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Losing the Exchange

“Curing autism” made its way back into the news again recently.

If you haven’t yet read it, the New York Times Magazine ran an article, The Kids Who Beat Autism, about how research is showing that up to 10 percent of children diagnosed with autism no longer meet the criteria for the disorder after undergoing treatment, the coveted “optimal outcome”.

This was, naturally, immediately followed by a fresh wave of “cure” talk circulating with “optimal outcome” and a dash of rah-rah-go-team-let’s-beat-it for good measure. Being closer to a cure for autism is a good thing, right?

I. Defining “recovered”

“Recovered”. Are the parents and evaluators here defining this as merely becoming asymptomatic, or is it something more than that?

There’s plenty of detail there about the first part; the article introduces several families whose children, after intensive treatment through early childhood and beyond, have reached “optimal outcomes”.

We’re now learning through research that a person with ASD may become asymptomatic by learning to manage sensory input, undergoing intense behavioral conditioning, carefully replacing old habits with new ones. One could, potentially, even go further in the “reprogramming” by retraining oneself to the point of experiencing things the same way a neurotypical person would. That may or may not be what has happened in these examples of recovery. Understandably, the researchers who studied what, if anything, made the difference were precise in their language, not breathless:

Autism spectrum disorders (ASDs) were once considered lifelong disorders, but recent findings indicate that some children with ASDs no longer meet diagnostic criteria for any ASD and reach normal cognitive function. These children are considered to have achieved “optimal

outcomes” (OO). The present study aimed to retrospectively examine group differences in the intervention history of children and adolescents with OO and those with high-functioning autism (HFA).

From this, it seems pretty clear that the research conversation is using symptoms (“the criteria for the disorder”) as the yardstick. So far, so good.

And then, as is often the case with exciting science news that hits the front pages, we get a little more exuberant. Early intervention leads to optimal outcome more often! No symptoms, no autism, right? Problem solved. We are closing in on a cure, clearly, because we have found a way to make the bad things go away.

Here, the NYT article discusses the same outcome:

In May, another set of researchers published a study that tracked 85 children from their autism diagnosis (at age 2) for nearly two decades and found that about 9 percent of them no longer met the criteria for the disorder. The research, led by Catherine Lord, a renowned leader in the

diagnosis and evaluation of autism who directs a large autism center and teaches at Weill Cornell Medical College, referred to those who were no longer autistic as “very positive outcome.”

Note how, in moving from research summary to public interpretation, we’ve now gone from “no longer meets diagnostic criteria for any ASD… normal cognitive function” to “no longer autistic”. Embedded in that semantic choice is a massive amount of assumptions and implications.
Are these therapies just changing behavior, or are they honestly altering the way these kids experience things and think about things at a deeper level than that? At what point are we training away someone’s own nature and particular talents in order to conform to social expectations? No one can answer that but the people who have gone through the treatments and come out the other side, so it will be some time before we can grasp the long-term paths of these success stories and how deep the metamorphosis has gone.

In our haste to help loved ones and make advances in behavioral science, we must take care not to overlook the ethical questions around the deeper levels of change.

II. An architecture of neurodiversity

Fundamentally, I like to describe the typical and the not-so-typical as two different frameworks for processing the world—two different ways of sensing and interpreting everything around you. Autism spectrum disorders, clearly, fall on the neurodiversity side, where they get neighborly with schizotypy, bipolar, and an array of other biological arrangements.

(Still with me? I know those are all words that provoke knee-jerk responses, like “autism” does, but don’t run off just yet.)

This is the crux of the cure conflict- nothing is 100% bad or good, and not everything that is different is pathological by nature. The disordered extremes draw our attention, our effort, and our projected bullshit too. It’s exciting to talk both about curing autism, and about how maybe people with ASDs are, who knows, latent geniuses or something else fun to speculate about. Einstein probably had Asperger’s, says the rumor mill.

But beyond that, in the more boring place that doesn’t get media attention or grant money, is a humankind that is better off having an array of people who all see the world in different ways. As many higher-functioning folks with autism spectrum conditions argue, there’s room for autism to exist without necessarily being a disorder.

Quite a while ago, neurodiversity activist Jim Sinclair wrote:

“Read that again. This is what we hear when you mourn over our existence. This is what we hear when you pray for a cure. This is what we know, when you tell us of your fondest hopes and dreams for us: that your greatest wish is that one day we will cease to be, and strangers you can love will move in behind our faces.”

