Editor’s Note: Over the next several months, Mad in the UK and Mad in America will publish a serialized version of Sami Timimi’s book, Insane Medicine. In Part 2 of chapter 4, he discusses the lack of findings for any genetic or neurobiological basis for ASD, as well as the diagnostic criteria and testing for ASD. Each Tuesday, a new section of the book will be published, and all chapters will be archived here.
ASD genetics: Has the null hypothesis been disproven?
As previously discussed, the correct scientific stance is to assume that what we are characterising as autism or ASD does not exist as a natural category until we can demonstrate that this null hypothesis can’t be true. If we want to classify ASD as a genetically predetermined neuro-developmental disorder we have to demonstrate that the null hypothesis—that there are no specific genes or neurological abnormalities/differences—can’t be true.
The argument that autism is a strongly genetic condition rests primarily upon twin studies. I explained in the last chapter on ADHD why estimating genetic heritability using the twin method does not help you in distinguishing environmental from genetic causes. The only reliable way to establish the relevance of the genetic component is through molecular genetic studies, of which there is a growing database involving whole genome scans of thousands of children with the autism label.
No specific, characteristic, rare, common, or polygenetic genes for autism have been discovered, but not for want of looking. Various candidate genes, linkage studies, genome scans, and chromosome studies have all failed to produce and reliably replicate any particular genes associated specifically with autism. The more failures pile up, the more proponents of the genetic explanation paradigm start desperately talking about how autism genetics is “complex” and that there must be some sort of mysterious polygenetic interactions that accounts for the “missing heritability.”
The most likely explanation for this finding, or rather lack of finding— that there is no such thing as genes that cause autism—remains unmentionable.
The continuing failure to identify specifics seems to have resulted in the majority of the human chromosome being identified as potentially harbouring autism genes, with major expert reviews typically concluding: “Many research teams have searched for genes that may be involved. They haven’t turned up any prime candidates yet, only dozens, maybe hundreds of bit players” (Hughes writing in 2012) and “With the advent of next generation sequencing techniques, the number of genes found that are associated with ASD is increasing to over 800 genes; consequently, it is becoming even more challenging to find unified explanations and functional associations between the genes involved” (Al-jawahiri and Milne writing in 2017).
The high ratio of males to females in ASD diagnoses also poses a problem for genetic theories. Genetic mechanisms need to account for this (such as autism being transmitted through the X chromosome), and thus far no molecular genetic studies have found an X or Y chromosome link.
Instead of facing up to the possibility that genes are not revealing themselves because they are not there, we are instead moving into an era where multiple research teams come together to create banks of “big data” in the hope that this can reveal tiny associations. It is hard to face the possibility that this mass of research money has led to a wasted endeavour, so instead they carry on getting the lion’s share of wasted research money because, “Sequencing technology quickly confirmed that the aetiology of ASD was multigenic and highly heterogeneous, with very few of the same pathogenic variants present in a significant percentage of afflicted individuals” (Rylaarsdam and Guemez-Gamboa, writing in 2019) and so “It may take many more decades of research before the scientific community has an accurate picture of how these modulators contribute to the aetiology of ASD. However, this understanding is critical for the development of effective therapies.”
Yes, keep throwing your research money at us. We’ve failed so far, but we need decades more of these failures to really know how badly we’ve failed, because we don’t understand the basic principles of scientific methodology. But hey, we’re scientists, we look like scientists, talk like scientists, so you should believe us.
Scientifically speaking, then, we have to assume that with regards to genetics, the cupboard is empty and the null hypothesis stands: There is no characteristic identifiable genetic abnormality/profile associated with ASD.
ASD brain imaging studies: Has the null hypothesis been disproven?
An important consideration to take into account in any analysis of neuroimaging profiles is that of “neuroplasticity.” This refers to the remarkable ability of the nervous system (particularly in children) to grow and change in response to environmental stimuli. The amazing plasticity of the human brain makes it difficult to determine precise cause and effect when individuals with different life experiences subsequently show what appear to be differences in neurological structure or functioning. This inconvenience makes it difficult for researchers to pin down behavioural features that children display as being caused by any neurological abnormalities or differences.
