A close-up photograph shows a pale-skinned person walking barefoot on soft earth, surrounded by forest. The focus is on their feet and lower legs, emphasizing movement and sensory experience.

In the spring of 2025, developmental psychologist Steven K. Kapp published a bold new paper in Frontiers in Integrative Neuroscience. Kapp’s paper is part of a growing shift in how science understands autism. Drawing from decades of clinical studies, brain research, and listening to lived Autistic experience, Kapp shows that autism isn’t mainly about social or behavioral differences. Instead, he describes it as a lifelong pattern of sensory–movement divergence—something that begins at birth, if not earlier, and shapes development from the start.1 And while his theory is backed by cutting-edge research, it echoes something many Autistic people have been saying for years: autism isn’t something that happens to one—it’s something one is.

Introduction

In framing autism this way, Kapp challenges one of the most entrenched and harmful narratives in modern medical and political discourse: the idea that autism must be caused by something—an injury, a toxin, a loss—and therefore, potentially, something that can be prevented or cured. This cause/cure framework fuels whole industries of speculative research, early intervention programs, and grief-driven advocacy from parents. Each one builds on the hope that if we could just find the moment things went wrong, we might somehow ‘undo the damage’.

But as Kapp demonstrates, this model misreads both the science and the Autistic experience. What may appear to others as regression is, in many cases, better understood as a mismatch between developmental expectations and underlying sensory–movement differences—not a genuine loss of skills. The search for a single cause rests on this flawed premise, overlooking how autism emerges from a distinctive developmental trajectory that begins at or before birth.2

I want to set Kapp’s work into its larger context, into a wider reflection on what it means to understand autism not as an error to fix, but as a form of embodiment with its own logic, value, and place in the world. Not only is autism not caused by a singular event or exposure, it is not a problem to be solved at all. Autism is an expression of human biodiversity—an essential facet of how the nervous system can be configured. Drawing on decades of research, from fetal brain imaging to placental gene expression studies, let’s look at the evidence for autism’s prenatal and intrinsic nature. We will also explore the cultural costs of the cause/cure paradigm, and consider what it might mean to instead see autism as a form of embodied difference that strengthens the collective—neither puzzle nor pathology, but presence.

The Cause/Cure Framework: Looking for Something That Was Never Lost

For decades, many researchers and advocates have poured time and money into trying to figure out what causes autism. Was it something in the water? A vaccine? A stressful pregnancy? A difficult birth? The questions have shifted slightly with each generation, but the impulse remains the same: to look for something that went wrong, and to imagine that if we could only name it, we could fix it. This is the heart of what we might call the cause/cure framework—the belief that autism is a deviation from the norm caused by something external, something preventable, something repairable.

This framework didn’t emerge in a vacuum. It developed alongside medical models of disability that define difference as deficit, and it has been reinforced by systems that reward linear success stories: the heroic scientist, the cured child, the relieved parent. Under this model, any evidence that autism might be present from birth—or that it might not be a tragedy at all—is quietly sidelined.

It’s not hard to see why this idea gained traction. When a child’s development starts to diverge from what doctors or educators expect, it’s common for parents to ask: what changed? What happened? But the question itself assumes there was a change. It assumes there was a time before autism—some “normal” state that was lost. As Kapp points out, this assumption leads to misinterpretations of developmental difference as decline.3 A child who stops speaking in sentences may not be losing ability at all—they may be overwhelmed, dysregulated, or shifting how they communicate. But through the lens of regression, that shift gets framed as damage. And damage, of course, demands a cause.

From this point, it’s a short leap to desperate searches for culprits—vaccines, pollutants, parenting styles—and a long trail of disproven theories. A large meta-analysis covering more than 1.2 million children found no evidence linking autism to vaccines of any kind.4 Other studies have ruled out thimerosal, MMR, and cumulative antigen load.5 Still, the belief persists. Once a framework takes root—especially one built on fear and urgency—it becomes hard to unseat, even when the evidence says otherwise.

But the science does say otherwise. Over and over again, studies show that autism is not something that suddenly appears or takes hold after a triggering event. It is something that begins at—or before—birth, and unfolds over time.

