Imagine a simple, everyday sound—like the hum of a refrigerator—suddenly becoming a grating, overwhelming roar.
For many autistic individuals, this extreme sensory experience is a fact of life, ranging from hypersensitivity to sound and touch to a lack of response to pain.
While these different sensory experiences are now part of the diagnostic criteria for autism, they are neither universally present in autistic people nor unique to the condition.
This led scientists to wonder: what if the real common denominator for sensory issues isn’t autism, but something else entirely?
Key Points
- Alexithymia, or difficulty identifying and describing your own emotions, might be the missing link between autism and sensory sensitivities.
- When researchers accounted for alexithymia, the genetic connection between autism and sensory symptoms disappeared.
- However, the genetic relationship between alexithymia and sensory symptoms remained significant even after accounting for autism.
- This suggests that alexithymia and sensory issues share a direct genetic foundation that is independent of autism.
- The findings imply that sensory symptoms in autism may actually be caused by co-occurring alexithymia, not autism itself.
The Search for the Missing Genetic Link
A team of researchers utilized a quantitative genetic study involving adolescent twins to trace the origins of these traits.
Their goal was to untangle the complex genetic overlap between three factors: autism (measured by Best Estimate Diagnosis or BED), sensory symptoms (measured by the Short Sensory Profile or SSP), and alexithymia (measured by the “uninsightful” subscale of the Observer Alexithymia Scale or OAS).
Alexithymia is a condition characterized by a profound difficulty identifying and describing one’s own feelings.
It’s highly prevalent in autistic individuals, affecting 40-65% of the population, compared to just 5-10% in non-autistic people.
Essentially, alexithymia makes it hard to “read” your own internal world.
Previous research had already established a moderate-to-strong genetic connection between autistic traits and sensory symptoms.
The prevailing assumption was that a shared genetic mechanism linked the two.
However, the new twin study proposed a paradigm shift: that alexithymia is the key, genetically linked to sensory symptoms, and its common co-occurrence with autism makes it look like autism is the primary cause.
The Emotional Wiring Connection
The study confirmed that both autism and alexithymia are highly heritable, at approximately 82% and 84%, respectively.
Importantly, they found significant phenotypic and genetic associations between all three traits: autism, alexithymia, and sensory symptoms.
The puzzle was to determine which associations were direct and which were merely artifacts of the others.
The critical analysis involved testing the genetic correlation between two traits while statistically controlling for the third.
Think of it like a detective work: once you remove a suspect, does the crime still make sense?
The first revelation centered on the original presumed link:
- The genetic correlation between autism and sensory symptoms became non-significant after controlling for alexithymia.
This suggests that the genetic factors shared by autism and sensory processing issues are entirely or mostly accounted for by alexithymia.
The genetic “glue” holding autism and sensory symptoms together is alexithymia.
The second, equally important finding cemented alexithymia’s central role:
- The genetic correlation between alexithymia and sensory symptoms remained significant even after controlling for the variance explained by autism.
This means that alexithymia and sensory difficulties share a common genetic foundation that is independent of autism. They are genetically linked in their own right.
Why You Can’t Feel and What That Means for Your Senses
This discovery provides a powerful conceptual model.
When a person struggles to register or interpret internal bodily signals (a difficulty known as atypical interoception, often associated with alexithymia), the brain might increase its focus on external stimuli, leading to hypersensitivity.
If your internal emotional “background noise” is muted, the external sensory world (touch, sound, light) gets turned up to compensate.
The authors propose that this difficulty with one’s internal emotional state is a “transdiagnostic risk-factor” for sensory issues.
It’s not just a feature of autism; it might be the underlying issue in sensory symptoms found in other conditions like ADHD and Schizophrenia as well.
Real-World Impact and Next Steps
This research offers profound implications, moving beyond the mere description of symptoms to identify a potential root cause.
- For Diagnosis: The findings suggest a need to consider the influence of alexithymia both when diagnosing autism and when providing support. Autism with co-occurring alexithymia and sensory difficulties could represent a distinct subtype that may respond similarly to targeted interventions.
- For Therapy: Instead of only managing sensory overload with external adaptations (like noise-canceling headphones), therapies might also target alexithymia. Interventions that improve interoception—the ability to perceive and understand internal bodily states—could potentially reduce the need for the brain to over-focus on external sensory information.
- For Everyone: The study reframes sensory sensitivity as being less about the autism diagnosis itself and more about a shared underlying difficulty in processing internal emotional information. This opens the door for research across multiple conditions to see if treating alexithymia is the key to alleviating sensory distress for a much broader population.
In essence, the study suggests that to understand the sensory experience of autism, we must first understand the emotional experience of alexithymia.
Reference
Yorke, I., Murphy, J., Rijsdijk, F., Colvert, E., Lietz, S., Happé, F., & Bird, G. (2025). Alexithymia may explain the genetic relationship between autism and sensory sensitivity. Translational Psychiatry, 15, 75. https://doi.org/10.1038/s41398-025-03254-1