We see this neuroplasticity at play in all sorts of ways, from the ability that children have to compensate over time for brain injuries, to the findings that London cab drivers have larger volumes than almost anyone else of brain areas that are highly involved in navigating and spatial awareness. Thus, any brain differences found could be the result of environmental factors affecting brain development (like psychological trauma), differences in the rates that maturation takes place (for example, we know that on average girls develop a little faster than boys) and variations resulting from other features in the research subjects (for example, their intellectual ability).
It means that we can’t assume any differences we find are the result of a pre-existing biological problem. After all, the brain is the body organ whose function is that of enabling the organism to adapt to the environment. It would be surprising if the brain was not influenced by the experiences the organism has.
However, the biggest problem for autism studies, as with ADHD, comes from the lack of consistently replicated findings. This consistent inconsistency plagues research in this area. For example, some studies focussing on an area of the brain called the “cerebellum” have documented an increase in cerebellar volume among children diagnosed with an ASD, while others have found smaller than average cerebellar volumes; yet others have reported no significant differences between children with ASD and non-ASD subjects.
Similarly, studies on another area called the “amygdala” have been widely inconsistent, including some studies that found significant differences in volume and others that found no differences. This is the picture that emerges from this research. With clockwork regularity, a team of researchers announce their latest finding: “We have found that the connections between the two halves of the brain are smaller in autism, suggesting ASD is a disorder of brain connectivity,” and this then goes round the world media, but then we never hear of the subsequent research teams who can’t replicate these findings.
This shambolic, confused, and contradictory reality of autism brain research was brought home to me when I participated in a debate about autism with a colleague at an academic event in March 2017. We each had to put forward papers supporting our view. The colleague I was debating with, who believes that autism is a “known” disorder of the nervous system and that with sufficient research we will discover its neurological basis, put forward three papers to support his position. They were:
- “The emerging picture of autism spectrum disorder: Genetics and pathology,” a 2015 paper by Chen and colleagues. This paper proposes that research points to a primary role in ASD for the limbic system and cerebellum.
- “Neuroimaging in autism spectrum disorder: Brain structure and function across the lifespan,” a 2015 paper by Ecker and colleagues. This paper focuses on frontal and temporal lobes and the cerebral cortex as the primary sites of interest in causing ASD.
- “Autistic spectrum disorders: A review of clinical features, theories and diagnosis,” a 2015 paper by Fakhoury. This paper plumps for the primary issue in ASD being the balance of excitatory and inhibitory synapses.
It’s a complete mess. No common theme emerged from these three “state of the art” research reviews. There is little overlap in their favoured theories. None of the papers properly discussed the effects of environment or possible other factors (like levels of intellectual impairment in the research samples) on the results.
Theories come and go, and no one has a clue really what, how, or where this apparent neurodevelopmental abnormality or difference is. It is a swirling cauldron of self-proclaimed scientists that cannot face up to a scary reality—that their science hasn’t met the basics required of the scientific method. Most seem unprepared to state the obvious—that the null hypothesis stands and their research maybe heading down one blind alley after another into a cacophony of dead ends.
Finally, some researchers are waking up to the idea that maybe they will not find anything. A 2016 paper entitled “ASD validity,” which includes the renowned autism researcher Professor Christopher Gillberg amongst its authors, concludes, “The findings reviewed indicate that the ASD diagnosis lacks biological and construct validity,” and they recommend disbanding the ASD diagnoses as a basis for research. Sadly, they go on to suggest a broader neurodevelopmental construct instead. None of this evidence (or rather lack of it) seems to have the slightest dent in the continuing expansion in the numbers receiving ASD labels or in the assumption that there exists a natural thing called autism.
Here too then, as far as the science is concerned, the cupboard is also empty. No one has come near to finding a characteristic abnormality, and as a result there is no biological marker or brain scan used to diagnose autism. The null hypothesis stands—there is no characteristic brain abnormality associated with ASD.
What is autism anyway?
ASD did not develop out of any scientific discovery, and it has been created and popularised through social and political drivers.
We should not be surprised by the lack of progress in discovering the biological foundations. We don’t really know how to make a useable and exclusive definition of a case. If our definition of a case includes a wide variety of features that are spread in different ways across populations, you shouldn’t be surprised when research findings show a similar wide variation of findings.