Always Been There: What the Science Actually Shows

If autism isn’t caused by something going wrong, then what is it? For researchers like Kapp who aren’t invested in the cure story and can look with fresh eyes, the answer has been quietly unfolding for decades. Study after study suggests the same thing: that autism is a form of neurodevelopmental difference that begins before and/or during gestation—long before any vaccines, dietary exposures, or parenting styles could possibly play a role.

Some of the clearest evidence comes from studies of infant brain development. In a landmark longitudinal study, researchers used MRI scans to track infants who had an older autistic sibling and therefore had a higher chance of being autistic themselves. They found that by 6 to 12 months of age—well before any child had been diagnosed—those who would go on to receive an autism diagnosis already showed differences in brain growth, especially in how the surface of the brain was expanding over time.6 By the time they turned two, these same children also showed differences in brain volume. These changes weren’t reactions to the outside world. They were part of the developmental process itself.

Other studies have found differences even earlier. At six months old, some autistic babies have more cerebrospinal fluid around their brains than their non-autistic peers.7 In another study, researchers reviewing old home videos noticed subtle movement differences—like asymmetrical crawling or delayed righting reflexes—in babies who would later be diagnosed with autism. These differences were visible within the first months of life, sometimes even in the first days.8

But perhaps most striking are the studies looking at what’s happening before birth. Researchers examining placental tissue have found patterns of gene expression and epigenetic differences—small changes in how genes are regulated—that appear more often in children who go on to be diagnosed with autism.9 These differences aren’t caused by parenting or trauma. They are part of how a nervous system takes shape.

None of these findings point to a single cause, and none of them are predictive on their own. What they do offer is a consistent picture: that autism is not something that suddenly arrives. It’s a way a body and brain grow. A way a person comes into being.

The Real Cost of Searching for a Cure

When we spend our energy trying to figure out what causes autism—or how to prevent it—we miss the opportunity to understand what autism actually is. And more than that, we risk causing harm. The cause/cure framework doesn’t just steer science down unproductive paths. It shapes how people talk about autism, how children are treated, and how Autistic people come to see themselves.

Many Autistic adults grew up hearing that they were puzzles to solve or tragedies to grieve. Some were told directly, while others absorbed it from media, professionals, or the quiet tension in their families. Even when the language was gentle, the message was clear: something had gone wrong. That kind of framing leaves marks. It affects self-esteem, mental health, and the ability to build an identity rooted in self-respect.10

For parents, too, the promise of a cure can be a trap. It offers hope—but at a cost. When parents are told that their child’s autism is the result of something they did—or didn’t do—it often leads to guilt, grief, and a constant chase for answers. That chase can become consuming. Instead of getting support for the family you have, you’re encouraged to keep searching for the child you think you lost. This cycle has been reinforced by theories of “regression” that treat natural shifts in development as signs of loss or failure, fueling anxiety and disorientation instead of clarity.11

And for society as a whole, the cost is collective. When we treat autism as a problem to fix, we pour resources into prevention instead of support. We center fear instead of understanding. We create systems that reward compliance, not communication—and then we call it progress when someone learns to mask, destroying their own mental health in the process.12

Kapp’s work helps us pause that pattern. It invites us to step back and see autism not as something that needs solving, but as something that needs space. What would it mean to stop searching for what went wrong—and start creating conditions where Autistic people can thrive as they are?

Diversity: What Systems Need to Thrive

If we step back from the fear-based narratives about autism, we can begin to ask a different kind of question. Not how do we prevent this, but what do we lose when we try? The answer: more than we can afford.

Every living system depends on variation. In ecosystems, biodiversity protects against collapse. In immune systems, diversity helps the body respond to new threats. Even in agriculture, planting one single crop across a wide area invites disaster. Diversity isn’t noise—it’s resilience.

The same is true for human minds. The neurodiversity paradigm, developed by Autistic scholars and self-advocates,13 invites us to see neurological variation not as a flaw, but as a natural and vital part of human complexity. Just as other systems need many kinds of organisms to adapt to different niches, human culture needs many kinds of minds to navigate an unpredictable world. Monocultures are fragile. Mixed systems survive and thrive.

