily on the neurophysiological and biogenetic aspect of autism research. Genetics,8 This point is treated at great length in Hacking, Ian, The Social Construction of What? (Cambridge, MA: Harvard University Press, 1999). See especially Ch. 4.3industrial pollutants, vaccinations, viral infections, and immunological variables will be treated,as they are currently the most fashionable and productive avenues of scientific research andpublic debate. The state of the science paints a picture of autism as overdetermined, withindividual cases of autism caused by heterogenous interactions of genetic predispositions withsocial and environmental factors; indeed, autism itself is beginning to look less like a unitarydisorder, so much as a family of disorders that share certain biological pathways and cognitiveand behavioural expressions.Chapter 2 draws on the debates outlined in the first Chapter to address the centralquestions of this thesis. In it I will attempt to analyze the impact that etiological research has onthe claims of the neurodiversity movement, and explicate the ways in which the tension betweenthe “dominant” scientific view of autism and the neurodiversity view traces out the contours ofmuch broader debates in bioethics, disability studies, and the philosophy of medicine dealingwith the nature of disease and the goals of medicine. I focus my analysis on the normativestandards and evaluative judgements implicit in the scientific research discussed in Chapter 1,also discussing the ethical dimensions of technologies currently proposed or in development thatdeal with autism in one way or another. I hope to use the neurodiversity debate to demonstratethe ways in which scientific knowledge of this kind is inherently value-laden. I close this thesiswith some lingering questions and thoughts on future research directions.1.2 NeurodiversityThe concept of “neurodiversity” was first employed in the late 1990s in response to a number ofperceived problems in the way autism was understood in the popular imagination and depicted in4the media. Autism was frequently portrayed as a “tragedy,” with autistic persons regularlysuffering bullying, abuse, and workplace discrimination; correspondingly, autism was mainlyregarded as a medical problem to be addressed through the rubric of behavioural therapies,medication, and special education. Promoting an attitude of acceptance and respect towardautistic persons and the “neurodiverse,” Judy Singer used the term in her 1999 essay “Why can'tyou be normal for once in your life?” writing thatthe key significance of the 'autism spectrum' lies in its call for and anticipation of a politics of neurological diversity, or neurodiversity. The 'neurologically different' represent a new addition to the familiar political categories of class/gender/race and will augment the insights of the social model of disability.9Though Singer is often cited as coining the term “neurodiversity” in this essay, earlier, in 1998,Harvey Blume wrote an article for The Atlantic titled “Neurodiversity: On the NeurologicalUnderpinnings of Geekdom” which discusses the supposedly elevated rates of autism spectrumdisorders, especially Asperger syndrome, in Silicon Valley. Blume's article trades on thestereotype of the mildly autistic person as being talented with technology and computers,suggesting that Asperger syndrome may be beneficial for the development of future technologiesand thus “Neurodiversity may be every bit as crucial for the human race as biodiversity is for lifein general.”10 During the decade of the 2000s, the idea spread quickly across the internet, beingadopted by bloggers, activists, websites and organizations dedicated to autism self-advocacy.Today, these include large advocacy organizations such as the Autism Self Advocacy Network,119 Singer, Judy. "Why Can’t You Be Normal for Once in Your Life? From a Problem with No Name to the Emergence of a New Category of Difference." in Disability Discourse, ed. Mairian Corker and Sally French (Philadelphia: Open University Press, 1999), 64.10 Blume, “Neurodiversity.”11 See for Freedom,12 and Autism Network International,13 as well as countless individualbloggers, webpages, newsgroups and the like.The neurodiversity movement poses a bit of a problem for anyone who would like tomake categorical statements about it, composed as it is of a heterogeneous collection ofindividuals and organizations who all state their beliefs in different ways. Nevertheless, theposition of the individuals and organizations who align themselves with this ideology sharemany commonalities which can be roughly broken into five interrelated claims.  These are:1. Autism is a natural variation among humans, not a disease or disability,2. Autism does not need to be (or cannot be) cured,3. Autism is an integral part of a person's identity,4. Autistic persons deserve the same rights and social acceptance as anyone else, and5. Autism, like many other conditions, is best understood through the social model ofdisability.It would be overstating the case to say that all of these tenets are universally accepted within themovement, but as each one is espoused quite commonly by prominent organizations andmembers of the neurodiversity community, we shall consider this list to be representative of thegeneral position of the movement and note contentions and disagreements where they occur.1412 See See Cf. Fenton, Andrew, and Tim Krahn, “Autism, Neurodiversity and Equality Beyond the 'Normal',” Journal of Ethics in Mental Health 2, no. 2 (2009); Jaarsma, Pier, and Stellan Welin, “Autism as a Natural Human Variation: Reflections on the Claims of the Neurodiversity Movement,” Health Care Analysis 20, no. 1 (2012); Kapp, Steven K., et al., “Deficit, Difference, or Both? Autism and Neurodiversity,” Developmental Psychology 49, no. 1 (2013); Bumiller, Kristin, “Quirky Citizens: Autism, Gender, and Reimagining Disability,” Signs 33, no. 4 (2008); Bagatell, Nancy, “Orchestrating Voices: Autism, Identity and the Power of Discourse,” Disability & Society 22, no. 4 (2007); Nicolaidis, Christina, “What Can Physicians Learn from the Neurodiversity Movement?” Virtual Mentor, American Medical Association Journal of Ethics 14, no. 6 (2012); Baker, Dana Lee, “Neurodiversity, Neurological Disability and the Public Sector: Notes on the Autism Spectrum,” Disability & Society 21, no. 1 (2006); Owren, Thomas, “Neurodiversity: Accepting Autistic Difference,” Learning Disability Practice 16, no. 4 (2013).6Each of these claims will be discussed in turn.1.2.1 Natural human variationThe first claim in this taxonomy is Autism is a natural variation among humans, not a disease ordisability.15 John Elder Robison, an activist and advocate with Asperger syndrome who haswritten several books including the bestselling autobiography Look Me in the Eye, as well asformerly sitting on the advisory committee for Autism Speaks,16 writes thatneurodiversity is the idea that neurological differences like autism and ADHD are the result of normal, natural variation in the human genome. This represents a new and fundamentally different way of looking at conditions that were traditionally pathologized;it’s a viewpoint that is not universally accepted though it is increasingly supported by science. . . .  We are not sick. We are different.17This claim is echoed in neurodiversity publications across the Internet, from simple statementson personal blogs stating that “[neurodiversity holds that] Autism is a natural human variation,” 18to the National Symposium on Neurodiversity at Syracuse University, whose website states that“neurodiversity is viewed is a concept and social movement that advocates for viewing autism asa variation of human wiring, rather than a disease.”19The neurodiversity movement characterizes autism as a variation among humans,15 See Jaarsma and Welin, “Autism,” 23; Bumiller, “Quirky Citizens,” 970-1; Kapp et al., “Deficit,” 60.16 Robison recently resigned from his position in protest of an op-ed piece published by Suzanne Wright, one of the founders of Autism Speaks. Wright's article was perceived by Robison and many autistic persons as “pro-cure.”17 Robison, John Elder, “Neurodiversity and Me,” Look Me in the Eye (blog), October 20, 2013 (10:15 a.m.), abfh.“Full Disclosure,” Whose Planet is it Anyway? (blog), September 11, 2007 (2:51 p.m.), “What is Neurodiversity?” National Symposium on Neurodiversity at Syracuse University, accessed July 1 2014, to use the language of difference in lieu of the traditional medicalized language ofdiseases and disabilities to emphasize their opposition to the dominant, medicalized concept ofautism. They describe these differences or variations as natural or normal, often making explicitreference to the genetic cause of the condition, or its neurological underpinnings. (Thischaracterization of autism as a variation in “brain wiring” or a “neurological variation” is, ofcourse, where the term “neurodiversity” gets its name from.) In short, this tenet posits a natural,endogenous, and fully “biologized” account of autism. This fact, as well as the possiblemeanings of the words “normal” and “natural” used in this context will be discussed furtherwhen we turn our attention to the etiological research currently underway.1.2.2 IdentityThe second claim of the neurodiversity movement is Autism is an integral part of a person'sidentity.20 Jim Sinclair, an autistic author and self-advocate well-known in the neurodiversitycommunity, explains in the essay “Don't Mourn for Us” thatAutism isn't something a person has, or a “shell” that a person is trapped inside. There's no normal child hidden behind the autism. Autism is a way of being. It is pervasive; it colors every experience, every sensation, perception, thought, emotion, and encounter, every aspect of existence. It is not possible to separate the autism from the person – and ifit were possible, the person you'd have left would not be the same person you started with.21Many prominent autistic figures have made similar remarks about their own experiences with20 See Bagatell, “Orchestrating Voices,” 2007, and Hacking, Ian, “Genetics, Biosocial Groups & the Future of Identity,” Daedalus 135, no. 4 (2006): 91-2.21 Sinclair, Jim, “Don't Mourn for Us,” Autonomy, the Critical Journal of Interdisciplinary Autism Studies 1, no. 1 (2012): 1.8autism. Temple Grandin, an animal scientist, professor, best-selling author, and autistic self-advocate, is often quoted in support of this claim as saying, “If I could snap my fingers and benonautistic, I would not. Autism is a part of what I am.”22 Autistic blogger Lisa D. expressessimilar sentiments, writingI am autistic, and my autism is not separate from my identity. “Autistic” is part of what defines me, just like “college student” and “American” and “short.” If it's okay for me to say that being female is part of who I am, then why can't I say that about autism? Or is it because disability is something that's so terrible that we need to reject it and pretend it doesn't exist?23Lisa D. here points to the way that neurodiverse persons deliberately blur the line between“disability” and identity. Reappropriating the “autism” label is empowering, giving autisticpersons the ability to take pride in and ownership of their “quirks,” and to feel as though theybelong to a small, but perhaps uniquely privileged, community.24Somewhat parenthetically, it should be noted that this sense of ownership and identitysurrounding autism has motivated many activists to oppose the use of “person-first” languagewhen speaking about autism. That is, the use of phrases such as “person with autism” have comeunder fire from neurodiversity advocates as they are seen to imply that autism is a disease,22 Grandin, Temple, Thinking in pictures: And Other Reports from My Life with Autism. New York: Random House, 1996: 50. Grandin has since revised her position, stating “Autism is an important part of me, and I do not want to change, but my career is my identity, not autism.”  Grandin worries that too much focus on autism identity politics leads to people “becoming their label.” See Grandin, Temple, “Temple Grandin: Autism Is Not My Identity,” TakePart, October 14, 2012, Lisa D. “'Overcoming Autism' is Not on My To Do List,” Reports from a Resident Alien (blog), March 19, 2014 (12:10 a.m.), While it is a central tenet of the neurodiversity movement that autism is an identity, I should clarify that not all autistic people feel this way. Most notably, perhaps, the autistic author Donna Williams has stated that “Autism is not me.  Autism is just an information processing problem that controls who I am.” Quoted in Grandin, “Thinking in Pictures,” 50.9illness, or condition “overlaid” upon, and separable from, an otherwise healthy person. Theseindividuals feel that this usage denies their identity and implicitly endorses the “cure mentality.”It has been suggested, rather, that “identity-first” language such as “autistic person,” “ASDperson,” or simply “autistic” (used as a noun) be employed instead, which are seen to accordwith their view that autism is an integral part of the identity of the person.25 While I have nodesire to make premature judgements through slipshod word choice (these kinds of identityclaims are, after all, partly what is at stake in this discussion), I will follow the convention amongneurodiversity publications and use identity-first language in the following pages.Individuals who have received a formal diagnosis of ASD or who have self-diagnosedthemselves with the condition, especially as adults, often feel that the label powerfullyrecontextualizes and, crucially, explains behaviours and experiences in their lives that they werepreviously unable to understand. Dawn Prince-Hughes, an autistic primatologist and authorwrites of her experience being diagnosed as an adult that “everything suddenly made sense. Ilooked back over my life, perhaps the way people do before they die, and thought of all thepainful memories that could now be explained. . . . It made me feel both better and worseknowing that I hadn't meant to disturb or hurt anyone.”26 Experiences such as difficulty fitting inwith peers, the inability to participate in unstructured activities, and characteristically autisticbehaviours such as rocking, hand-wringing, or echolalia previously described as “crazy” take on25 See for example Brown, Lydia, “The Significance of Semantics: Person-First Language: Why It Matters,” Autistic Hoya (blog), August 4, 2011,; “Identity-First Language,” Autistic Self Advocacy Network, accessed July 1, 2014,; and Sinclair, Jim, “Why I Dislike 'Person First' Language,” Autism Mythbusters, accessed July 1, 2014, Prince-Hughes, Dawn, Songs of the Gorilla Nation: My Journey Through Autism, (New York: Harmony Books, 2004), 174.10new meaning in a life narrative newly structured around a nosological category.27It is unclear, however, whether a diagnosis of ASD really has the power to explain any ofthese things. Although, as stated above, mention may be given to genetics or differences in“brain wiring,” a diagnosis of ASD, as with all conditions in the DSM-5, is ultimately based onbehavioural characteristics. As the DSM-5, like its predecessors, is explicitly agnostic about theetiology of the conditions it lists,28 the conditions it purports to diagnose are implicitly defined bythe presence of certain constellations of symptoms. The categories of disorder in the DSM-5 arepurely descriptive; in this sense, the label of “autism” is just that – a name that denotes a familyof behaviours. To say, then, that a diagnosis of autism “explains” the behaviours of the personwould be akin to saying that a person's shyness is explained by the fact that she is shy. In the caseof autism, as in the majority of mental illnesses defined in this manner, however, no causallyeffective pathology has yet been identified, thus etiological research may have an important roleto play in helping autistic persons to understand their own