These days the same behaviourally defined syndrome (ASD) is applied to residents of institutions with little hope of living independently and a long list of the great and the good such as Mozart, Van Gogh, Edison, Darwin, Einstein—all of whom, along with many others, have been retrospectively diagnosed as having an ASD (just type “famous people with autism” into Google and see what comes up).
From an “impairment” perspective, this is the entire human spectrum. Are people who support the idea that ASD is a recognisable condition seriously saying that what might be helpful for these cultural icons is the same as for residents of institutions with little functioning language?
This problem of having a vast repertoire of presenting behaviours and levels of functioning that can lead to a diagnosis is referred to as the problem of “heterogeneity” (defined as the quality or state of being diverse in character or content). Not only do the “core” features, such as difficulties in social communication, have a large crossover with people who would not consider themselves as having a “disorder,” but what are considered as autism symptoms are also commonly listed in a variety of mental health diagnoses—from ADHD to depression and anxiety to psychosis.
Heterogeneity is widely accepted as an issue in “mainstream” publications about autism. However, far from seeing this as a major problem with regard the scientific and medical validity of the concept, it is often explained away as a reflection of the “complexity” of autism. This leads to the ludicrous situation where, at a conference I was at, a consultant for a new autism assessment unit was proudly talking about the first 100 patients they had diagnosed with ASD at their new national clinic and how, “if you put those 100 people together in a room and talked to them you would struggle to see what they had in common.”
This was put forward to explain how varied ASD presents in real people, but the pointlessness and bizarreness (just from a common sense, let alone scientific, point of view) of giving people who had little in common the same label, seemed lost on this presenter (and sadly, most professionals in the autism industry).
Wherever you look, heterogeneity and a lack of conceptual clarity about what autism is, is evident. This confusion is apparent when examining “diagnostic criteria” for other common “diagnoses.” For example, in the criteria for “conduct disorder” you can find “inability to form bonds with peers and egocentrism, which is shown by a readiness to manipulate others for favours without any effort to reciprocate, together with a general lack of feelings for others.” This description bears (arguably) a closer resemblance to the descriptions of the cases Hans Asperger wrote about than Lorna Wing’s cases (as discussed in Part 1).
One of the core features of the autistic spectrum is meant to be a lack of empathy, a lack that is meant to cause enduring difficulties in social interactions. How is this type of “lack of empathy” to be differentiated from the lack of empathy found in conduct disorder, or indeed the “personality disordered” criminal? Other “disorders,” such as “attachment disorder,” also describe children who lack empathy and have what is referred to as “dysfunctional patterns of social interaction.”
Attachment disorder is described as often associated with some form of neglect, abuse, or trauma; however, in the absence of robust evidence on what causes attachment disorder or autism, making the distinction between “social dysfunction” in the context of conduct disorder, attachment disorder, or ASD becomes little more than a matter of the semantics carried by the subjective opinion of the diagnoser. This confusion of symptom crossover is not limited to conduct and attachment disorders, but spans potentially the entire spectrum of psychiatric diagnoses.
How about the “symptom” of “restricted and repetitive behaviours”? You will find versions of this in criteria described in obsessive compulsive disorder, obsessive personality disorder, schizoid personality disorder, ADHD (such as with computer games), major depressive disorder (morbid preoccupation with negative aspects of life), eating disorders (fixation with food and/or weight), and so on.
Away from manuals and medicalised symptoms you can also find this with: most men (e.g. with football/soccer!), sportsmen and women (with their sport and training regimes), and humanity in general, as an obsessive interest in a restricted sphere is characteristic not only of a depressed state of mind, but also of the application needed for discovery and exploration. Most high achievers thus have the capacity to “fixate” on their area of interest/expertise. In the weird circularity of reasoning, this then becomes the motivation for labelling the long list of great achievers mentioned earlier as having ASD—their capacity for fixating on a subject becomes evidence for their supposedly “having” ASD.
What about the “symptom” of “lack of empathy”? As already mentioned, you can see this in many formal diagnoses, such as conduct disorder and attachment disorder, but also in depression, psychosis, ADHD, personality disorders, and so on. It can also appear as a result of a lack of self-confidence in social situations. Perceived poor achievement or a sense of inferiority in a competitive culture may also lead people to turn away from a range of common interests. In fact, if you think about it, any experience connected to a preoccupation with your own problems tends to reduce interest in other people’s lives and interests. The extent to which you can feign interest in all subjects or empathise with all predicaments is limited. As expectations for social empathy (e.g. in school and in the workplace) increase, so more may appear to lack this capacity.