Autism brings gifts too often uncelebrated: pattern recognition, unconventional insight, sensory attunement, deep honesty, nonlinear processing.14 These aren’t deficits, though each has been framed as a flaw by various researchers, practitioners, and educators. They are traits shaped by a different kind of nervous system—one that, given the right conditions, offers enormous value (value far deeper and more meaningful than surface calculations like capitalistic productivity) not despite differences, but because of them.

When we pathologize those differences—trying to make every brain conform to a single standard of communication, behavior, or productivity—we lose what makes the social system strong. We might make it more efficient, by starving out people who can’t fit in (then blaming them for suffering.) But that makes the system more rigid and brittle, harming people who can solve problems society doesn’t yet acknowledge it has.

Kapp Heralds a Different Kind of Future

Steven Kapp’s work15 doesn’t just challenge a flawed idea. It offers a new foundation.

Instead of asking how to prevent autism, Kapp asks how we can better understand the kind of embodiment autism represents. Instead of looking for what went wrong, he invites us to notice what’s already here: a different developmental path, shaped by sensory–movement patterns that begin before words, before diagnosis, before the world starts demanding performance. A body moving through space in its own rhythm. A nervous system tuned to signals others might miss. A way of being that is not broken, just less common.

This is the future we’re being asked to imagine—not one where autism is eliminated, but one where it’s understood. One where support is shaped to fit the person, not the other way around. One where Autistic people are not just accommodated, but trusted. Not fixed, but followed.

And perhaps most importantly, a future where autism is not seen as a mystery to solve or a crisis to avert—but as one of many ways a human life can unfold.

Footnotes

  1. Kapp, S. K. (2025). Sensory–movement underpinnings of lifelong neurodivergence: Getting a grip on autism. Frontiers in Integrative Neuroscience, 19, 1489322. https://doi.org/10.3389/fnint.2025.1489322 ↩︎
  2. Ibid., see “Autistic regression or autistic resilience?” and “Conceptual and empirical foundations of sensory–movement differences.” ↩︎
  3. Ibid. ↩︎
  4. Taylor, L. E., Swerdfeger, A. L., & Eslick, G. D. (2014). Vaccines are not associated with autism: An evidence-based meta-analysis of case-control and cohort studies. Vaccine, 32(29), 3623–3629. https://pubmed.ncbi.nlm.nih.gov/24814559
    ↩︎
  5. DeStefano, F., Price, C. S., & Weintraub, E. S. (2013). Increasing exposure to antibody-stimulating proteins and polysaccharides in vaccines is not associated with risk of autism. The Journal of Pediatrics, 163(2), 561–567.e1. https://pubmed.ncbi.nlm.nih.gov/23472704 ↩︎
  6. Hazlett, H. C., et al. (2017). Early brain development in infants at high risk for autism spectrum disorder. Nature, 542(7641), 348–351. https://www.nature.com/articles/nature21369 ↩︎
  7. Shen, M. D., et al. (2017). Increased extra-axial cerebrospinal fluid in high-risk infants who later develop autism. Biological Psychiatry, 82(3), 186–193. https://pubmed.ncbi.nlm.nih.gov/28392081 ↩︎
  8. Teitelbaum, P., et al. (1998). Movement analysis in infancy may be useful for early diagnosis of autism. PNAS, 95(23), 13982–13987. ↩︎
  9. Zhu, Y., et al. (2022). Placental epigenetics and neurodevelopment: Evidence from methylation changes associated with autism. Genome Biology, 23, 105. https://genomebiology.biomedcentral.com/articles/10.1186/s13059-022-02613-1 ↩︎
  10. Kapp, S. K., Gillespie-Lynch, K., Sherman, L. E., & Hutman, T. (2013). Deficit, difference, or both? Autism and neurodiversity. Developmental Psychology, 49(1), 59–71. https://doi.org/10.1037/a0028353 ↩︎
  11. Ozonoff, S., & Iosif, A.-M. (2019). Changing conceptualizations of regression: What do recent findings mean for autism research? Neuropsychology Review, 29(2), 270–278. https://doi.org/10.1007/s11065-019-09411-1 ↩︎
  12. Cage, E., Di Monaco, J., & Newell, V. (2018). Experiences of autism acceptance and mental health in autistic adults. Journal of Autism and Developmental Disorders, 48, 473–484. https://doi.org/10.1007/s10803-017-3342-7; Hull, L., Mandy, W., Petrides, K. V., et al. (2017). “Putting on My Best Normal”: Social camouflaging in adults with autism spectrum conditions. Journal of Autism and Developmental Disorders, 47, 2519–2534. https://doi.org/10.1007/s10803-017-3166-5 ↩︎
  13. Walker, N. (2021). Neuroqueer Heresies: Notes on the Neurodiversity Paradigm, Autistic Empowerment, and Postnormal Possibilities. Autonomous Press. ↩︎
  14. Mottron, L. (2021). A radical change in our autism research strategy is needed: Back to prototypes. Autism Research, 14(11), 2213–2220. https://doi.org/10.1002/aur.2599
    ↩︎
  15. Kapp, S. K. (2025). Sensory–movement underpinnings of lifelong neurodivergence: Getting a grip on autism. Frontiers in Integrative Neuroscience, 19, 1489322. ↩︎