experiences, as will be discussedfurther in the following sections.1.2.3 Anti-cureFollowing closely from previous two claims is the claim that Autism should not be cured, treatedor prevented.29 Given that autism is a natural human variation, “neurodiversity activists reject theidea that autism should be cured, advocating instead for celebrating autistic forms ofcommunication and self-expression, and for promoting support systems that allow autistic people27 This point is treated at greater length in Hacking, “Genetics,” and Hacking, Ian, “Kinds of People: Moving Targets,” Proceedings of the British Academy 151 (2007).28 American Psychiatric Association, DSM-5.29 See Fenton and Krahn, “Autism,” 2, and Bumiller, “Quirky Citizens,” 968.11to live as autistic people.”30 Casting autism as a variation, advocates claim that in the same senseas we would think it ridiculous to say that we ought to “cure” someone of their gender, sexualorientation, or skin colour, we ought also to think it ridiculous to try to “cure” autism.This claim may also be stated as Autism cannot be cured. This follows from the secondclaim in this taxonomy, that autism is an integral part of the person's identity. In Sinclair's view,the integrality of autism to one's identity implies that a “cure” would annihilate the individual.He claims that parents who wish their autistic child could be cured are, in effect, wishing that“the autistic child [they] have did not exist, and [they] had a different (non-autistic) childinstead.”31 This statement has been challenged by parents of autistic persons who pursuepotential cures and treatments; seeing their actions as motivated by their love and concern fortheir child's well-being, they understandably resent being told that their actions indicate that theydo not truly love their child, but rather the child they “love” is an imaginary, nonautistic one.Neurodiversity advocates oppose painful, uncomfortable, and potentially dangeroustreatments such as chelation therapy and certain forms of applied behavioural analysis (ABA),for example.32 Especially opposed are treatments aimed at “normalizing” the autistic child, andmany advocates feel that characteristically autistic “stimming” behaviours targeted by thesetreatments such as hand-flapping and rocking are harmless, and may even be beneficial for theperson in question. Not all potential treatments are opposed by all members of the movement,30 “What is Neurodiversity?” National Symposium on Neurodiversity at Syracuse University, accessed July 1 2014, Sinclair, “Don't Mourn,” 1.32 Chelation therapy is an effective treatment for some forms of heavy metal toxicity which has been used by someparents with the belief that autism results from some kind of chemical poisoning, such as that from adjuvants in vaccinations. It has not been approved for treatment of autism and has the potential for harmful side effects; chelation therapy has resulted in the death of at least one autistic child. See Atwood, Kimball C., et al., “Why the NIH Trial to Assess Chelation Therapy (TACT) Should be Abandoned,” The Medscape Journal of Medicine 10, no. 5 (2008): 115.12however. Certain behavioural interventions and medications, for example, aimed at amelioratingthe most disabling symptoms of autism, such as self-injurious or obsessive-compulsive-likebehaviours, are often considered beneficial to the well-being of autistics. Therapy and educationaimed at improving the autistic persons ability to function in society, communicating with“neurotypicals,” gaining employment appropriate to their abilities, and so forth, are alsogenerally looked favourably upon.33 Therapy, cure, and prevention methods will be discussed atgreater length in Chapter Rights and acceptanceThe next claim is Autistic persons deserve equal rights, appropriate accommodations, socialacceptance, and self-determination.34 The Autism Self Advocacy Network characterizes theneurodiversity movement as one whichpromotes social acceptance of neurological difference as part of the broad landscape of human diversity and seeks to bring about a world in which Autistic people enjoy the sameaccess, rights, and opportunities as all other citizens. Acceptance of difference is essentialto understanding, accepting, and benefiting from the contributions of everyone in our society, thus allowing all people to live up to their potential.35Many autistic persons feel ostracized or discriminated against due to their condition (or due to33 When neurodiversity activists decide which kinds of treatments are acceptable and which are not, one can see this act as an act of essentialism – they are actively engaged in defining the essence of autism. “Characteristically autistic behaviours” such as echolalia and restricted patterns of interest are not to be interfered with – they belong to the essence of autism.  “Accidental symptoms” such as self-injury do not, even though they may be equally caused by the same underlying condition. This point is treated at much greater length in Nadesan, Majia Holmer, Constructing Autism: Unravelling the 'Truth' and Understanding the Social, (New York: Routledge, 2005). See especially Chapter 7.34 See Fenton and Krahn, “Autism,” 1, and Jaarsma and Welin, “Autism,” 23-4.35 “Position Statements,” Autistic Self Advocacy Network, accessed July 1, 2014, conditions, as will be discussed in the next subsection), and the neurodiversity movementis thus explicitly aimed at addressing these problems. This includes educational campaignsdesigned to increase public awareness of autism, attempts to reduce bullying in schoolenvironments, reintegrating autistic children into “mainstream” classroom environments, andhelping autistic persons secure employment and gain necessary workplace accommodations.High-profile, successful autistics such as Temple Grandin are often employed to help changepublic perceptions and reduce prejudicial attitudes.Perhaps the most important part of this claim is the insistence on self-determination.Many decisions, such as those relating to therapeutic options, school placement, andinstitutionalization, are made on behalf of autistic persons in ways that are seen to interfere withtheir autonomy. Thus the neurodiversity movement is explicitly one of self-advocacy, arguingthat autistic persons are in the best position to make choices in their own lives, and there ought tobe no decisions made about autistic persons without the inclusion of autistic persons in thedecision making process.1.2.5 Social model of disabilityMany neurodiversity advocates also explicitly embrace the social model of disability,36 wherein itis understood that one's body or mind is never disabled in isolation – only in the context of one'ssocial and physical milieu does disability emerge. The social model draws a distinction betweenimpairments, which relate to the physical and mental capacities of individuals, and disabilities,which are seen as socially constructed. These disabling social conditions are embedded in thenorms, expectations, and institutional practices in one's environment.36 See Kapp et al., “Deficit”, 60, Baker, “Neurodiversity,” 17, and Singer, “Why Can't You Be Normal,” 64.14In this capacity, autism is frequently compared with homosexuality.  In a homophobicsociety, it is argued, homosexual people will routinely appear mentally disordered or disableddue to hegemonic social conditions that systematically disable homosexuals as compared withheterosexuals. Workplace discrimination, hate crimes, the inability to marry, and so forth allcontribute to construct homosexuals as ill. These observations may go a long way towardexplaining why (but not excusing the fact that) homosexuality was still “officially” considered amental illness until the 1970s. Neurodiversity advocates argue that a similar kind ofdiscriminatory social framework is in place today with regard to autistic and other neurodiversepersons. Social stigma, popular misconceptions, and inadequate accommodations for autisticpersons in particular may make it difficult for them to secure gainful employment or forgemeaningful personal relationships. These pervasive social conditions moreso than any featuresinherent to autism itself, it is argued, systematically construct the condition as “disabling” andcontribute to the oppression of autistic persons. Thus, the neurodiversity movement is one whichexplicitly addresses the normative dimension of medical and social practices....These various claims overlap and intersect with one another in important ways, and the choice tobreak the neurodiversity position into five separate subclaims is somewhat arbitrary. Althoughmany of the writers and organizations mentioned above are speaking specifically about autismand autism spectrum disorders, and the word “neurodiversity” is most often seen in that context,the concept and the movement have been expanded by some activists to encompass an inclusiveattitude toward people with many different types of neurological differences. Many activistsmake this explicit, as in the case of the blog Neurodiversity Now, which states that15“Neurodiversity is a concept where neurological differences are to be recognized and respectedas any other human variation. These differences can include those labeled with Dyspraxia,Dyslexia, Attention Deficit Hyperactivity Disorder, Dyscalculia, Autistic Spectrum, TouretteSyndrome, and others.”37 This deliberate inclusiveness38 is no doubt important to theneurodiversity movement, but will be mostly glossed over in the following pages, as I will betreating the etiology of autism.1.3 Controversy and criticismNeurodiversity itself is not an uncontested concept. Even among autistic persons, there is notcomplete consensus on what the term means, and some reject the concept entirely, as one autisticperson who defines neurodiversity as “The idea that we autistic folks are not 'abnormal,' just adifferent kind of normal. (This is bullshit.)”39 Similarly a blogger by the name of Johnathandescribes himself as “An Autistic who wishes a cure could be found, though I know that mightnot happen in my lifetime,” making it his goal with his blog to “try to mostly show what a scamneurodiversity is.”40 The pro-cure position is well represented by parents of autistic children andorganizations such as Autism Speaks41 and Talk About Curing Autism,42 but pro-cure autisticindividuals seem to have a weaker Internet presence than does the neurodiversity movement.Perhaps this is because they are less common than autistic persons who adhere to the37 Megan R., “What Do You Mean by Neurodiversity?” Neurodiversity Now (blog), January 24, 2013 (9:45 a.m.),  See also Fenton and Krahn, “Autism,” 1.38 There is an interesting exclusive side to this type of neurodiversity, insofar as it includes some but not all of the “neurologically different” under its banner, and in so doing may commit some of the same marginalizing normative judgements of which its advocates are otherwise so critical. This point perhaps needs further investigation but is beyond the scope of this thesis.39 Quoted in Kapp et al., “Deficit,” 64.40 Jonathan, “Autism's Gadfly,” Autism's Gadfly (blog), n.d., ideology, or perhaps because their views are already well represented by thedominant stream of scientific research and pro-cure activism.One objection raised by critics of the neurodiversity programme is a potential for self-selection bias in the available literature. It has been suggested that since autism self-advocatesmust be capable, at the very least, of communicating in some modality – typically in print – thathigher-functioning individuals, such as those with Asperger syndrome, are thereforeoverrepresented in the neurodiversity movement, and especially in neurodiversity publications.43The worry is that the de facto exclusion of low-functioning individuals results in a failure of themovement to represent the full spectrum of diversity amongst autistic persons; thus, when self-advocates claim that autism is not a disability but an identity, that autism ought not be cured, orthat autism is a normal human variation, they may be (implicitly or explicitly) speaking on behalfof all autistic persons, or speaking about autism as if it were a unitary, homogenous condition,and thereby marginalizing the experiences of those autistic people who are unable to advocatefor themselves due to their communication difficulties.The problem here is twofold. The demedicalized understanding of autism proposed byneurodiversity advocates carries the risk of marginalizing people who are severely impaired bytheir condition, as the “disability” label can actually be quite helpful for low-functioning ASDpersons. This label may enable them to gain access to disability benefits and other services thatthey need to carry out the basic functions of life. Conversely, retaining our current socialunderstanding of autism as an illness stigmatizes autistic persons and perpetuates disabling socialconditions, making it difficult for even high-functioning individuals to obtain meaningful43 This is a common criticism, but has been contested by members of the neurodiversity movement. Cf. Jaarsma and Welin, “Autism,” Nicolaidis, “What Can Physicians Learn,” and Joseph, “All Autistics Who Oppose Neurodiversity Are High Functioning,” Natural Variation – Autism Blog, February 24, 2009 (4:42 a.m.),, for example. This is to say that both the current medical model of ASD and theproposed demedicalized autistic identity position risk making overgeneralizations about autismas a condition, and in so doing, marginalizing the needs and life experiences of those people whodon't fit the cast.To this end, Jaarsma and Welin argue that the neurodiversity claims ought to be acceptedas they pertain to “high-functioning” individuals, such as those with Asperger's disorder, but notin the case of “low-functioning” autistic persons. They argue that since, in addition to deficitsand disabling consequences, high-functioning autism “can also have desirable and enablingconsequences, both to the individual and to society”44 and since “high-functioning autists mostoften can have rather independent lives in the right kind of environment,”45 we ought to honourthe neurodiversity movement with respect to high-functioning autism. But low-functioningautism is seen by Jaarsma and Welin to have more undesirable effects and fewer mitigatingfactors, with little opportunity for a productive, independent life, and ought therefore to beconsidered a disability.This narrow conception of neurodiversity, however, is problematic insofar as it drawslines somewhat arbitrarily between high and low functioning autism, relying on normativejudgements of precisely the kind that the neurodiversity movement rejects. Further, although byconvention high- and low-functioning autism are distinguished on the basis of whether or not thepatient's IQ falls within the “normal” range or whether the patient has language delays,46 this44 Jaarsma and Welin, “Autism,” 22.45 Ibid., 28.46 Baron-Cohen, Simon, “Is Asperger Syndrome/High-functioning Autism Necessarily a Disability?” Developmentand Psychopathology 12, no. 03 (2000): 490. By convention, the “normal” IQ range is two standard deviations from the average. The average IQ is defined to be 100, and the standard deviation is defined to be 15, making the “normal” range between 70 and 130. Approximately 95% of the population falls between these bounds. See Neisser, Ulric, “Rising Scores on Intelligence Tests,” American scientist 85 (1997).18kind of univariate formulation of a complex idea such as “function” has been contested. Personson the autism “spectrum” often experience a range of deficits (and often some benefits) ondifferent axes of ability including “spoken language, written communication, adaptive skills,different types of intelligence, need for consistency, sensory processing, and so on.”47 Accordingto Nicolaidis, we must, therefore,resist the temptation to categorize people as high- or low-functioning, inasmuch as such categorizations