Autism 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 if it were possible, the person you’d have left would not be the same person you started with.
This is important, so take a moment to consider it: Autism is a way of being. It is not possible to separate the person from the autism.
Therefore, when parents say, I wish my child did not have autism,
what they’re really saying is, I wish the autistic child I have did not exist, and I had a different (non-autistic) child instead.
“Read that again. This is what we hear when you mourn over our existence. This is what we hear when you pray for a cure. This is what we know, when you tell us of your fondest hopes and dreams for us: that your greatest wish is that one day we will cease to be, and strangers you can love will move in behind our faces.”

Artists and creatives of all kinds have always known that those gifts of seeing and feeling differently, the ones so admired by the public, often come with a price as well. And yet, we don’t speak of “curing” creativity or of curing the negatives that are sometimes associated with it. Addiction, bipolar disorder, depression, anxiety…

Society likes to avoid and romanticize this at the same time, in everything from the fascination with Hemingway’s life to A Beautiful Mind, but every so often the public engages in some way with the idea that there are biological complications of being wired for a certain threshold of creativity. Too recently, the inner struggle of creativity became the subject of public conversation yet again.

Katherine P. Rankin, Ph.D. and colleagues at the University of California-San Francisco comment,

“It is well-established that people with affective disorders tend to be overrepresented in the creative artist population… [affective disorders] may carry certain advantages for creativity, especially in those who have milder symptoms.”

Wait, why are we talking about depression and bipolar now? Hold onto that thought.

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III. Moving beyond symptoms

Autism spectrum disorders, like many psychiatric disorders, are still diagnosed in a rather 19th-century manner compared to most other medical conditions. A professional observes disordered symptoms, renders a diagnosis and suggests treatment based on a brief window of observed behavior, and sends the patient off to log time in treatment, hoping for progress in the form of diminished symptoms. No blood tests or biopsies, just an advanced game of trial and error, compounded by conflicts over diagnostic categories and instruments.

After a century of making comparatively little headway in the face of debilitating psychiatric conditions, researchers from around the world embarked in 2007 on an open-source genomics project to better understand a handful of critical disorders with staggeringly high social costs: autism spectrum disorder, attention deficit-hyperactivity disorder, bipolar disorder, major depressive disorder, and schizophrenia.

An NIH study published in 2013 revealed the first documented evidence of genetic links among the five disorders in the Psychiatric Genomics Consortium:

This analysis provides the first genome-wide evidence that individual and aggregate molecular genetic risk factors are shared between five childhood-onset or adult-onset psychiatric disorders that are treated as distinct categories in clinical practice. As such, our findings are relevant to the goal of moving beyond descriptive syndromes in psychiatry and towards a nosology informed by disease cause.
The finding that genetic variants have cross-disorder effects is an empirical step towards helping clinicians understand the common co-occurrence of clinical phenotypes in individual patients. Our results implicate a specific biological pathway — voltage-gated calcium-channel signalling — as a contributor to the pathogenesis of several psychiatric disorders, and support the potential of this pathway as a therapeutic target for psychiatric disease.
These results add to literature in several specialties (including autoimmune and metabolic diseases) that have begun to document widespread pleiotropy of genetic risk factors across traditional diagnostic boundaries.

“These results provide evidence relevant to the goal of moving beyond descriptive syndromes in psychiatry, and towards a nosology informed by disease cause.”

 
Well, that’s an interesting twist in the story.

It’s well-documented that many ASD folks are comorbid with ADD or bipolar, that depressive tendencies are a feature of ASD, and that the various pervasive developmental conditions were originally bundled together under the term “childhood schizophrenia”. And now? All these separate conditions are now known to share specific genetic links, possibly to the point of being different expressions of a larger diffuse condition. We asked for research, for something that would get us past hit-or-miss behavioral observations and into something testable, and here it comes.

IV. Becoming neurotypical?

Personal story time: I have experienced what it’s like to be “recovered”, though not on purpose.

Over a long stretch of time, from high school until a couple years ago, my sensory issues declined to the point where, for at least several years, I wasn’t experiencing things much differently from an NT person. I was still an introvert, still a systems-oriented thinker, but getting around in the world and circulating with people became smoother and more natural over time. I didn’t feel as smart as when I was younger, but the decline was so gradual I thought it was just a function of age. I was working out a bunch of other things, but other than what I mistakenly thought at the time was hearing loss, the sensory issues and other factors were long gone.

(I didn’t have any cognizance that I had a PDD at this point in time; I just knew that I was a weird hyperlexic child, and I had an odd array of issues when I was young that people said I would grow out of as I got older.)

Then I was diagnosed with a genetic folate-processing disorder, and my M.D. prescribed me a fancy supplement as treatment, saying, “this is pretty new, and everyone has a different result, so anything could happen. Here’s my home phone number; let me know what comes up for you.”

And it all came roaring back. All of it, the bad and the good.