Thus, what are considered primary symptoms of ASD like “social communication difficulties,” “lack of empathy,” and “restricted and repetitive behaviours” cannot be thought of as isolated individual pathology/difference without an understanding of the context in which they appear. When you start to dig around the undergrowth that constructs our idea of autism, it becomes apparent that it is so shallow; nothing can realistically take hold there. It’s no surprise that all we have is scientism holding up autism as a concept. If we can’t find any, even vague, boundary to hold the concept together, how on earth do we expect to find biological correlates or markers? The reason we can’t find any is thus obvious. According to the real science, then, ASD is a fact of culture not a fact of nature.
ASD, therefore, doesn’t even work well as a descriptive classification. It’s what narrative therapists would call a “thin description” because it leaves out all sorts of other things that might be important to understand in that person’s life (family, social environment, school, traumas, etc.) as well as their skills, abilities, and things they do well in. These other features recede into becoming of lesser importance than the more prominent “diagnosis,” through which other descriptors and events may now be read and seen as secondary.
Not only are the “symptoms” flimsy constructs, but there are many situations in which you don’t need a mysterious concept like autism to describe the presentation, as fairly ordinary and relatively easy to understand processes could be at work.
For example, ASD has been found to be more common in immigrant children. Where a person’s family background differs culturally to a significant degree from the rest of the local community, together with the accompanying stress and psychosocial adversity that often accompanies such a dramatic change in peoples’ circumstance, and particularly if there isn’t an already existent community that could provide support and cultural familiarity, could this not lead to autism type “symptoms” such as lack of social reciprocity, withdrawal etc.?
Similarly, children and young people with a variety of “imperfections” (poor motor coordination, facial disfigurement, speech difficulties, etc.) could also find themselves struggling to make friends and, out of necessity, withdraw into pursuing solitary interests. Changes in lifestyle may also cause changes in patterns of socialisation similar to those that are described by ASD symptoms. Use of extensive screen-based technology, particularly in the early years, could reduce interest in face-to-face socialisation and instead forge a preference for the escapism found in TV, computer games, and YouTube.
I am in touch with a group of practitioners (including psychiatrists and therapists) in France and North Africa, who have been documenting this association and prescribing interventions that include withdrawing or limiting screen time with, after a few weeks or months, a reported disappearance of most of the ASD “symptoms” in some children.
Thus, in addition to the social construction of the meanings associated with the behaviours said to be indicative of autism, we also have a diverse set of possibilities for the potential pathways that may lead to experiencing such behaviours. For some, cerebral abnormalities causing difficulties in learning and proper functioning of the body and nervous system may result in struggling to keep up with peers, make friends, or, at a more severe level of brain injury, the inability to make sense of the basics of language and communication. A more solitary world is an understandable outcome.
For some, severe environmental insult (such as the deprivation experienced by many in the infamous Romanian orphanages) may impair development. For many, a unique set of circumstances involving the interaction of biological and psychological factors could be relevant. Minor biological differences responsible for physical traits, including hand-eye coordination and sensory processing, can have significant psychological impacts, especially if experienced throughout childhood in a climate of intense social competition. A clumsy boy will have difficulty mixing with other boys who play the ever-popular ball games that require good fine motor control and visual-spatial skills.
A combination of subtle differentiating factors may be at stake. A child may come from a culturally atypical family and, owing to some clumsiness, fail to integrate into the local community peer group, leaving her vulnerable to exclusion. A friendless child may then withdraw into an atomised world, sometimes centred on the addictive attractions of electronic gadgetry, making it easier than ever before in human history for the disillusioned simply to join a parallel virtual universe.
There is another issue worth mentioning that arises when we talk about something being on a “spectrum.” A spectrum means we are all, to some degree, on this spectrum. However, people who get classified with an “autistic spectrum disorder” are put into a different category from the rest of us. A diagnosis is a binary classification. You either have it or you don’t. Calling something a “disorder” turns a spectrum into, at some point, no longer on a spectrum, but something that exists as a separate category.