only serve to inadvertently harm our patients. We risk unnecessarily depriving patients categorized as “low-functioning” of their self-determination and opportunities to reach their potential. Similarly, we often deprive our patients categorized as “high-functioning” of necessary supports and services, or we make dangerously false assumptions about their ability to understand what we say or carry out our recommendations. Instead, we must try to understand an individual’s complex combinations of strengths and challenges, as well as the potential for wide variations in functioning.48This focus on the function of autistic persons and the performativity of autism has itself beensubject to criticism, as it is seen not as an objective evaluation of a person's “severity” of autism,but rather a value judgement about the person's worth or utility.49 “High-functioning” in thissense may be a euphemism meaning “functional enough to work and contribute to society,” in amanner reminiscent of the use of the word “well” to mean “well enough to work.”50Similar questions persist for the broader conception of neurodiversity favoured by most47 Nicolaidis, “What Can Physicians Learn,” 507.48 Ibid.49 Murray, Stuart. “Autism Functions/The Function of Autism.” Disability Studies Quarterly 30, no. 1 (2010).50 See Berlant, Lauren, “Risky Bigness: On Obesity, Eating and the Ambiguity of 'Health',” in Against Health: How Health Became the New Morality, ed. Jonathan M. Metzl and Anna Kirkland (New York: New York University Press 2010): 28.19advocates. If autism is a simply natural human variation and another, equally valid way of beinga person, why ought we worry about depriving “high-functioning” (or, for that matter, “low-functioning”) autistic persons from support and services? Clearly, what Nicolaidis and manyother advocates have in mind is an approach to understanding and treating autism that goesbeyond the simpleminded ill/well binary. These themes will be readdressed in Chapter 2....Despite this controversy, or perhaps because of it, the neurodiversity movement continues to gainsupporters among the autistic and nonautistic communities alike. The movement has staked out aterritory in the contentious terrain of mental health, opposing the normative judgements thereofand maintaining that autism is not pathological. This claim, however, takes place in a partialepistemological vacuum – one that is increasingly being filled by scientific research currentlyunderway. It is to this research that we now turn.1.4 Etiologies of autismSeventy years after autism was first identified, its cause remains elusive. Originally thought to bea nascent form of schizophrenia, autism initially went largely unnoticed by psychiatricresearchers and professionals.51 It was not until 1980, with the publication of the DSM-III, thatautism first gained official recognition. At this point, autism was no longer associated withschizophrenia, but considered a “pervasive developmental disorder” – a class of idiopathic,behaviourally-defined conditions affecting young children. The 1987 revision of the Diagnosticand Statistical Manual, the DSM-III-R, modified the diagnostic criteria for autism and saw the51 Baker, Jeffrey P., “Autism at 70 – Redrawing the Boundaries,” The New England Journal of Medicine 369, no. 12 (2013): 1089.20addition of “pervasive developmental disorder – not otherwise specified” (PDD-NOS) as a newdiagnosis for people who met some but not sufficiently many of the criteria for a diagnosis ofautism.52In 1994, the American Psychiatric Association released the DSM-IV, which again saw theexpansion of diagnostic categories under the heading of pervasive developmental disabilities,adding Asperger syndrome, Rett syndrome, and childhood disintegrative disorder (CDD).53These five diagnostic categories, autism, Asperger's, Rett's, CDD, and PDD-NOS, shared manysimilarities in their symptomatology, and were thought to represent different points on an“autism spectrum,” along which the “sufferer” could vary significantly in the severity of theirdeficits and their ability to function.54 Thus it was decided by the APA to remove thesedifferential diagnoses from the fifth edition of the DSM, released in 2013, in favour of the singleheading, “autism spectrum disorder.”55 Throughout these  years of classificatory change, the APAhas remained silent on the topic of the etiology of ASD, and rightly so. Despite decades of52 Ibid.53 Ibid. Rett syndrome is a disorder primarily affecting girls characterized by a period of normal development for 6to 18 months, followed by a loss of purposeful motor control, epilepsy, characteristically autistic behaviours andother symptoms. CDD follows a course similar to Rett's, with a period of normal development for up to 3 or 4 years of age followed by a rapid loss of linguistic capability and cognitive function, often accompanied by autistic behaviours. CDD remains idiopathic, and is quite rare compared to other autism spectrum disorders. Asperger syndrome, likely the most well-known of these new additions, is often referred to as a form of “high-functioning autism.” Asperger syndrome is a condition with deficits in social reciprocity and repetitive behaviours similar to those of autism, but without accompanying intellectual impairment or language delay.54 Although some of the problems with the idea of autistic “function” were discussed in the previous Section, this language is still in common currency, and the idea of autistic “function” is still regularly used as a metric for deciding whether an autistic person deserves disability services or should be removed from the mainstream classroom to “special education,” for example. As such, the use of this term is nearly impossible to avoid; this should not, however, be taken as an endorsement on my part of the idea of autistic “function” as a useful way of thinking about autism. Similarly, the language of “deficits,” “mental illness,” and other such value-laden terminology is pervasive in the way autism is discussed in the scientific literature – hopefully I might be forgiven the use of this language in the following discussion of said literature.55 This decision has been highly controversial. The removal of Asperger disorder has proven particularly contentious, as many people who have been diagnosed or self-diagnosed with Asperger disorder may feel that they are having their identities stripped from them. See Singh, Jennifer S., “The Vanishing Diagnosis of Asperger's Disorder,” Advances in Medical Sociology 12 (2011).21research, autism spectrum disorders have stubbornly resisted “reductionistic” attempts toconstruct their etiology in terms of “the gene for autism,” mercury poisoning from childimmunizations, overly aloof “refrigerator mothers,” or other univariate explanations that haveheld sway at different times and places.56 In this Section, I will summarize some of the major areas of etiological research thatscientists are currently undertaking with the goal of understanding autism. While I cannot hopeto do justice to the depth and diversity of research presently underway, my intent with thisSection is to communicate the flavour and dominant themes of current autism research, as wellas to convey the heterogeneity and lack of a unified understanding of the condition. In thefollowing pages I will discuss the dominant threads in autism etiology research, includingneurophysiology, genetics, environmental pollutants, vaccinations, viral infections, immunology,and parenting practices. Volumes have been written about these subjects, of course, so I do notaim for comprehensiveness, but my concern is perhaps less with what the “actual” etiology oretiologies of autism are, so much as what is claimed to be the etiology of autism, especially whenthose claims bear the weight of scientific authority, real or perceived. Perhaps what is mostimportant for how we understand autism is construction of a simple and coherent etiologicalnarrative, the complex reality notwithstanding.1.4.1 Neurological underpinningsResearch into the cause of autistic symptomatology has primarily been focused on the search forthe “autistic brain” – that is, the search for abnormal developmental signatures in the brain thatdifferentiate autistic from nonautistic persons. These studies, making use of imaging techniques56 See Nadesan, “Constructing Autism,” especially Chs. 5 and 6.22such as MRI, PET, and CT scans, or in some cases autopsy of autistic persons' brains, havepointed to a variety of neurophysiological mechanisms that may be at play in the expression ofautism. To start at a gross anatomical level, autistic persons typically have brains which are 5%to 10% larger than those of the general population. A study by Courchesne et al. reported that ofthose studied, 90% of two- to four-year old children with autism had a brain volume above thenormal healthy average, and 37% had brain volumes at least two standard deviations abovenormal, thus meeting the criteria for developmental macroencephaly.57 This overdevelopment ofthe brain is believed to begin in the first months of the child's life, as head circumferencemeasures of newborns show no difference between neurotypicals and those who are laterdiagnosed as autistic.This period of overdevelopment results in abnormally high volumes of white matter incerebral and cerebellar structures, and abnormally high volumes of grey matter in the cerebrum,especially the frontal lobes.58 The rapid development of these brain structures appears to ceaseprematurely within the first 2 to 4 years of life, often leaving older autistic children with smallerthan normal brain volumes.59 Periods of overdevelopment such as these can lead to localizedneuronal hyperconnectivity, which fact may explain some of the behavioural, cognitive, andaffective disturbances observed in autistic persons, especially sensorimotor overstimulation.60 Other studies have focused on the amygdala, a part of the limbic system, as the locus ofabnormal development implicated in the development of autism. The amygdala is a complex and57 Courchesne, Eric, et al., “Unusual Brain Growth Patterns in Early Life in Patients with Autistic Disorder: An MRI Study,” Neurology 57, no. 2 (2001).58 Carper, Ruth A., et al., “Cerebral Lobes in Autism: Early Hyperplasia and Abnormal Age Effects,” Neuroimage 16, no. 4 (2002).59 Courchesne, Eric, “Brain Development in Autism: Early Overgrowth Followed by Premature Arrest of Growth,”Mental Retardation and Developmental Disabilities Research Reviews 10, no. 2 (2004).60 Belmonte, Matthew K., et al., “Autism and Abnormal Development of Brain Connectivity,” The Journal of Neuroscience 24, no. 42 (2004).23still poorly understood structure which is involved in numerous different tasks, includingmemory consolidation, danger response, fear, anxiety, and other emotions.  Its role in autism washypothesized by Baron-Cohen et al. due to the involvement of the amygdala in social interactionand emotional intelligence.61 The amygdala is also implicated in obsessive-compulsivebehaviours commonly observed in autistic persons. Most research has found abnormally large oroverdeveloped amygdalae in autistic children,62 however a recent study by Inui has pointedtoward damage or underdevelopment of the fetal amygdala as a potential cause of autism.63 Other potential neurological culprits include the poor regulation of neurotransmitters,including dopamine, oxytocin, and especially serotonin, which has repeatedly been found atelevated levels in  sample autistic populations.64 Some research has also pointed to disturbancesin the ability of neurons to migrate to the cerebral cortex during pregnancy.65 Many of thepurported causes of autism are also implicated in other mental illnesses, perhaps explaining thehigh comorbidity of autism with other conditions. The neurological overdetermination of autism,its overlapping etiologies and high comorbidity with other mental illnesses has cast some doubton whether our psychiatric nosologies truly represent something about the way the brain works,or whether they are simply convenient classificatory fictions.6661 Baron-Cohen, Simon, et al., “The Amygdala Theory of Autism,” Neuroscience & Biobehavioural Reviews 24, no. 3 (2000).62 See Bellani, M., et al., “Brain Anatomy of Autism Spectrum Disorders II. Focus on Amygdala,” Epidemiology and Psychiatric Sciences 22, no. 4 (2013) for a recent review.63 Inui, Toshio, “Toward a Unified Framework for Understanding the Various Symptoms and Etiology of Autism and Williams Syndrome,” Japanese Psychological Research 55, no. 2 (2013).64 See McBride, P. Anne, et al., “Effects of Diagnosis, Race, and Puberty on Platelet Serotonin Levels in Autism and Mental Retardation,” Journal of the American Academy of Child & Adolescent Psychiatry 37, no. 7 (1998).65 See Schmitz, Christoph, and Payam Rezaie, “The Neuropathology of Autism: Where Do We Stand?” Neuropathology and Applied Neurobiology 34, no. 1 (2008) for a review of these topics.66 See Nadesan, “Constructing Autism,” especially Ch. GeneticsAutism is one of the most heritable of mental illnesses. Studies on monozygotic twins havedemonstrated concordance rates between 70% and 90%,67 and while twin studies cannot rule outenvironmental factors entirely – indeed, environmental influences are needed to explain whymonozygotic twins are not always either both autistic or both neurotypical – numerous studieshave consistently shown heritability to be approximately 80%.68 There are three general types ofgenetic variations that can give rise to autism: single-gene disorders, broad phenotypic variationstemming from multiple genes, and de novo genetic mutations.Single-gene or “Mendelian” disorders that can cause autism include Fragile X syndromeand Rett syndrome. Fragile X syndrome is caused by a mutation of the FMR1 gene on the Xchromosome and may result in many different types of intellectual impairments, includingADHD, ASD, or OCD, as well as other physical and psychological effects. As it is a disorder ofthe X chromosome, boys are preferentially affected at a rate of 1 in 3600, compared withapproximately 1 in 6000 in girls.69 Similarly, Rett syndrome is a disorder caused by mutations tothe MECP2 gene on the X chromosome affecting synthesis of the MECP2 protein, which causesautism-like symptomatology. Rett syndrome, however, almost exclusively affects girls – malefetuses without a functioning MECP2 gene typically miscarry before reaching full term, whereasfemales with the disorder typically retain a functioning copy of the MECP2 gene, providing themwith sufficient protein synthesis to survive, but not to experience normal neurological67 Monozygotic concordance refers to the probability that, given one autistic twin, the other twin will also be autistic in a set of identical twins. See Eapen, Valsamma, “Genetic Basis of Autism: Is There a Way Forward?” Current Opinion in Psychiatry 24, no. 3 (2011).68 Ibid. “Heritability” describes the proportion of phenotypic variation attributable to genetic, rather than environmental, variations.69 Rousseau, Francois, et al., “Prevalence of Carriers of Premutation-size Alleles of the FMRI Gene – and Implications for the Population Genetics of the Fragile X Syndrome,” American Journal of Human Genetics 57, no. 5 (1995).25development.70 Between 10-15% of cases of autism are thought to stem from single-geneconditions such as these.71Beyond Mendelian single-gene disorders, most cases of autism are thought to involve avariety of genes, with “each of these variations being common and distributed continually in thegeneral population, but resulting in varying clinical phenotypes when it reaches a certainthreshold through complex gene–gene and gene–environment interactions.”72 In these cases, no“genetic disorder” is present, but it is thought that the confluence of many factors, which inisolation would create modest or no effects, produces clinically significant symptomatologywhen present in a single individual. The number of distinct genes that can contribute to autisticsymptoms in children is believed to be immense – a recent study claimed as many as 400different loci may be implicated.73 These individual “predisposing” genes are rarely claimed toexplain more than a few percent each of the variability in symptomatology between subjects andcontrols, and despite the innumerable studies claiming to find associations between particulargenes and ASD, the replicability of such studies has generally been poor, owing the exceedingrarity of these genes, or perhaps publication bias.The third type of genetic influence is so-called de novo genetic mutations.  