Sensory issues in autism may stem from co-occurring emotional blindness, not autism itself

A new twin study published in Translational Psychiatry suggests that the sensory sensitivities often seen in autistic individuals may not be caused by autism itself. Instead, these sensory traits appear to be genetically linked to alexithymia—a condition characterized by difficulties in identifying and describing one’s own emotions. After accounting for alexithymia, the researchers found no remaining genetic association between autism and sensory symptoms. These findings challenge long-standing assumptions about the nature of autism and point to the possibility that some hallmark features attributed to the condition may instead arise from overlapping but distinct traits.

Autism spectrum conditions are typically associated with a range of difficulties in social interaction and communication, as well as repetitive behaviors and restricted interests. In recent years, sensory processing issues—such as being overly sensitive to sounds or textures—have been recognized as part of the diagnostic criteria. Yet not all autistic individuals experience these symptoms, and sensory sensitivities are also common in other conditions like attention-deficit hyperactivity disorder and schizophrenia. This has raised questions about what causes these experiences and whether they are specific to autism.

One possible explanation is that another trait, alexithymia, may be responsible for the sensory challenges commonly seen in autism. Alexithymia affects the way people perceive and process their own emotions, and it is significantly more common in autistic individuals than in the general population. Importantly, alexithymia is also seen across many other mental health conditions. This led the researchers to ask whether the genes that influence alexithymia might also account for the sensory traits attributed to autism.

“Our previous research has suggested a lot of the things that we think are features of autism (lack of empathy, poor recognition of facial expressions, lack of eye contact etc) are not due to autism at all. They are due to a co-occurring condition called alexithymia, which about half of autistic people have but is completely independent of autism itself,” said study author Geoffrey Bird, a professor at the University of Oxford and University College London.

“It might be the case that alexithymia is related to atypical interoception (the ability to perceive the state of your body), making it possible that the atypical sensory experiences which affect some of the autistic community might be explained by autism as well.”

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To test this idea, the researchers conducted a large twin study using data from the Twins Early Development Study in the United Kingdom. They focused on a sample of 207 twin pairs, including 55 identical pairs and 152 fraternal pairs. One or both twins in each pair either met diagnostic criteria for autism or were matched controls. The researchers used a combination of gold-standard diagnostic interviews and parent-completed questionnaires to assess autism traits, sensory symptoms, and alexithymia.

Sensory symptoms were measured using the Short Sensory Profile, a widely used parent-report tool that evaluates behaviors like sensitivity to noise, touch, or visual stimuli. Alexithymia was assessed using the Observer Alexithymia Scale, specifically focusing on the subscale that captures lack of insight into personal emotions. This aspect of alexithymia was chosen because it is most likely to relate to differences in sensory experience.

Using a method called bivariate twin modeling, the researchers explored how much of the relationship between autism and sensory symptoms could be explained by shared genetic factors, and how much was due to overlapping genetics with alexithymia. Twin studies are particularly useful for teasing apart genetic and environmental contributions because identical twins share nearly all of their genes, while fraternal twins share only about half.

The first set of analyses confirmed that all three traits—autism, sensory symptoms, and alexithymia—were strongly heritable. Autism showed a heritability estimate of about 82 percent, consistent with previous research. Alexithymia was also highly heritable at 84 percent, somewhat higher than past estimates, likely due to differences in how it was measured. Sensory symptoms showed moderate heritability at about 57 percent, with additional contributions from shared and unique environmental factors.

Next, the researchers looked at how these traits were related to one another. As expected, autism was moderately correlated with both alexithymia and sensory symptoms. The correlation between autism and sensory issues was largely genetic in origin. However, when the researchers accounted for alexithymia, the genetic link between autism and sensory symptoms disappeared. This suggests that genes related to alexithymia, not autism, were driving the observed connection between autism and sensory differences.

By contrast, the link between alexithymia and sensory symptoms remained significant even after controlling for autism. Although the overall correlation between alexithymia and sensory sensitivity weakened somewhat after removing the influence of autism, the shared genetic component remained just as strong. This means that alexithymia and sensory sensitivity are genetically related in a way that is independent of autism.

These findings suggest “that the sensory differences due to autism might not be due to autism at all, rather they might be associated with alexithymia,” Bird told PsyPost. “Thus, like a lot of things we previously associated with autism, we might need to update our view of what autism is. Our results suggest it is genes associated with alexithymia, not autism, that cause sensory differences.”

The results also support a broader view of alexithymia as a “transdiagnostic” factor—something that contributes to symptoms across a range of mental health conditions. Because alexithymia is common not only in autism but also in disorders like anxiety, depression, and eating disorders, understanding its role could help researchers and clinicians make sense of overlapping symptoms across diagnoses.

Despite the strength of the findings, the study had limitations. The researchers relied on parent-report measures, which can introduce bias, especially if one parent completed assessments for both twins. There was also some missing data, particularly among families of autistic participants, which may have reduced the ability to detect certain effects. Additionally, only one component of alexithymia was examined, and the measurement scale was slightly altered, which could affect comparisons to previous research.

Another limitation is that the study design did not allow the researchers to fully test whether alexithymia explains the link between autism and sensory symptoms in both directions. For instance, they could not assess whether controlling for the genetic contribution of alexithymia to autism would similarly weaken the autism-sensory link. This means the conclusions, while compelling, remain provisional.

Despite these caveats, the findings prompt a rethinking of how autism is defined and understood. If sensory symptoms are not directly caused by autism, but rather by alexithymia, then the current diagnostic criteria may need to be reconsidered. It may also mean that some individuals are misdiagnosed or that their sensory issues are misunderstood if clinicians do not take alexithymia into account.

Bird said that the next steps include exploring whether alexithymia can be reduced—and whether doing so would improve outcomes for people who experience sensory difficulties. This line of inquiry could have wide-ranging benefits, not just for autistic individuals, but for anyone with alexithymia, regardless of diagnosis.

The study, “Alexithymia may explain the genetic relationship between autism and sensory sensitivity,” was authored by Isabel Yorke, Jennifer Murphy, Fruhling Rijsdijk, Emma Colvert, Stephanie Lietz, Francesca Happé, and Geoffrey Bird.