Works Cited

Cage, E., Di Monaco, J., & Newell, V. (2018). Experiences of autism acceptance and mental health in autistic adults. Journal of Autism and Developmental Disorders, 48, 473–484. https://doi.org/10.1007/s10803-017-3342-7

DeStefano, F., Price, C. S., & Weintraub, E. S. (2013). Increasing exposure to antibody-stimulating proteins and polysaccharides in vaccines is not associated with risk of autism. The Journal of Pediatrics, 163(2), 561–567.e1. https://pubmed.ncbi.nlm.nih.gov/23472704

Hazlett, H. C., et al. (2017). Early brain development in infants at high risk for autism spectrum disorder. Nature, 542(7641), 348–351. https://www.nature.com/articles/nature21369

Hull, L., Mandy, W., Petrides, K. V., et al. (2017). “Putting on My Best Normal”: Social camouflaging in adults with autism spectrum conditions. Journal of Autism and Developmental Disorders, 47, 2519–2534. https://doi.org/10.1007/s10803-017-3166-5

Kapp, S. K., Gillespie-Lynch, K., Sherman, L. E., & Hutman, T. (2013). Deficit, difference, or both? Autism and neurodiversity. Developmental Psychology, 49(1), 59–71. https://doi.org/10.1037/a0028353

Kapp, S. K. (2025). Sensory–movement underpinnings of lifelong neurodivergence: Getting a grip on autism. Frontiers in Integrative Neuroscience, 19, 1489322. https://doi.org/10.3389/fnint.2025.1489322

Mottron, L. (2021). A radical change in our autism research strategy is needed: Back to prototypes. Autism Research, 14(11), 2213–2220. https://doi.org/10.1002/aur.2599

Ozonoff, S., & Iosif, A.-M. (2019). Changing conceptualizations of regression: What do recent findings mean for autism research? Neuropsychology Review, 29(2), 270–278. https://doi.org/10.1007/s11065-019-09411-1

Shen, M. D., et al. (2017). Increased extra-axial cerebrospinal fluid in high-risk infants who later develop autism. Biological Psychiatry, 82(3), 186–193. https://pubmed.ncbi.nlm.nih.gov/28392081

Taylor, L. E., Swerdfeger, A. L., & Eslick, G. D. (2014). Vaccines are not associated with autism: An evidence-based meta-analysis of case-control and cohort studies. Vaccine, 32(29), 3623–3629. https://pubmed.ncbi.nlm.nih.gov/24814559

Teitelbaum, P., et al. (1998). Movement analysis in infancy may be useful for early diagnosis of autism. PNAS, 95(23), 13982–13987.

Walker, N. (2021). Neuroqueer Heresies: Notes on the Neurodiversity Paradigm, Autistic Empowerment, and Postnormal Possibilities. Autonomous Press.

Zhu, Y., et al. (2022). Placental epigenetics and neurodevelopment: Evidence from methylation changes associated with autism. Genome Biology, 23, 105. https://genomebiology.biomedcentral.com/articles/10.1186/s13059-022-02613-1