De novomutations are those that are possessed by the child but are present in neither parent, and thereforeexist as the result of new mutations in the germ cells of one of the parents.  These mutations,usually inherited from the father, often result in severe and specific deficits in the affected child.70 Amir, Ruthie E., et al., “Rett Syndrome is Caused by Mutations in X-linked MECP2, Encoding Methyl-CpG-binding Protein 2,” Nature Genetics 23, no. 2 (1999).71 Folstein, Susan E., and Beth Rosen-Sheidley, “Genetics of Austim: Complex Aetiology for a Heterogeneous Disorder,” Nature Reviews Genetics 2, no. 12 (2001): 950.72 Eapen, “Genetic Basis.”73 Iossifov, Ivan, et al., “De Novo Gene Disruptions in Children on the Autistic Spectrum,” Neuron 74, no. 2 (2012)26Although autism resulting from de novo mutations constitutes only about 15% of cases,74 theprobability of these mutations and the corresponding risk of autism increases with the father'sage at the time of conception.75The heterogeneity of genetic influences implicated in the development of autism-likesymptoms, as well as the presence of many “autistic genes” among nonautistic populationssuggests that the role genetics play is one of predisposing children toward developing autism.76This idea of “genetic susceptibility” to autism suggests that genetic factors are responsible forsome children having, for example, a poor ability to process heavy metals, or a malfunctioningimmune system which “overreacts” to viral infections early in life – these environmental factorsare then believed to push the child “over the edge,” as it were.1.4.3 Heavy metals and other environmental pollutantsAs it is thought that genetics alone is unable to explain the observed increase in the prevalence ofautism and other neurodevelopmental disorders, researchers have begun to look at environmentalfactors, including heavy metals and other common industrial chemicals in the environment. Intwo recent review articles, Grandjean and Landrigan identified 11 industrial chemicals found inthe environment that have been implicated in the development of autism, ADHD, and otherconditions. These chemicals include lead, methylmercury, polychlorinated biphenyls, arsenic,toluene, manganese, fluoride, chlorpyrifos, dichlorodiphenyl-trichloroethane, tetrachloro-74 Ibid., and Sebat, Jonathan, et al., “Strong Association of De Novo Copy Number Mutations with Autism,” Science 316, no. 5823 (2007).75 O’Roak, Brian J., et al., “Sporadic Autism Exomes Reveal a Highly Interconnected Protein Network of De Novo Mutations,” Nature 485, no. 7397 (2012).76 Meek, Shantel E., et al., “A Review Of Gene–Environment Correlations And Their Implications For Autism: A Conceptual Model,” Psychological Review 120, no. 3 (2013).27ethylene, and polybrominated diphenyl ethers.77 Many of these chemicals are transmitted throughbreastmilk to the infant, whence they are able to cross the blood-brain barrier. Other of thesechemicals are present in the bloodstream of the mother and may pass unimpeded through theplacenta.Exposure to such contaminants in critical developmental periods affects the function anddevelopment of the brain in various unsavoury ways. Prenatal exposure to methylmercury hasbeen shown through use of fMRI to be associated later in life with unusually high levels ofactivation in certain cortical regions in response to sensorimotor tasks, congruent with the“overstimulation” reported by many autistics in response to everyday sensorimotor stimuli.78Fetal exposure to phthalates, a class of chemical compounds used in many consumer productssuch as cosmetics and children's toys, as well as being commonly used in packaging, has alsobeen shown to be associated with autism. Phthalates are absorbed into the body through skincontact and consumption, and travel freely through the placenta to reach the fetus where they actas endocrine disruptors.79 These chemicals impede the thyroid's ability to distribute hormonesthroughout the body by “competing” for receptor sites on the transport proteins.80Other environmental contaminants which may play a role in the increase in autismprevalence include commonly-used organophosphate pesticides; perfluorooctanoic acid, achemical used in the manufacture of many products such as Teflon and Gore-Tex;81 and various77 Grandjean, Philippe, and Philip J. Landrigan, “Developmental Neurotoxicity of Industrial Chemicals,” The Lancet 368, no. 9553 (2006), and Grandjean, Philippe, and Philip J. Landrigan, “Neurobehavioural Effects of Developmental Toxicity,” The Lancet Neurology 13, no. 3 (2014).78 White, Roberta F., et al., “Functional MRI Approach to Developmental Methylmercury and Polychlorinated Biphenyl Neurotoxicity,” Neurotoxicology 32, no. 6 (2011).79 Miodovnik, Amir, et al., “Endocrine Disruptors and Childhood Social Impairment,” Neurotoxicology 32, no. 2 (2011).80 Colborn, Theo, “Neurodevelopment and Endocrine Disruption,” Environmental health perspectives 112, no. 9 (2004).81 De Cock, Marijke, Yolanda G. H. Maas, and Margot van de Bor, “Does Perinatal Exposure to Endocrine Disruptors Induce Autism Spectrum and Attention Deficit Hyperactivity Disorders? Review,” Acta Paediatrica 28types of air pollution including particulate matter from automobile traffic.82 The number ofenvironmental pollutants known or suspected to play a role in the development of ASD growsseemingly without bound. On this point, Grandjean and Landrigan emphasize thatThe number of chemicals that can cause neurotoxicity in laboratory studies probably exceeds 1000, which is far more than the estimated 200 that have caused documented human neurotoxicity. However, in the absence of systematic testing, the true extent of the neurotoxic potential of industrial chemicals is unknown. The physiology of brain development and experimental evidence suggest that developmental neurotoxicity is likely for all of them, except perhaps for some of the compounds that require metabolic transformation to become neurotoxic, in which immature metabolism may provide some degree of protection. The few substances proven to be toxic to human neurodevelopment should therefore be viewed as the tip of a very large iceberg.83While they are speaking here of neurodevelopmental disabilities generally, some of the chemicalpollutants alluded to by these authors have already been claimed to contribute to the rise inautism prevalence, and more will almost certainly be added to the list as the science develops.1.4.4 VaccinesOne industrial chemical that has received particular scientific and media attention is thiomersal,an organomercury compound commonly used as a preservative in vaccines. The popular notionthat vaccines increase the risk of childhood autism originated in a 1998 paper published in TheLancet titled “Ileal-lymphoid-nodular hyperplasia, non-specific colitis, and pervasive101, no. 8 (2012).82 Volk, Heather E., et al., “Traffic-Related Air Pollution, Particulate Matter, and Autism,” JAMA Psychiatry 70, no. 1 (2013).83 Grandjean and Landrigan, “Developmental Neurotoxicity,” 2175.29developmental disorder in children”84 which argued for, among other things, a possible linkbetween the measles, mumps, and rubella (MMR) vaccine and the onset of neurodevelopmentaldisorders such as autism. Over the next several years, through the ensuing media coverage, theidea that vaccines increase the risk of autism took hold in the public imagination despitemounting scientific evidence to the contrary. Eventually Andrew Wakefield, the principalinvestigator of the original study, was revealed to have falsified data and to have had financialconflicts of interest, leading to the official 2010 retraction of the paper.In response to public outcry, thiomersal, believed to be the cause of this purportedconnection, was removed from vaccines in North America and Europe by 2000, an action that isoften interpreted by anti-vaccine organizations as an admission of guilt on the part of vaccinemanufacturers.85 This act did not placate the troubled parents, however, and blame quicklyshifted to other organomercury adjuvants used in vaccines, or to the administration of particularpathogens or combinations of pathogens. For example, administering the particular combinationof pathogens in an MMR vaccine at a critical period in the child's development is believed bysome anti-vaccine activists to precipitate the development of autism by “overwhelming” thechild's fragile immune system in those predisposed.There is no scientific evidence to support these claims. Hundreds of individual trials,reviews and meta-analyses carried out by scientist in different fields have consistently found noassociation between childhood vaccinations and increased prevalence of autism.86 Nevertheless,84 Wakefield, Andrew J., et al., “Ileal-lymphoid-nodular Hyperplasia, Non-specific Colitis, and Pervasive Developmental Disorder in Children,” The Lancet 351, no. 9103 (1998). Retraction published in The Lancet 375, no. 9713 (2010): 445.85 Baker, Jeffrey P., “Mercury, Vaccines, and Autism: One Controversy, Three Histories,” American Journal of Public Health 98, no. 2 (2008).86 For a very recent review of the literature, see Taylor, Luke E., Amy L. Swerdeger, and Guy D. Eslick, “Vaccines Are Not Associated with Autism: An Evidence-Based Meta-Analysis of Case-Control and Cohort Studies,” Vaccine 32, no. 29 (2014). Neurodiversity proponent and blogger Catherina keeps an updated list of scientific 30the influence and visibility of anti-vaccine organizations such as Generation Rescue andprominent anti-vaccine spokespersons such as Jenny McCarthy in the popular press have had asignificant influence on public perceptions of ASD, and thus it bore mention.1.4.5 Viral infections and immunologyThe antivaccine movement, though thoroughly discredited, draws some apparent support fromthe legitimate scientific research being carried out in the field of immunology. Maternal viralinfections during gestation or infections during the first few years of life of the infant have beenpostulated as potential catalysts for autism and other mental illnesses, though the “mechanism,by which viral infection may lead to autism, be it through direct infection of the central nervoussystem (CNS), through infection elsewhere in the body acting as a trigger for disease in the CNS,through alteration of the immune response of the mother or offspring, or through a combinationof these, is not yet known.”87Although this is a relatively new area of research in autism etiology, several recentstudies in animal models have established a link between maternal immune system activationduring pregnancy and the development of autism-like symptoms in offspring.88 Elmer et al.performed a study on rats showing a relationship between MCHI protein concentration andmaternal viral infection.89 MCHI (major histocompatibility complex class I) proteins play ajournal articles demonstrating the lack of causal connection between vaccines and autism. See Catherina, “75 Studies that Show No Link Between Vaccines and Autism UPDATED to 107,” Just the Vax (blog), March 7, 2014 (3:18 p.m.), Libbey, Jane E. et al., “Autistic Disorder and Viral Infections,” Journal of Neurovirology 11, no. 1 (2005): 1.88 Cf. Bauman, Melissa D., et al., “Activation of the Maternal Immune System During Pregnancy Alters Behavioral Development of Rhesus Monkey Offspring,” Biological Psychiatry 75, no. 4 (2014) and Shi, Limin, et al., “Activation of the Maternal Immune System Alters Cerebellar Development in the Offspring,” Brain, Behavior, and Immunity 23, no. 1 (2009).89 Elmer, Bradford M., et al., “MHCI Requires MEF2 Transcription Factors to Negatively Regulate Synapse Density During Development and in Disease,” The Journal of Neuroscience 33, no. 34 (2013).31crucial role in the development of the central nervous system, including negatively regulating thedevelopment of synapses between cortical neurons. These proteins were found in much higheramounts in the cortical neurons of offspring whose mothers' immune systems had been activatedby viral infection during gestation, causing changes in synaptic density in the cerebral cortices ofthe rats. As synaptic density in the cerebral cortex is one of the potential indicators of autism, asimilar abundance of MCHI protein in human children could catalyze the development of autism.However, a cohort study of 7379 participants carried out in Denmark investigated therelationship between autism and early childhood infections. While the study found a higherincidence of ASD diagnoses among children who were admitted to the hospital at some point forbacterial or viral infections, the results were not significantly different by type of infection – thatis, children hospitalized with measles were not statistically more likely to be diagnosed withASD than children hospitalized with upper respiratory tract infections, for example. For thisreason, the authors of the study conclude that the relationship between hospitalization forinfectious diseases and ASD diagnoses is not a causal one.90 As this line of research is fairlyyoung, few definitive conclusions have been reached.1.4.6 Parenting practices and behavioural interventionsThe final area of research discussed here deals with parenting practices and the socialenvironment of the child, suggesting these factors may play a role in autistic symptomatology. Inretrospect this perhaps seems obvious; if behavioural interventions have any effect on theseverity of autistic deficits, then social-environmental practices affect children in ways more or90 Atladóttir, Hjördís Ósk, et al., “Association of Hospitalization for Infection in Childhood with Diagnosis of Autism Spectrum Disorders: A Danish Cohort Study,” Archives of Pediatrics & Adolescent Medicine 164, no. 5 (2010).32less conducive to the expression of autism. This area of research has been slow to develop, due tothe understandable stigma attached to such explanations. This dates as far back as Leo Kanner's1943 paper where he postulates that cold and aloof mothers are to blame for their children'sautism, coining the term “refrigerator mother.”91 While the “refrigerator mother,” with itsmisogynistic overtones, is now universally dismissed by the scientific community as a root causeof autism,92 a recent study by Smith et al. has shown a relationship between maternal warmth andpraise and the amelioration of certain symptoms among autistic adults, including increased socialreciprocity and decreased repetitive behaviours.93This is echoed by other researchers who have found that parental limit-setting behaviouris associated with fewer behavioural problems from their autistic children,94 and that parentalmindfulness is associated with decreased aggression and self-harm,95 for example. The researchsuggests, however, that the role of social factors such as parental warmth is one of mitigation,rather than prevention. Autism is not caused by a particular parenting style, however overbearingor neglectful. Rather, it is thought that particular parenting styles and behavioural interventionsmay be adopted with the knowledge that the child is already autistic, in an attempt to achieve the“best” outcome for the child, where “best” is typically understood to mean that the child scoreshigher on measures of social reciprocity, verbal behaviour, and intelligence, or displays fewercharacteristically autistic behaviours such as