You don’t see this in the rest of medicine. You don’t find people saying you have an “asthma disorder” or “diabetes disorder” or “heart failure disorder.” By sticking the word “disorder” on the end we make it into a condition, so when we classify somebody with ASD we’re not saying “You’re on the ninetieth percentile of the spectrum,” you just have a disorder or you don’t.
Whichever way you look at it, ASD is useless, unscientific, limiting, and, I would argue, a destructive construct.
But surely we “test” for autism, don’t we?
The marketisation of ASD has resulted in the growth of what are now deceptively called “tests” for ASD. Using this medicalised language of a “test” gives the aura of something scientific and medical going on that gives you some sort of accurate result and measurement—something that can answer the question “does my child have ASD?” These tests are based either on observing and rating a person doing set tasks or on answers given to a questionnaire. Each question or task gets scored in some way, so at the end you have a total score and an answer as to whether they have scored above or below the cut-off point.
The use of numbers gives them further credibility in the eyes of the public, as it looks like the assessor is measuring something. But all they are doing is writing a number that corresponds to their interpretation of the answers given by a particular person at a particular moment in time, or their interpretation of observations made on a particular person in a particular context at a particular moment in time. This arbitrary number is then compared to another arbitrary number (the presumed cut-off point) to decide whether they have ASD or not. These “tests” do not provide any physical data on the internal functioning of the mind or body, and so cannot be viewed as having the same status as medical tests that measure physical features and that act as an aid to diagnosis.
If we did physical medicine in the same manner, then instead of putting a sphygmomanometer round your arm to measure your blood pressure, we would have a questionnaire and some observations which we would score as we go along and then if you scored above a certain number we would say “you have a Blood Pressure Disorder.” In the way most ASD assessment units operate now, that would be your job done: “We have tested you and found that you have a Blood Pressure Disorder. It’s a lifelong disorder. Here are some leaflets and links to some websites about Blood Pressure Disorder. Have a good life. Bye.”
In 2017, I attended, along with 13 other participants, a two-day training on the administration of one of these autism testing instruments (yes they are sometimes referred to as “instruments”)—the Autism Diagnostic Observation Schedule (ADOS), probably the most widely used “test” for autism. The first version was first published in 1989, with several updates since then.
For the course, the ADOS was advertised as being a “semi-structured standardised measure of communication, social deficits, and play associated with ASD.” The language of “standardised,” “measure,” and “deficits” all help promote the illusion that this is an empirically valid and quantifiable approach to identifying a medical problem. There are 5 modules to choose from. Each module rates similar phenomena, but uses some different activities for different ages or intellectual levels.
It’s worth remembering the overall context, which reflects several levels of assumptions. This includes that ASD exists as a discrete, natural “thing,” that this “thing” can be identified and quantified, that identification and measurement can be done validly and reliably through specific assessment tools, that ADOS is one such tool, that the items in ADOS encompass and identify the “symptoms” that make up ASD, that ADOS has good enough reliability to enable you not to get false positives (people who are given an ASD label but don’t “have it”), and that you can be trained to administer ADOS in a “standardised” way, to make ADOS subject to little inter-rater variation. Each assumptive level is an open question. If any of these assumptions are unwarranted, then the validity of ADOS crumbles.
The ADOS assessment involves an interviewer (whom I shall refer to as the “examiner”) and a subject (whom I shall refer to as the “patient”). The examiner presents a series of tasks for the patient to complete in a limited time and then removes each task at the end of this time and moves on to the next one. The whole process is meant to take a standardised minimum of 40 minutes and maximum of 60 minutes. The behaviour of the patient is observed and given numerical ratings, which the examiner puts in an observation booklet.
The examiner is not allowed to change or modify their approach in response to the patient’s behaviour, including the requirement to produce all the tasks in sequence. Tasks include free play; describing a picture book story; play with miniature figures; completing a puzzle; and, with older patients, questions about their social life, understanding of relationships, and hopes for the future. Throughout the assessment, the examiner is looking for the presence of certain “symptoms” or the absence of “normal” behaviours, which will then be used to complete the numerical rating system.