It was like being a kid again, and I went around for weeks saying “my brain is back!” because I felt sharp again, colors were brighter, the world seemed clearer, I could put things together in my head more easily, visual puzzles were supremely satisfying again, the spatial reasoning skills I used to be so proud of and thought had become irretrievably dull sharpened back up. And the sensory problems did too. Too loud, too bright, too fast, too tight. I was more easily distracted or overloaded than ever, if I couldn’t moderate the input flooding my system.

I finally sought out a formal diagnosis because it became clear that all those things weren’t outgrown at all; it was more like certain aspects of my internal architecture had been lulled to sleep, lying dormant until my neurochemical pathways had a full supply of those missing ingredients again. The extra branches in the “magic trees of mind” had withered for a season, but still lived.

So that was a thing.

I’ve seen how the other side lives, and it is easier. Of course people want what’s easier for their children, for them to suffer less, to fit in better, to live out the dreams their births represented. How could we not? No one wants their loved ones to live a difficult life if it could be prevented somehow.

Every day I take that pill is a day where, on some level, I actively choose the spectrum over “normal”. I don’t think stopping folate treatment would un-wave the magic wand entirely, but I am keenly aware that even the existence of that possibility is an exquisitely rare position to be in.

And yet I have no desire to go back to my pseudo-NT existence, even if I could. This lens through which I look at the world, the delicate web of connections and signals and ephemera around me, though all too often difficult and different, is mine. I don’t want to experience life the same way everyone else does. Sensory overload is the price of having those doors of perception flung open ever wider, but I can learn to mitigate the downsides without losing what to me are irreplaceable advantages.

Someone else in my shoes may very well wish the opposite, though. Preserving that choice, in whatever capacity it exists, within the scope of therapies and treatments is a thorny ethical issue embedded deep inside the autism advocacy community.

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V. The exchange sacrifice

One of the most exciting frontiers of autism treatment research of late, referenced in the Times article, is the evidence that early intervention treatments are acting on the neuroplasticity of the brain — physically rewiring the child’s brain by actively creating new neural pathways.

The study showed that the brain scans of children receiving early intervention treatments approached neurotypical levels over time, which is exciting and, like anything really cool that happens in behavioral science, serves up a shiny new bioethical Pandora’s box.

Teaching skills and autonomy to a child with autism is critical, but we need to be honest with ourselves about the fact that employing treatments that would remove the entire essence of their difference is erasing something more fundamental than a disorder.

The temptation to not just observe and assist, but organically intervene at ever earlier, deeper levels has consequences we have no way of predicting.

So let’s take the idea of a true cure to its dictionary-definition conclusion — not just managing or learning to live with autism, but eradicating it altogether.

It’s possible, even probable, that further research could lead to the capacity to accurately predict the onset of these conditions. And then what? If the cause is an aggregate of various genetic traits, a genetic susceptibility that develops into a full-blown disorder with an environmental trigger, “cure” talk leads us directly into the icky space of eugenics.

In research on bipolar disorder, heritability has been well-documented for some time now, and there is an existing conversation around the ethical implications of preventing bipolar disorder through genetic means. Professor Grant Gillett of the University of Otago, New Zealand, has said,

“The diagnosis of bipolar disorder has been linked to giftedness of various sorts and this raises a special problem in that it is likely that the condition has a genetic basis. Therefore it seems possible that in the near future we will be able to detect and eliminate the gene predisposing to the disorder.
“This may mean, however, that, as a society, we lose the associated gifts. We might then face a difficult decision either way in that it is unclear that we are preventing an unalloyed bad when we diagnose and eliminate bipolar disorder through prenatal genetic testing and yet if we allow the individual to be born we are condemning that person to being an unwitting sacrifice in that they might well suffer considerable net distress as a result of our need to keep our gene pool enriched in the relevant way.”

So, even in the other related conditions we end up back in the hall of bioethics funhouse mirrors.

VI. Beyond disorders

Things that are different aren’t necessarily disorders.

This is not a screed against parents who are struggling to help their children. One of the sad divides in the autism community is the yawning chasm between the “stop trying to fix us” self-advocates and the high-impairment “hurry up with a cure, because this current situation is bullshit” group, surrounded (and too often exacerbated) by a constellation of parents who are struggling to do as much as possible to help their children while mourning their own dreams of what might have been.

Stepping into that space, where we are all existing and interacting in that liminal space between neurotypical and whatever lies beyond, pushes all of us to our limits, patients and family alike. That is the one experience shared by everyone with a personal stake in this.

Treatment and therapy is critical because the everyday world isn’t going anywhere anytime soon, and getting treatment early is the best possible option. But if we must talk about cures, let’s stay focused on curing the disorder part and temper the enthusiasm for “ending autism” for now.

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Photos by Pen Waggener, Omer Unlu, and the University of Michigan.

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