hand flapping or self-harm.9691 Kanner, Leo, “Autistic Disturbances of Affective Contact,” Nervous Child 2, no. 3 (1943).92 Rajendran, Gnanathusharan, and Peter Mitchel, “Cognitive Theories of Autism,” Developmental Review 27, no. 2 (2007). See also Nadesan, “Constructing Autism.”93 Smith, Leann E., et al., “Symptoms and Behavior Problems of Adolescents and Adults with Autism: Effects of Mother-Child Relationship Quality, Warmth, and Praise,” American Journal of Mental Retardation, 113, no. 5 (2008).94 Osborne, Lisa A., et al., “The Effect of Parenting Behaviors on Subsequent Child Behavior Problems in Autistic Spectrum Conditions,” Research in Autism Spectrum Disorders 2, no. 2 (2008).95 Singh, Nirbhay N., et al., “Mindful Parenting Decreases Aggression, Noncompliance, and Self-Injury in Children with Autism,” Journal of Emotional and Behavioral Disorders 14, no. 3 (2006).96 Numerous studies have been conducted demonstrating the effectiveness of diverse therapies such as applied 33...This list is not exhaustive. In a recent review article on the relationship between genetic andenvironmental factors in autism, Meek et al. notedAs is evident through a brief review of autism genetic research, there are likely multiple genetic influences and distinct biological pathways involved in the development of autism. While the field faces many challenges, including genetic and phenotypic heterogeneity, the dearth of research incorporating both genetic and social environmental measures may be among the most limiting factors to the field’s progress.97The picture of autism painted by scientists is an interactional one – in most cases of autism inwhich a single-gene disorder like Fragile X or Rett syndrome is not present, it is thought thatgenetic predisposition combined with a variety of different environmental “insults” all contributeto precipitating the development of autism in the child. This is an especially intuitive hypothesisin cases where children show a period of normal development followed by rapid deterioration ofmotor, cognitive, and linguistic abilities, as in the case of CDD.Indeed, it is likely that the category we now call “autism spectrum disorders” does notrepresent a common underlying pathology, but rather that there are many distinct etiologies thatfind common expression in the constellation of symptoms we now classify as autistic, potentiallybehaviour analysis, speech therapy, music therapy, holding therapy, dietary restrictions, sensory integration therapy, etc., along these measures. See, for example, Makrygianni, Maria K., and Phil Reed, “A Meta-analytic Review of the Effectiveness of Behavioural Early Intervention Programs for Children with Autistic Spectrum Disorders,” Research in Autism Spectrum Disorders 4, no. 4 (2010), and Howlin, Patricia, Iliana Magiati, and Tony Charman, “Systematic Review of Early Intensive Behavioral Interventions for Children with Autism,” American Journal on Intellectual and Developmental Disabilities 114, no. 1 (2009). One could object, however, that the metrics used in these studies are normative ones, and the goal of these therapies is normalization of autistic persons. We might therefore be inclined to be more cautious and say that these therapies have been demonstrated to be effective in producing autistic children who conform more closely to the hypothetical norms embedded in the evaluative metrics employed, regardless of whether those outcomes are more adaptive to the autistic child in question, broadly understood. 97 Meek, “A Review.”34explaining why there is such a heterogeneity among so-called autistic persons in the expressionof their symptoms, as well as why there is such a wide spectrum of “function.” Clearly, the fieldis still far from constructing a coherent narrative describing the cause of autism, and much moreresearch will be required to do this, especially focusing on the interactions between genetics,environment, and upbringing. But even these inchoate etiologies suggest new ways to understandautism, as well as new “treatments,” “therapies,” or other medical interventions aimed atpreventing new cases of autism or ameliorating symptoms in those already diagnosed. These newways of understanding autism, and how they conflict, concur, and interact with the claims of theneurodiversity movement will be the subject of the following Chapter.352. (De)medicalizing autismPrima facie, this research into the cause of autism need not be any more committed topathologizing autism than research into the cause of blue eyes need be committed topathologizing eye colour.  Searching for the genetic, neurological, and environmental influencesthat affect the course of autism development in children is no doubt a legitimate area of scientificinquiry, in this sense. But overwhelmingly researchers cast their investigations in the language ofhealth and illness, systematically constructing autism as a mental health problem to be addressedthrough medical interventions.In a recent review article on the relationship between vaccines and autism, for example,Tomljenovic and Shaw begin with the claim that “Autism spectrum disorders (ASD) are seriousmultisystem developmental disorders and an urgent global public health concern,”98 while Sebatet al. have described autism as a “major burden to society.”99 Grandjean and Landrigan, whosework was discussed above, devote a section of their review article to the economic costsassociated with autism and other neurodevelopmental disorders, claiming that ASD isresponsible for the loss of some 7 million IQ points in the United States alone, corresponding toa loss of some $126 trillion in potential lifetime earnings in 2008 dollars.100 Their concern, itseems, is motivated by the potential loss of economic productivity, insisting on an economicallyinstrumental valuation of persons. They are motivated to propose prevention measures forconditions such as ASD not because they cause suffering to individuals, but because they hinderthe growth of the economy.98 Tomljenovic and Shaw, “Do Aluminum Vaccine Adjuvants Contribute.”99 Sebat et al., “Strong Association.”100 Grandjean and Landrigan, “Neurobehavioural Effects,” 334-5.36Research conducted on these terms constructs and is constructed by a pathologicalunderstanding of autism – indeed, one that goes beyond treating autism as an individualaffliction, but as a scourge on society as a whole. The use of rhetorical strategies such as theseexposes these researchers as committed to pathologizing autism, but at least it has the benefit ofbeing overt – one can hardly call autism a “burden to society” or “public health concern” anddeny their belief in its status as disease. But the research has other implications, perhaps moreinsidious, that also construct autism as pathological – and in so doing raise important questionsabout suffering and disease. In this chapter, I will discuss the ways, both direct and indirect, inwhich this etiological research contributes to a pathological construction of autism. I will thenaddress the role of normality in the neurodiversity program, and the complex relationship thisconcept has with what we might call the nature of disease. I will argue that the insistence onnormality ultimately commits the neurodiversity movement to a problematic model of disease,and that they might be better served by remaining agnostic on the questions of normality andetiology. I close with some final thoughts on identity and authority.2.1 Genetics and reproductive technology construct autism as a diseaseEtiologies suggest treatments. The state of our knowledge of the heterogeneous genetic factorsthat dispose children to developing autism motivated Joseph Buxbaum of the Mt. Sinai School ofMedicine to state in 2005 that a prenatal test for autism would be available within 10 years.101This statement was widely criticized by the neurodiversity movement for its perceived eugenicovertones, and lead to the creation of an “Autism Genocide Clock” posted on the blog of a101 Herera, Sue, “Autism Research Focuses on Early Intervention,” CNBC, February 23, 2005, advocate that counted down the days until the proposed test was supposed tobecome available.102 Predictions of this kind are unreliable at best, of course, and the genetics ofautism has proven much more complex than Buxbaum initially supposed. Nevertheless,Campbell made a similar suggestion in 2010, claiming that we have already sufficient knowledgeof the genetic determinants of autism to warrant genetic testing for Mendelian disorders such asRett syndrome, and we should be able to produce a clinically useful genetic test for other formsof autism in the near future.103 Indeed, a nascent form of preimplantation genetic selection isalready underway in the state of Western Australia, where sex selection techniques for in vitrofertilization patients have been approved as a method of reducing the likelihood of having a childwith autism for parents thought to be at high risk. As boys are four times more likely than girls tobe autistic, the Reproductive Technology Council of Western Australia approved the use of sexselection for female children as an effective method of reducing the risk of having an autisticchild.104 While the method is crude – a bit like trying to avoid seeing one's ex-wife at a cocktailparty by moving to a different country – it nevertheless clears the path for future, more closelytargeted genetic tests.The existence of a test of this kind puts expecting parents in the position of deciding onthe genetic future of their children, a thought that no doubt makes many people uneasy, as itseems to foster an attitude of control and discourage the kind of “openness to the unbidden”102 The clock has since been removed. See Ventura33, “Autism Research and Prenatal Testing,” The Ventura33 Fanfiction Universe (blog), n.d., Campbell, Daniel B, “Advances and Challenges in the Genetics of Autism,” FOCUS: The Journal of Lifelong Learning in Psychiatry 8, no. 3 (2010).104 First announced in O'Leary, Cathy, “WA Allows Embryo Screening for Autism,” The West Australian, October 19, 2013, See also Western Australian Reproductive Technology Council 2013 Annual Report, June 30, 2013,, especially p. 13.38some see as necessary to love and appreciate a child.105 But the promise of genetic engineering toallow us to prevent debilitating genetic disorders and freely select benign character traits for ourchildren is a tempting one. On this point, Savulescu and Kahane argue that as a corollary to ourduty to provide our children with the best lives we can, parents have a moral obligation, whenpossible, “to select the child, of the possible children they could have, whose life can be expectedto go best”106 According to this “Principle of Procreative Beneficence,” as they call it, parentshave a duty to use any genetic selection techniques available to them in an effort to give theirfuture children the “best possible future.” While it is not at all clear what they have in mind bythe “best possible future” or what it means for someone's life to “go best” – the authors gesturevaguely toward “well-being” and “advantages” – they make it clear that those conditions wetypically call developmental disabilities, such as Down syndrome or autism, are excluded.Jaarsma and Welin disagree with this assessment. They argue that not only do we nothave a duty to select against an autistic fetus, but that parents who so desire ought to be allowedto select for a mildly autistic child.107 This is a qualified claim however – as discussed above,they support a narrow conception of neurodiversity, in which they honour the identity claims ofhigh-functioning autistics only, not low-functioning ones. But although Jaarsma and Welin seemto agree with at least a restricted version of the neurodiversity claim, this agreement is based onthe attributes thought to accompany high-functioning autism.108 A high-functioning autistic mayhave social deficits, flattened affect, and repetitive behaviours, for example, but these “hypo-105 Sandel, Michael J., The Case Against Perfection: Ethics in the Age of Genetic Engineering (Cambridge, MA: Harvard University Press, 2007): 45.106 Savulescu, Julian, and Guy Kahane, “The Moral Obligation to Create Children with the Best Chance of the BestLife,” Bioethics 23, no. 5 (2009): 277.107 Jaarsma, Pier, and Stellan Welin, “Human Capabilities, Mild Autism, Deafness and the Morality of Embryo Selection,” Medicine, Health Care and Philosophy 16, no. 4 (2013).108 Jaarsma and Welin, “Autism.”39empathizing” behaviours may be compensated for by a “hyper-systematizing” cognitive stylethat gives high-functioning autistic persons exceptional abilities in scientific, mathematical, andcreative domains.Savulescu and Kahane's assessment differs in its prescriptions from Jaarsma and Welin's,but ultimately both are based on an instrumental valuation of persons according to the normativestandards of independence, employability, and so forth – in other words, “to function.” Savulescuand Kahane appear to recognize this fact, noting that often the worst consequences of disabilitiesare due to prevailing social conditions, yet they would prefer to see such difficulties addressedthrough the medium of preventative genetic medicine rather than social change. Given thiscommitment, as well as the ambiguity in what it might mean for someone's life to “go best,” wecould understandably infer from their principle that we have a “significant moral obligation” toselect for male over female children in a patriarchal culture, straight over gay children in ahomophobic culture, light-skinned over dark-skinned children in a racist culture, and so forth,given the myriad privileges associated with each of these characteristics. In this sense, Savulscuand Kahane's commitment to “procreative beneficence” is also a tacit commitment to reinforcingsocial ills such as racism and sexism, not to mention discrimination against the disabled or theneurodiverse.No doubt this is not what Savulescu and Kahane have in mind, and they probably wouldnot advocate, if asked, selecting against black or gay or female babies, feeling that these areproblems to be addressed through social change and not genetic change, but in so doing they aredividing the arena into health problems and social problems, drawing (what they feel to be) aclear line between them.109 Under this rubric, autism and other developmental disabilities are to109 Savulescu and Kahane cannot argue that female children ought not be selected against because gender is not a 40be considered health problems rather than social problems (although there might be some socialproblems associated with then). But by classifying autism under the rubric of health and notsocial problems, they have precisely begged the question – they have decided the issue inadvance against neurodiversity.Whatever their utility, these ethical musings bring into focus the implicit valuations thattechnologies of this type inherently carry. A useful comparison would perhaps be the prenatal(postimplantation) genetic test by amniocentesis commonly used to test for Down syndrome, theuse of which places parents at an increased risk of miscarriage. To parents who intend to keepand care for the child no matter its condition, such a test makes no sense – there is little merit intaking the risk unless it were assumed that the parents intended to abort the fetus should the testcome back positive. These tests only make sense in a context that allows for selection (in thiscase, elective abortion); thus to take the test is to accept the value implicit in those selectiveprocedures. But even the very existence of a genetic test for a condition that might be considered“undesirable” forces upon prospective parents a choice of whether or not to use it, with theknowledge that even refusing the test constitutes a tacit judgement on the worth of children withsaid condition.Preimplantation genetic tests would allow for selection without increased risk ofmiscarriage or the need for elective abortion, but they do not necessarily avoid making implicitnormative judgements.    