To learn how to administer the ADOS, the course participants (me included) watched a number of video-recorded ADOS assessment sessions, made our own ratings of what we observed, and were then taught by the course facilitator what the “correct” ratings were and how to use these ratings to make a diagnosis (or not).
The language used is based in assumptions that went unnoticed (or not commented upon if they were) during the course. There was no acknowledgement that these assessments take place in a particular context and setting (such as a medical clinic following concerns expressed by someone about a child) or that the behaviour of the examiner could have an impact on how the patient subsequently behaved. The assumption was that the context and examiner side of the relational dynamic in the assessment room are non-significant, so that what emerges during the assessment is purely the result of the biology of the patient.
The quasi-autistic rigidity of seeing only “real” internal qualities in the patients was a recurrent theme. Most of the questions I asked during the course stemmed from genuine puzzlement as to how certain patient behaviours in the videos of assessment interviews that we watched could be interpreted as solely the consequence of symptoms in the patient. This led to circularity in logic where the course facilitator insisted that what was being observed could only be understood as being the manifestations of ASD spilling out into the assessment session, due to the expertise/experience of the examiner in conducting a standardised assessment.
Thus, as the facilitator guided us through the scoring, they kept referring to the “fact” that this or that symptom occurred. Non-pathologising interpretations were not tolerated. We were all being trained to become examiners with a keen eye for noticing every minutiae of the “not normal” about the patient.
What arises from this is a mechanistic view of social interactions. The scenarios/tasks are set up as if the examiner, their actions, and the environment, exist as controllable variables so that what emerges irrefutably demonstrates the patients’ social abnormalities. In one example, the course facilitator, discussing a previous patient’s interactions with his mother, demonstrated this one sided view of social interaction. In this example she recounted a story told to her by a parent of a child brought to their clinic.
Apparently, this mother had asked her child, “Why do you never look at me?” The child then started to look at her. The mother now complained, “Why do you stare at me?” The confused boy now decided maybe he should learn to look at her and then away from her. His mother now complained, “Why do you move your eyes from one place to another?” According to this story, the boy eventually developed a complex formula for how long to look at her and away from her. In recounting this tale the facilitator made no comment about the mother’s role in this developing relational discomfort—it was all the result of this child’s (at the time undiagnosed) ASD.
No allowance was made for gender or for the cultural relevance of the activities/questions in the ADOS. The illusion of objectivity starts dissolving when you see the wording of what you are being asked to rate. For example, for rating “Stereotyped/idiosyncratic use of words or phrases,” a mark of 2 (indicating high degree of abnormality) is given if the patient “often uses stereotyped utterances or odd words or phrases, with some other language.” A mark of 1 (indicating some level of abnormality) is “Use of words or phrases tends to be more repetitive than that of most individuals at the same level of expressive language, but not obviously odd.”
For “Quality of social overtures,” 1 is “Slightly unusual quality of some social overtures. Overtures may be restricted to personal demands or related to the child’s own interests, but with some attempt to involve the assessor,” 2 is “Significant minority (or more) of inappropriate overtures; many overtures lack integration into context and/or social quality.” Note that words like “often,” “unusual,” “quality,” “some,” “significant,” and so on. All require an examiner to interpret—they do not lend themselves to establishing objective facts. All the ratings are like this.
How the f**k are you meant to decide what an “unusual quality of some social overtures” looks like? Oh, wait a minute, of course, it’s an expert who knows how to see that. Great, so how do you become an expert then? By learning to administer the ADOS, stupid.
Reliance on the interpretive bias of the examiner was regularly revealed. For example, in one video assessment we observed, I saw the child regularly smiling, but the course facilitator said this was not smiling but the symptom of “smirking.” Even if it was “smirking,” it’s difficult to understand why that should be considered a medical “symptom.”
Other behaviours rated included: “unusual” use of words; quality of child’s attempt to initiate interaction; whether the child requests things from the examiner; not spontaneously giving toys or other objects back to the examiner; not showing toys or other objects (e.g. by holding them up) to the examiner; lack of flexible, creative use of objects (e.g. a doll) in a representational manner; unusual sensory interests; and so on, all open to interpretive variation.
All the ratings are of this nature. They bring up questions of who has the authority and how did they come to the conclusion about what should be considered appropriate/inappropriate, normal/abnormal, healthy/symptomatic, and so on.