The sex-selection technique approved in Western Australia exemplifiesthis as, contra Jaarsma and Welin, the technique has been approved to select against autisticdisability, as they are very careful not to draw any moral distinctions that line up with distinctions of disability or illness to avoid claims of discrimingation or eugenics. Nevertheless, they admit that selecting a smarter fetus,for example, is a moral obligation, even if the alternative is a child of average intelligence. Why not, in that case, select for a more privileged gender, sexuality, or race? See Savulescu and Kahane, “Moral Obligation,” 284-9.41children only, leading some neurodiversity advocates to accuse the state of practicing eugenics.110Here the value judgement is explicit – autism is regarded as an undesirable disability, and thetechnology is made available to those parents who wish to avoid the tragic fate. But suppose weindulged the fantasy of Jaarsma and Welin, and allowed selection for mildly autistic children.Since ASD typically trades in predispositions rather than “genes for autism,” might we feel likeselecting for children with Asperger syndrome would put them at risk for more severe forms ofASD? Or, perhaps we should go further and allow selection for any and all forms of ASD,however severe.111 Would doing so be honouring the neurodiversity programme? Or would thevery existence of a genetic selection procedure somehow challenge the autistic claim to identityand normality?We might be inclined to wonder why there is such intense interest in the possibility of aprenatal genetic test for autism in the first place. That such time, energy, and money is spent inthe search for the genetic determinants of autism suggests that there is significant interest inmaking such a test available for use. It is not difficult to imagine that most parents, given thechoice, would opt for a neurotypical child, given the well-known difficulties associated withraising autistic children.112 The presence of such a test, then, could serve not only to reinforce a110 Durbin-Westby, Paula C., “Baby Sex Checks for Autism: Eugenics Concerns,” Paula C. Durban-Westby Autistic Advocacy Blog, October 20, 2013 (8:18 p.m.), That parents might wish to select for a child with Asperger syndrome or even “low-functioning” autism is not sofar-fetched. By way of comparison, members of the Deaf community have already used preimplantation genetic tests in efforts to increase their chances of having deaf children. These Deaf persons have often expressed sentiments similar to those of the neurodiversity movement, including the belief that deafness is an identity, rather than a disability, yet their actions have proven controversial. Deaf community members claim that since deafness is an identity like any other they have done nothing wrong in choosing an identity for their children, while others among the bioethics community and general public have expressed outrage that parents would deliberately attempt to bring a disabled child into the world. See Sandel, The Case Against Perfection, 1-5.112 Many of the most vehement opponents of the neurodiversity movement are parents of autistic children themselves, as they are all too familiar with the stresses and challenges concomitant to raising an autistic child. See, for example, Rao, Patricia A., and Deborah C. Beidel, “The Impact of Children with High-Functioning Autism on Parental Stress, Sibling Adjustment, and Family Functioning," Behavior Modification 33, no. 4 (2009), and Davis, Naomi Ornstein, and Alice S. Carter, “Parenting Stress in Mothers and Fathers of Toddlers 42pathological understanding of ASD, but also as a way of moving the discussion away from therights and acceptance claims of the neurodiversity movement (Claim 4) and into the realm ofpreventative medicine instead. Providing the opportunity for prospective parents to geneticallyselect against autism or other “disabilities” devalues the lives of persons living with thoseconditions selected against, treating them as medical problems to be addressed through theframework of preventative genetic medicine, and ignoring the social and institutional barriersthat create the disabilities experienced by autistics. Under this framework, the “disability itself”is viewed as the problem, not the failure of social justice.113 The existence of such a genetic test,or even its proposal, is not value-neutral – rather, it serves to reinforce the battle lines drawnbetween the neurodiversity movement and the popular and scientific conceptions of autism.2.2 Environmental pollutants construct autism as a diseaseThe discovery that industrial pollutants, heavy metals, and other environmental toxins areimplicated in the development of autism raises similar questions and normative challenges.Would we feel more or less disposed to regard autism as an identity if it were caused byenvironmental “insults”? Further, given that exposure to toluene and methylmercury mayprecipitate the development of autism in genetically predisposed children, for example, ought weattempt to eliminate those chemicals from the environment? Grandjean and Landrigan think so.Claiming that the increase in neurodevelopmental disorders represents a “pandemic,” and usingthe language of disease and disability, they propose a strategy based on the Precautionarywith Autism Spectrum Disorders: Associations with Child Characteristics,” Journal of autism and developmental disorders 38, no. 7 (2008).113 Roberts, Dorothy, “The Social Immorality of Health in the Gene Age: Race, Disability, and Inequality,” in Against Health: How Health Became the New Morality, ed. Jonathan M. Metzl and Anna Kirkland (New York: New York University Press, 2010).43Principle aimed at the elimination of neurotoxic industrial chemicals causing developmentaldisabilities such as autism and ADHD.114 Their view is certainly not unprecedented. As mentioned above, thiomersal was removedfrom vaccines in 2000 due to public outcry, despite virtual scientific consensus that the chemicalposed no risk for the development of autism or other neurological conditions. Even after theremoval of thiomersal, some anti-vaccine activists still contend that childhood vaccines areimplicated in autism, opting to prevent their children from being vaccinated over taking thepurportedly increased risk of ASD. Here we have a clear indication of their commitments – notonly do we have a duty to remove potentially toxic chemicals from the environment of childrenwho may be at risk of developing autism due to exposure, but further, autism is such anundesirable condition that it is worth placing one's own children and the children of others at riskfor serious infectious disease to avoid it. Here, the identification of a causally efficacious agent –even one based on scanty evidence and conjecture – in the development of autism stabilizes andreinforces the belief that autism is pathological.The presence of thiomersal and other mercury compounds in vaccines and their dubiousrelationship with autism has, understandably, been the subject of much controversy, as well asthe subject of a number of best-selling books in which thiomersal has been compared with thethalidomide scandal of the mid-20th century.115 There are parallels between the two cases,naturally. In both, we see the introduction of a foreign substance into the body of the affectedperson or the mother during pregnancy resulting ultimately in (alleged) physiological or114 Grandjean and Landrigan, “Neurobehavioural Effects.”115 Thalidomide, of course, is a drug that was marketed to pregnant mothers in the 1950s and 1960s to help reduce morning sickness, but was quickly pulled from circulation when it was shown to cause marked birth defects in the children of mothers who had used the drug. See Dachel, Anne, “Thalidomide / Thimerosal,” Age of Autism (blog), September 5, 2012 (5:46 a.m.), changes in the child. But we also have a similar dynamic in play in the case of, forexample, vaccinations (disregarding the thiomersal connection) – an administered externalchemical agent affects the physiology of the child, in this case triggering their immune system toproduce antibodies for specific communicable diseases. In order for the comparison betweenthalidomide and thiomersal (or the comparison between gross anatomical birth defects andautism) to have the desired rhetorical force, the authors must assume that the effects ofthalidomide were pathological and, in so doing, they are able to argue, or perhaps simply assume,that autism is pathological as well. And the comparison seems to make sense, at leastsuperficially – but we're willing to accept this argument so readily only because most of usalready believe that thalidomide-induced birth defects (and autism) are pathological.There is a distinctly essentialist flavour to this kind of argument. There seems to be a kindof essential person lurking under the surface here, and conditions such as autism or birth defectsare seen to get in the way of who that person was meant to be, in some sense. Perhaps this couldbe cast in terms of genetic endowment; we might think that thalidomide-induced birth defects orchemically- or virally-induced autism disturb the essential person, imposing a detrimental traitupon someone's otherwise preordained genetic destiny. But surely it can't be as simple as this, ifthe idea of a “genetic disease” such as Huntington's is to make any sense. Nor can such a naivefocus on the genetic account for the critically important role of the environment in not onlycreating diseases and impediments, but also those people we call “healthy.” This kind of ghostlyessential person is closely related to the concept of normality, and it also makes an appearance inthe arguments of the neurodiversity movement, in particular their insistence on autism as normaland as an integral part of identity. This point will be discussed at greater length in the following45sections.If we assume that some of the aforementioned chemicals are truly implicated in thedevelopment of autism spectrum disorders, what, then, is our duty? Do we follow the lead of theanti-vaccine activists in one arena, and many scientists and activists in another, to recommendthat these chemicals be banned immediately to safeguard our children's health? Answering thisquestion would seem to also stake out a claim on the question of autism as a pathology. If autismwere truly just a neurological difference, to be valued no greater or less than any other humandifferences, it is difficult to see why should it matter whether the condition is caused byanthropogenic chemicals, genetics or viral infections. That so many people in both the scientificand lay communities seem to feel that there is in fact a difference between chemically-inducedautism and genetic autism, however, reveals something about the way we think about disease andthe important role etiology has to play in distinguishing health from illness and normality fromabnormality.2.3 Neurodiversity and “normality”Bearing the weight of scientific authority, these kinds of etiological claims and their associatednormative flavours have an uneasy relationship with the neurodiversity movement, not leastbecause the claims are often in direct contradiction with one another. As discussed in Section 1.2,the first claim of the neurodiversity movement is that ASD is a natural human variation, oftencouched in the language of genetics. A claim of this type predicates the validity of autism as anidentity on a shaky foundation of speculative causation – a foundation that is vulnerable tocollapse as the science moves toward constructing a coherent etiology that does not square neatly46with these preconceptions. And while scientists point to sole genetic causes in the case ofsyndromes such as Rett's, the most general picture of autism painted by scientists is morecomplex, resulting from an interplay of genetic predisposition and myriad environmental factors.Many neurodiversity advocates avoid mentioning ultimate causes such as genetics orpollutants, but maintain that autism represents a variation in “brain wiring.” This turn of phraseis delightfully vague, but there is no doubt that it is true under an appropriate interpretation. Tothe extent that the ontology or the functional organization of a mind is responsible for thedifferences in behaviour, affect, and cognition experienced by autistic persons, and to the extentthat these ontological or organizational differences derive from differences in a person's brain,we should have no prima facie objection to this kind of description.116 Yet, as Nadesan points out,this kind of “reductionistic” focus on neurophysiology is misleading, and can serve to moveattention away from the social forces involved in the production of autism, broadly construed.117In this sense, etiological investigation into the interplay of these kinds of social forces may beseen to undermine the authority of of neurodiversity advocates who have completely“neurologized” autism.These observations point toward an apparent inconsistency in the neurodiversityprogramme.  That is, a commitment to the genetic, neurologic, or any particular origin of autismas a premise for the acceptance of the neurodiversity claims not only puts one at risk of losing116 I must resist the urge to digress at length on the philosophical topics that ultimately bear only very minimally onthe topic at hand, and also resist the temptation to uncritically adopt a potentially controversial position such as mind-brain identity simply because it is currently fashionable among philosophers of mind and neuroscientists. Iwish to remain silent on these topics, but I take it as uncontroversial that there is some kind of causal relationship between brain and mind, and that we have no prima facie reason to believe that this kind of relationship would be necessarily incapable of producing the kinds of cognitive, affective, and behavioural differences characteristic of autism.117 “Social forces” could include not just such obvious things as parenting practices and socioeconomic factors, but also more broadly include diet and environmental pollutants, for example, insofar as these factors are thoroughly embedded in social practices. See Nadesan, “Constructing Autism,” especially Ch. 6.47legitimacy as the science develops, but also commits oneself to a problematic model ofpathology. This line of argument implies  that if it were the case that autism were an abnormalgenetic variation, or a nongenetic variation (i.e. if autism had some other etiology), then wewould be justified in calling it pathological. John Elder Robison, quoted above in support of thefirst neurodiversity claim, has made this argument more explicitly, claiming “Autism that’s aresult of chemical poisoning is a very different thing from the condition I grew up with . . . Beingborn different is one thing; crippling ourselves through preventable injury or ingestion ofchemicals is something else entirely. No one wants to accept that.”118 The neurodiversitymovement is generally in agreement with Robison on this point, and it seems to make good sense– yet it is difficult to say exactly why. If we accept the claim that autism is to be respected as anyother human variation – indeed, that autism is simply an identity, like being male versus beingfemale – then there is no immediately obvious reason why the cause of the identity shouldmatter. What is it about environmental pollutants, as opposed to genetics, that should make usfeel differently?  Is it the fact that it is due to chemicals? The fact that the pollutants are man-made? Or the fact that the results of exposure to these chemicals was unanticipated andaccidental?Pathologization resists simpleminded equations such as these. Autism in particular poseschallenges for those who would like to make a simple delineation between “genetic autism” and“chemically-induced autism” (or what have you): There is a wide range of “function” amongautistics – or, perhaps it would be better to say that there is a wide spectrum between peoplewhose autism offers them a few quirks and eccentricities compared to neurotypicals and thosewhose autism colours every aspect of their lives. Similarly, the main lesson of autism genetics is118 Robison, “Neurodiversity and Me.” 48that autism generally deals in predispositions, and thus we are left not with two obvious andsharply demarcated categories of “endogenous autism” and “exogenous autism,” but anetiological spectrum – and we are certainly unable to tell the difference in practice. For thesereasons, we should perhaps be hesitant to draw clear lines between persons whose autism isincidental to the person and those whose autism is integral to the person, lest we be forced toanswer difficult questions about whose autism truly “counts” as an identity and whose does not.Shall we only respect the identity claims of those autistic people whose autism is wholly geneticin origin? What about someone whose autism is almost entirely genetic in origin? Even if therewere a way for us to tell the difference, where ought we draw the line between natural humanvariation and pathology? Putting the question in these terms calls into stark relief the theoreticalcommitments at stake. To draw a meaningful boundary between autism that is nonpathologicaland autism that is pathological (or even to construct autism as uniformly nonpathological) oneneeds to assume that there is a meaningful distinction between pathology and health, and that thisdistinction lines up with some kind of identifiable property – in this case, it is assumed to line upwith “normal genetic variations” on the one side, and, presumably, abnormal genetic variationsand environmental insults, on the other. In other words, the boundary between pathology andhealth is drawn along etiological, rather than symptomatological, lines, in which some kind ofabnormality of structure or function (i.e. an identifiable etiology) is taken to be evidence ofpathology. According to this view, then, our understanding of the roles played by environmentaltoxins, viral infections, and the like bears directly on the question of whether autism is, indeed,“normal.”119119 There is something suspicious about this right from the start. Arguing that autism is not a disease because it is a normal genetic variation puts normality and disease in opposition to one another, when, in fact, disease is normal, in some sense of the word. Everyone gets sick at one point or another; isn't illness just a normal part of being human? This statement could be made more precise, but to do so would take us too far afield and 492.4 The “normal” function modelThese views characterize a particular model of disease – what has been called the “normalfunction model,” the “species-typical function model,” or the “medical model” of disease. Thismodel, which treats abnormalities of structure or function as constitutive of disease, plays animportant role in the medical-scientific conception of health, as well as an important role in therealm of bioethics. Ideally, it gives us an objective and non-arbitrary way to distinguish diseaseand disability from health, according to Norman Daniels, as “disease and disability are seen asdepartures from species-typical normal functional organization or functioning.”120 According toDaniels, this model is not only an accurate and commonsensical account of disease, but servestwo important political ends as well. The first is that it allows us to distinguish treatment fromenhancement. Medical interventions that are aimed at restoring a patient's capacities to “normal”are regarded as medical treatments, while interventions aimed at increasing a patient's capacitiesto beyond the normal range are regarded as enhancements (e.g. the use of nootropic drugs toenhance cognition). This distinction has an important role to play for Daniels in health care – onhis view, a fair and just health insurance policy or national healthcare system should, atminimum, provide its clients with access to medical treatments, but not necessarilyenhancements. This treatment/enhancement distinction is an important concept in bioethics withan extensive body of literature, but it bears little on the present discussion.Secondly, the normal function model is thought to help protect against the kind ofaggressive pathologization of the same type that neurodiversity advocates are critical of. Themodel explicitly recognizes that there is a range of “normal” persons, each with differentcontribute little to the argument, I think.120 Daniels, Norman. “Normal Functioning and the Treatment-Enhancement Distinction.” Cambridge Quarterly of Healthcare Ethics 9 (2000): 309-22.50capacities and endowments, thus the fact that one person is more shy than another, for example,need not immediately indicate the presence of disease. Daniels uses this model to delineate the“proper domain” of medicine, which is thought to include the amelioration of disease anddisability, but not to include complete physical or mental well-being. Thus, while there may besuch a thing as “pathological shyness” (i.e. social anxiety disorder), it is not the case, on thisview, that all shyness is necessarily to be viewed as disordered.The statements made by neurodiversity advocates quoted above make them implicitlybeholden to this kind of model of disease. Their emphasis on autism as “natural” or “normal” asa basis for demedicalization carries with it the corollary that “unnatural” or “abnormal”variations ought to be medicalized. What the word “normal” means to neurodiversity activists isnot immediately clear, however, as “normality” is a bit of a thorny concept, but ultimately provesto be crucially important.2.5 Three ways to be normalRobert Wachbroit distinguishes three ways that the word “normal” can be used: what he calls the“statistical,” “evaluative,” and “biological” concepts of normality.121 The first two of theseconcepts are simple enough. Statistical normality refers to the familiar measures of centraltendency, such as the mean and median. On this account, something is considered normal if it isaverage or within some bounds, say, within two standard deviations of average. This is amathematically exact concept, that can be applied precisely to problems amenable to quantitativeanalysis. The second concept is that of evaluative normality. This concept is broader than thefirst, encompassing such things as ethics, conventions, cultural norms and the like. Something121Wachbroit, Robert. “Normality as a Biological Concept.” Philosophy of Science 61, no. 4 (1994).51that is evaluatively normal need not be common or statistically normal – for example, althoughleft-handedness is uncommon, very few people (anymore) feel it is unacceptable. Conversely,something that is very common or statistically normal may not be evaluatively normal.Wachbroit distinguishes a third category of normality, what he calls “biologicalnormality.” Biological normality is an explicitly teleological stance – when we make statementsabout the “normal” heart or the “normal” lung, we are also making statements about the goal orthe function of the structure in question, as in “The function of the lungs is to draw oxygen intoand expel carbon dioxide from the body.” Function and biological normality go hand-in-hand forWachbroit – the normal organ (or mind, or body) is one that fulfills its function; the abnormaldoes not.122 It is this sense of biological normality Daniels has in mind in his “normal function”account – the medical model is one that explicitly looks for “abnormalities” of structure orfunction against the backdrop of the hypothetical norm. And while neurodiversity advocatesunequivocally agree that autism is an evaluatively normal condition, their vehement declarationsof particular etiologies as “normal” makes it clear that they also adhere to the view that autism isbiologically normal.Theories that invoke concepts of “biological normality” have been the subject of muchcriticism.123 Distinguishing between “normal” and “abnormal” can, in many cases, feel like a122 There is, evidently, some degree of overlap between these concepts of normality. There is certainly a degree of evaluation implicit in the decision of what constitutes statistical normality (e.g. how many standard deviations from the mean ought we think normal?). Similarly, evaluative judgements are pervasive in decisions about what constitutes biological normality or “health,” as will be discussed below. It is perhaps no surprise that normality is a thoroughly normative concept.123 Cf. Levy, Neil, Neuroethics: Challenges for the 21st Century (New York: Cambridge University Press, 2007): 94-104; Juengst, Eric T., “Can Enhancement Be Distinguished from Prevention in Genetic Medicine?” Journal of Medicine and Philosophy 22 (1997); Parens, Erik, “Is Better Always Good? The Enhancement Project,” Hastings Center Report 28, no. 1 (1998); Wolpe, Paul Root, “Treatment, Enhancement, and the Ethics of Neurotherapeutics,” Brain and Cognition 50 (2002); Hesslow, Germund, “Do We Need a Concept of Disease?” Theoretical Medicine 14, no. 1 (1993); King, Lester S., “What is Disease?” Philosophy of Science 21, no. 3 (1954); and Horwitz, Allan V., Creating Mental Illness, (Chicago: University of Chicago Press, 2002): 11-2.52pretty arbitrary affair, especially with regard to etiology. Taking at face value the claim made byRobison that chemically-induced autism is not normal (that is, it is pathological) but geneticallycaused autism is, we would be forced to conclude that two autistic persons with otherwiseidentical symptoms and abilities ought to be regarded differently depending on the etiology oftheir condition, despite the fact that they may experience the same kinds of life challenges andmixed blessings that autism carries. Other authors have made similar remarks about otherconditions – such as distinguishing between short-statured children on the basis of whether theyhave a human growth hormone deficiency or not.124 Such a distinction feels arbitrary andcapricious given that those with similar symptomatology will experience similar challenges.Why should etiology have a role to play in deciding which conditions “count” as diseases?The answer to the question lies in another facet of the normal function model that hasreceived criticism – that it relies upon a “theoretical account” of the design of the organism.125 Tosay that such-and-such condition is biologically normal requires knowledge of the “plan” or“schema” of how the organism “ought” to function: What is it supposed to look like? Whatcapacities is it supposed to have? This stance is explicitly teleological, and might be favourablycompared to the stance an auto mechanic takes when diagnosing and repairing a car. Knowingthe design specifications of the engine, the mechanic knows just how the engine is supposed tolook, what each belt and hose is supposed to do. Adopting a teleological stance toward anautomobile makes sense; automobiles are designed by human beings with intentions, thoseintentions are built into the design of the automobile, and we are able to know the “theoreticalaccount” of the design of the automobile because we have access to design specifications and124 Daniels, “Normal Function.”125 Parens, “Is Better Always Good?”53operations manuals. However, as human beings were not designed by someone with intentions,but rather developed incrementally through the process of evolution, we have no design manualsto inspect. Moreover, as evolution is an unthinking natural process and famously short-sighted, itwould not be overstating the case to say that humans were not designed for anything.126 Thus, ifwe are to have a “theoretical account” of the design of the human, then it is something we mustglean (or, rather, assign) through observation and inference. What is a human being supposed tolook like, anyway?This turns out to be a difficult question to answer, as there is a certain kind of circularityinvolved in establishing what constitutes “normality.”  King explains,We think health as freedom from disease, and disease as an aberration from health. This istravelling in circles . . . When we apply statistical methods we already have in mind the idea of health. We exert selection on the cases we study. Thus, to find the “normal” blood sugar level we eliminate known diabetics. And the basal metabolic rate, in health, we determine after omitting known thyroid disease.127Here, King has in mind the idea of statistical normality, but in other cases we might be lessinterested in statistics and more interested in an “ideal,” or what we have called “biologicalnormality.” King gives the example of dentistry, in which the healthy ideal is to have a full set of32 teeth, even though the average American adult only has about 25 remaining.128 Thus, eventhough most adults may vary from the ideal, the “theoretical model” of the human has 32 teeth,and deviation from this desideratum constitutes deviation from ideal health – what we might126 Even the use of the word “designed” here perhaps suggests too much agency on the part of evolution.127 King, “What is Disease?” 195.128 National Institute of Dental and Craniofacial Research, “Tooth loss in Adults (Age 20 to 64),” National Instituteof Dental and Craniofacial Research, accessed March 3, 2014, call “disease.”While missing a few teeth may not be what most people have in mind when they use theword “disease,” the above considerations capture several important points on the issue of whatdiseases consist in. King explains thatour concepts of disease are very closely related to our values. . . . Disease is the aggregateof those conditions which, judged by the prevailing culture, are deemed painful, or disabling, and which, at the same time, deviate from either the statistical norm or from some idealized status. Health, the opposite, is the state of well-being conforming to the ideals of the prevailing culture, or to the statistical norm.129This is one of the major problems with the normal function model. Not every departure from thehypothetical biological norm constitutes a disease, and those departures from the norm which doqualify as diseases do so for reasons that are intimately bound up with the way we value persons.Indeed, the very definition of the hypothetical biological norm is evaluative.130 In many casesthese evaluative judgements are relatively uncontroversial – few would argue that malaria is nota disease, on this or any account – but in some cases these kinds of judgements can serve tosystematically marginalize persons who, for whatever reason, do not conform to these norms.These norms are intimately bound up in the culture of the time and place, especially as regards“mental illness.”131 Autism in particular has all the hallmarks of a historically contingent129 King, “What is Disease?” 