My genuine interpretations using the ADOS scoring systems were quite different to that of what the facilitator explained were the correct, “objective” scores, particularly for the two younger patients in the videos. In fact when the first video was shown, I was convinced that this was being shown to illustrate an assessment of a normal child to show us the contrast, but it turned out all the videos showed someone who had been given a diagnosis of ASD.
I found some of the assessment videos painful to watch. The examiner moves quickly from one activity to another, giving each activity a few minutes. In the two videos of children who were around 3 and 5 years old, the objectification of their behaviours had more to do with power and a privileged construction of truth than the discovery of anything intrinsic to the child. Both children seemed to me to become uncomfortable and in different ways uncooperative due to, at least in part, the unusual context and behaviour of the examiner—a stranger they had just met.
We could only comment on and then code the patient’s behaviour, but were not allowed to interpret the patient’s possible feelings or the relational/contextual nature of interactions. It seemed to me that this “test” of social communication was done through setting up a deliberately provocative environment and expecting these young patients to acquiesce to the examiners unusual demands.
Thus, in the videos, ADOS looks more like a test of social conformity to a bossy adult’s constantly shifting demands. In one video, early in the session, after the examiner removes some toys the 5-year old patient was enjoying playing with, the patient stands with his back to the examiner and says “You’re not my friend.” The rest of the assessment session plays out a complex interaction, part hilarious rebellion by the young patient, part engagement, and part distressing to watch: the pressuring and cold detachment by the examiner.
To me, the repetitive questioning, at times exaggerated unnatural smiling, and high-pitched squeaky childish voice of the examiner appeared more unusual than the reaction of the child. However, using the ADOS, this child had ASD and was apparently the more “abnormal” of the two.
In the videos of the assessments for the older children, I wondered about the age appropriateness of toys, articles, and questions used. I am not sure how I would have answered, when I was younger (as the 12- and 17-year-olds in the video assessments had to), questions like “What does a friend mean to you?” “Do you ever think about a long term relationship or getting married?” “Do you take care of your own money?” “Do you have plans or dreams for the future?”
According to our rating scales, there are normal and pathological ways to answer these questions. Culture, gender, social class, none of these things matter either. Both of these older children spoke about experiences of being bullied. Even this was seen as further evidence that they are incompetent, with a hidden message that the ASD was the reason they were bullied (i.e. their “disorder” caused others to treat them badly).
The assessments created a tight funnel where there was no escape from shoehorning your interpretation of whatever happened as a potential “symptom”: Whether they engage, how they engage, how they talk, what they say, what they don’t say, how they look, what they do, what they don’t do, and so on.
ADOS is a trap. A massive money spinner for its creators, trainers, and promoters. An invented assessment, for an invented set of symptoms that is entirely subjective and lacks insight into the role of context and the inter-subjective nature of relationships. It attempts to identify relational “deficits” whilst demonstrating the instrument’s own lack of awareness about the nature of relationships. It relentlessly seeks to uncover evidence of “abnormalities” and creates a context where the examiner can readily find it.
It is a system that catches many in its net, from young kids who won’t do as the examiner instructs and in the way the examiner believes they should, to older ones who have an interesting turn of phrase. It constructs, rather than discovers, knowledge—with the creators, sellers, and now the many examiners who carry out ADOS assessments believing that they know how the universal, culture-, gender-, and sexuality-neutral person should and shouldn’t function. It is shamelessly promoted and sold around the world, subjecting ever more children and adults to its perverse normalisation/pathologisation agenda.
Autism is past its “use by” date
I believe that the concept of autism and ASD, just like ADHD, is not just an example of the rampant scientism that has colonised the fields of psychiatry and psychology, but further, that we should stop using them.
I am pleased that a movement grew to reclaim some sense of the self-worth that was stolen by the “disorder” paradigm of autism. However, I don’t believe the neurodiversity movement is likely to lead to the sort of shift I am thinking of. Whilst some might claim that the creation of the alternative categories of “neurotypical” and “neurodiverse” is a playful liberation from the pathologising medics, it still perpetuates the “us” and “them” dynamics and further solidifies the individualisation that feeds neoliberal politics. It replaces the marketisation opened up by autism as a disorder with marketisation in the sphere of neuro-identity.