197.130 Cf. Agich, George J., “Disease and Value: a Rejection of the Value-Neutrality Thesis,” Theoretical Medicine 4, no. 1 (1983); Engelhardt Jr, H. Tristram, “The Disease of Masturbation: Values and the Concept of Disease,” Bulletin of the History of Medicine 48, no. 2 (1974); Szasz, Thomas, The Medicalization of Everyday Life: Selected Essays (Syracuse: Syracuse University Press, 2007); and Lane, Christopher, “The Strangely Passive-Aggressive History of Passive-Aggressive Disorder,” in Against Health: How Health Became the New Morality,ed. Jonathan M. Metzl and Anna Kirkland (New York: New York University Press 2010), for examples.131 Horwitz, “Creating Mental Illness.”55disorder, as discussed by Nadesan in her book Constructing Autism;132 what today we medicalizeunder the banner of “autism spectrum disorders,” we might at a different point in time havecategorized as “eccentricities” (in the case of high-functioning individuals) or “feeble-mindedness” (in the case of low-functioning individuals).133 What constitutes “normal,” then, is abit of a moving target.The upshot of these observations is that so-called “normal function” models or the“medical model” rely heavily on value judgements and normativity to establish what does anddoes not “count” as normal – what, in other words, a human being is supposed to be like. Thefact that the dominant “medical model” is fraught with assumptions, political claims, andnormativity has motivated some neurodiversity advocates to adopt the “social model” of diseaseand disability (Claim 5). As discussed there, the social model understands an autistic person'sdisability as produced through the interaction of their capacities with the social and physicalenvironment. Disease, on this account, is not a “natural kind” – that is, not so much a category ofbiological fact as one of evaluative judgement. We do not call HIV a “disease” simply because ofthe presence of a virus, nor do we call teratoma a disease simply because of the presence of atumour – we call them diseases because of the normative judgements we make about them. HIVand teratoma are, quite simply, undesirable conditions to have.That many of the problems with the normal function model are the same problemsdecried by neurodiversity advocates regarding the “cure mentality” and the medical approach toautism makes it all the more surprising that such advocates would use the language of normalityto defend their position. While many neurodiversity advocates avow their adherence to the social132 Nadesan, “Constructing Autism.”133 Hacking, “Kinds of People.”56model, and while the social model of disability addresses the normative problems associated withthe medical model, there seems to be an incomplete adoption of the social model within andamong the positions of the neurodiversity movement.2.6 Identity revisitedIn this connection, it is perhaps also worth asking why neurodiversity advocates have set up whatseems like a false dichotomy by claiming that autism is an identity, rather than a pathology.Conditions that affect the mind – what we might conventionally call “mental illnesses” or“mental disabilities” – often have a difficult relationship with personal identity,134 and it is thistension that is pointed to by neurodiversity advocates who make the claim that autism is apositive identity – indeed, an inextricable part of the person, rather than a disorder or a disease.When we speak about autism as a “disease” or we describe someone as a “person with autism”we are exposing a tacit belief that autism is separable from the person, in contrast to the beliefthat autistic people simply have a different kind of brain or mind from neurotypicals.Interestingly, this sense of autism as an identity may actually be strengthened by increasingknowledge of its etiology. As mentioned above, the current paradigmatic definition of ASD is adescriptive one – it assigns the label to individuals who exhibit certain behavioural(ir)regularities, without reference to cause. Knowledge of the neurophysiology of autism, in thissense, provides an explanatory framework that the nosological category previously lacked.  134 For example, individuals with bipolar disorder, chronic depression, or anxiety disorders often struggle for years trying to find a regimen of psychiatric drugs, exercises, and therapies that alleviate their symptoms, and when they do so, report feeling like they are finally themselves. But many people, upon finding a treatment that relieves them of the symptoms of their condition by psychometric measures, are left feeling robotic, or otherwise “not themselves.” People with certain conditions, such as type I bipolar disorder, are notoriously difficult to keep medicated, as many would rather suffer the negative consequences of their condition than go through life feeling like someone other than themselves. See, for example, Karp, David A., Is It Me or My Meds? Living with Antidepressants (Cambridge, MA: Harvard University Press, 2007).57But it is not immediately obvious that these two categories – identity and pathology – aremutually exclusive.135 Other kinds of identification, such as “cancer survivor” or “alcoholic” blurthis distinction – or disregard it entirely, though they do so as a means of engaging with,addressing, and reappropriating what is otherwise a completely undesirable condition. Thosewho identify as cancer survivor do not necessarily do so because they want their cancer to berespected as any other human variation, but may do so as a way of reclaiming a painful andpotentially deadly condition as a means of strength and personal growth. Nor would mostalcoholics embrace alcoholism as a desirable condition, but identifying as an alcoholic is seen, insome approaches, as a necessary step toward recovery and treatment. In this sense, there is animportant disanalogy between these cases and the case of autism, in that embracing autism as anidentity and a pathology would mean accepting the values implicit in the pathology label.Treating autism as we treat cancer or alcoholism could be seen to locate the autist's suffering inthe autism, not in the social environment.But this also relates to the neurodiversity movement's tacit acceptance of the valuationsimplicit in the label of “disease,” which fact speaks to their indebtedness to “normal function”models, as discussed in the previous section. But also, insofar as the neurodiversity movementimplicitly accepts the ill/well dichotomy as presented, they have forced a dilemma uponthemselves.136 Namely, they have to either place autism into the category of pathology or health –or break the condition up along some simplistic, univariate axis of ability. Perhaps the obvious135 The complex and difficult relationships people have with their “pathologies” is treated at great length in Elliott, Carl, Better than Well: American Medicine Meets the American Dream (New York: W. W. Norton, 2003) and Elliott, Carl, A Philosophical Disease: Bioethics, Culture and Identity (New York: Routledge, 1999).136 Perhaps they have not forced it upon themselves so much as had it thrust upon them by the existing structures ofmedical, political, and social power that refuse to acknowledge the subtle and nuanced ways in which autistic and other neurodiverse persons are simultaneously enabled and disabled by their condition, and the many ways in which autistic persons differ greatly in their abilities.58solution is to reject the ill/well dichotomy entirely. Yet the language of disease has the power tobe simultaneously both stigmatizing and liberating. “Biologized” accounts of mental illnesses arebecoming increasingly common as neuroscience and cognitive psychology gain ground overtraditional psychological or psychoanalytic explanations of those conditions, but these newaccounts come with decidedly mixed blessings. Such explanations are no doubt well-intentioned,as in the case of the “brain disease” metaphor for drug addiction – an account of addiction as adisease can reduce feelings of guilt or blame for the condition, as well as making it easier foraddicts to receive treatment, but it can also reduce feelings of personal responsibility (perhapsnecessary for recovery) and increase social stigma.137 Social stigma may make it less likely forthe patient to seek medical treatment (even if said treatment is more easily available), experiencesocial isolation, and be a constant source of emotional pain.138 Thus, even if biogenetic accountsof autism or, for that matter, a label such as “disease” or “disability,” makes needed servicesmore easily available to autistic persons who need them, one may feel that, on balance, suchlabels and explanations are causing more harm than good to autistics. Taking a stance thatsimultaneously embraces autism as an identity and a disease could prove a much more radicalposition – one that transgresses the conventional binaries of ill and well, normal and abnormal.2.7 ConclusionThis debate between and among academics, scientists, neurodiversity advocates, and the laypublic provides rich terrain for the exploration of values and normativity in medicine. There are,of course, many questions here left unasked and unanswered that bear on these matters. Among137 Buchman, Daniel Z., Judy Illes, and Peter B. Reiner, “The Paradox of Addiction Neuroscience,” Neuroethics 4, no. 2 (2011).138 See Kvaale, Erlend P., William H. Gottdiener, and Nick Haslam, “Biogenetic Explanations and Stigma: A Meta-analytic Review of Associations Among Laypeople,” Social Science & Medicine 96 (2013).59them are such questions as these: Although normativity is pervasive in the way we conductmedicine, which may account for the current marginalization of autistic persons, is normativitycategorically undesirable in medicine? Are we even able to do medicine without at least somedegree of normativity, especially as regards mental illness – or conditions that are seen to affectthe mind? Specifically, can we always defer to the authority of the patient to make decisions ontheir own behalf, even when their condition calls their competence directly into question? Anddoes that phrasing implicitly beg the question?Ultimately, questions such as these probe the boundaries not just of the neurodiversitymovement, but also of the orthodox scientific conception of autism. We should ask: if we were totake the neurodiversity position seriously, would that mean “anything goes?” How would wedeal with difficult cases such as schizophrenics who may pose a danger to themselves or others,but nevertheless refuse treatment? Can these cases be adequately dealt with through a utilitarianapplication of the law, or would doing so simply be a rebranding of the normativity implicit inthe psychological programme of categorization, diagnosis, and treatment? On the other hand, theneurodiversity movement addresses serious problems with the psychological paradigm, and weignore these insights at our own peril. This movement points to a kind of perceived aggressivepathologization becoming increasingly common, which at its extreme entails a kind of“weaponizing” of the DSM, so to speak: using psychometric measures of behaviour andnosologies of mental illness as a means of political, social, and economic power.There is a need for much more scholarship and research regarding these questions, aswell as the question of autism's etiology. The science, as they say, is still in its infancy –scientists are still a long way from establishing a stable narrative or narratives explaining the60origins of the condition. Increasingly, it appears that the picture being painted of ASD is one of amessy, disunified category that lumps together people with certain superficial behavioural,cognitive, affective, or other characteristics. The production of these characteristics may beoverdetermined – produced by a complex dynamic interplay of social forces and biological ones,personal will and environmental determinism, genetics and socialization.But the neurodiversity movement has an uneasy relationship with questions of autism'setiology. Some of the claims of the movement are in direct conflict with emerging scientificknowledge, while in some cases a subtler conflict arises from underlying assumptions about thenature of suffering and disease. But the ultimate goal of the neurodiversity movement, it seems,is to promote awareness and acceptance of diversity in the human sphere, and promote the self-determination and rights of autistic persons specifically, and the “neurodiverse” more generally.This is no doubt a worthy goal, and insofar as the scientific research concerns itself with causalagents and matters of fact, there need be no conflict. But to the extent that etiological researchsimultaneously constructs and is constructed by a conceptual framework in which autism is a“mental illness” or “developmental disability,” this discourse systematically constructs autism ina way that calls into question the competence, and therefore self-determination, of autisticpersons.The neurodiversity movement hopes to counter this trend by situating autism in the realmof health through their use of the language of “normality” and “natural genetic variation.” Butjust as predicating the neurodiversity claim on the inchoate etiology of autism spectrum disordersleaves it vulnerable to being undermined as the science develops, similarly, staking out the claimthat autism is not a pathology because it is normal commits oneself to a problematic concept of61the nature of disease.  Perhaps a more robust tactic for neurodiversity advocates would be toremain explicitly agnostic on the question of autism's etiology. Many do. By deliberately movingthe focus away from etiology, neurodiversity advocates can focus the debate on the normativestandards implicit in the project of constructing nosologies of mental illness.If, in the preceding pages, I've done little more than explain the fairly obvious fact thatscientific research into the etiology of autism carries with it value judgements, normativeassumptions, and ethical quandaries, then so be it. That science is inherently value laden ishardly a novel statement. But the particular contours of that scientific research – and theparticular values it carries – have an important role to play in shaping the lives and experiencesof those who live with autism spectrum disorders daily. One wonders, though, about the stabilityof the neurodiversity movement. It may turn out to be the kind of activism and advocacy that canonly sustain itself in a (partial) scientific vacuum – in the liminal space between naming andidentifying a condition, on the one hand, and constructing a coherent etiology, perhaps in tandemwith a treatment, on the other. This may seem like a pessimistic prediction, but it has not beenmy goal here to make judgements on whether the autism “really is” normal or pathological – inmy opinion, these are the wrong questions to ask. I have instead endeavoured simply to show theways that these two ways of thinking – the “medical” and the “neurodiverse” – are in tensionwith one another. It may be the case that some of these tensions can be resolved, either through arevision of the neurodiversity programme, or by a more careful rhetorical approach by thescientific and lay communities. Scientific research aimed at discovering the cause of autism maybe more or less value neutral on the surface, but this research also suggests programmes for thetreatment and prevention of the condition, and is often motivated explicitly by this desire.62Technologies of this kind put ordinary people into situations of forced choice, in which makingethical decisions and value judgements about the desirability of autism – and by extension, itsstatus as pathology – are unavoidable. The normative contours of this etiological research,however well intentioned, are thus impossible to ignore.Of course, all these observations gloss over certain other questions I feel also need to beasked. Why, for example, did I speculate that scientific research might undermine theneurodiversity movement's foundation, and not vice versa? Why has the neurodiversitymovement received so much criticism from parents, scientists, and the like? Why are we so eagerto let scientists speak about autism, rather than autistic persons themselves? Perhaps, then, thekey insight of the neurodiversity paradigm is not that autism is “normal” nor that autistic personsdeserve respect, rights, and opportunities appropriate to their abilities, but that it calls into starkrelief the theoretical commitments and inherent ethical contours of neuroscientific researchdirected toward autism – as well as our own beliefs about who has the authority to speak onbehalf of whom. With these insights clearly in mind, perhaps we can tread more carefully in therealm of mental health.63BibliographyAgich, George J. “Disease and Value: a Rejection of the Value-Neutrality Thesis.” Theoretical Medicine 4, no. 1 (1983): 27-41.American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, FifthEdition. 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