As I have discussed, there is no measurable, characteristic “neuro” bit here. Those who believe that we have found it have been sold a lie. We are all, each one of us, unique and therefore we are all neurodiverse.
Autism is part of the paradigm of medicalising, pathologising, and individualising that serves neoliberal politics and economics well. The oppressive and insecure contexts that people, families, and communities must endure in the quest to have the ideal entrepreneurial, competitive, efficient, emotionally intelligent (to sell oneself or services, or cleverly manipulate others) qualities needed to be considered “normal,” means that when individuals can’t keep up, our societal constructs can blame this perceived failing on their interiority.
Autism is one of those “failings” that can be branded, given a scientific (scientism) badge, and marketised. The focus then shifts onto the failed person, who can be “supported/treated,” and the broader social context is freed from deeper examination. Politicians, bureaucrats, charities, and policy makers can look like they really care when they talk sympathetically about those blighted with this disability and how they are helping and supporting these people.
But at what cost do we continue to widen and widen the ASD net? Who has looked at the data of what happens to those caught in this net? Where is the evidence that a diagnosis improves the real-world outcomes for those diagnosed? Why are we not researching this basic question? How many are warned about the potential negative outcomes associated with a diagnosis?
I know, for example, that certain professions will not accept anyone who has an ASD diagnosis, but I don’t know how widespread this issue might be. I recently read that nationally “15% of adults with an autism spectrum disorder are in full time employment.” I don’t know what this means, but that seems like a worrying statistic to me. Labels carry associations and stereotypes few of us are able to see beyond. How many of us stop just seeing and trying to get to know “Jane” (or whoever) when we are told “she has autism”?
I understand that there are many who have found the act of naming helpful. Parents may be enabled to have a new sympathy for their child and adults may feel something about their life now makes sense. But at what price? How long do these initial feelings of relief last? What goes missing from that person’s narrative when a label that cannot explain is used to explain?
I worry about these questions and why I never see them being asked in mainstream literature on the subject. I worry about the potential for a subtle kind of violence that can be inflicted on someone thus labelled that may limit their own, their families’, and a whole host of people’s beliefs about what they can and can’t do, what they need protection from and don’t. I worry about how having the label of autism provides a cruel kind of hope. Parents may feel now that something is understood, experts will know what to do to help. As the days, months, and years accrue with matters not improving, what does that do to parents’ feelings about their “disordered” child? These are the types of dilemmas I regularly see in my consulting room.
In my practice I often meet families who have had a child diagnosed with autism, where matters haven’t improved, or worsened after a period of improvement, where parents feel disempowered because they believe that they cannot have the expertise to know what to do and they can’t seem to find the experts who do. I regularly meet young people whose own dilemmas are not given a full hearing, where the assumption is that they feel the way they do “because they are autistic.”
For some people, ASD is a ticket that gives them access to learning supports (for example) that could be helpful for other children who are denied this support because they don’t have “autism.” But I also see regular examples where an autism label excludes kids who could find input helpful. For example, their social anxiety is constructed as being “because they have autism” and so they are told there is nothing we can do about that.
Autism has become the new catch-all for young patients who don’t follow the increasingly narrow boundaries of expected behaviours, and to such an extent that we overlook histories that would obviously have an impact on their presentations. Autism now keeps coming up as a “maybe they have autism” suggestion in meetings and clinical reviews, as if that’s going to provide an explanation for behaviours that concern, frustrate, or infuriate us.
An ASD diagnosis can disempower parents and teachers by accident, because there is an assumption that they don’t have the expertise to know how to intervene and to know what the right way to support their child is. Ordinary things can fly out the window and so I’ve seen families where the power dynamics have switched because of parents’ concern that if they intervene in any way in their young person’s life they might make things worse. They end up walking on eggshells around the young person at the same time as panicking about their future, making for a very tense household. This assumption can paralyse parents and others, leaving them feeling deskilled and waiting for more “qualified” professionals to advise them, or even better, provide the “right expert therapy” to get through to their child.
Autism, like any other psychiatric diagnosis, is not a diagnosis. It has no explanatory power and so can’t tell you what will prove to be helpful or not with any particular individual, family, or community. Best to ignore its relevance.
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