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Is Misophonia Genetic?

Genome-wide research has reported a possible genetic association with misophonia. What the evidence says about heredity, family patterns, and what genes actually explain.

3 min read

In Brief

A genome-wide association study using 23andMe data reported an association between misophonia and rs2937573, a variant near the TENM2 gene. The finding is an important early lead, but it needs replication before it should be treated as a settled biological marker.

If you have misophonia, you have probably noticed it in someone else in your family. A parent who always seemed too bothered by noise at the table. A sibling who cannot tolerate certain sounds. Family clustering is commonly reported, and research is beginning to explore why.

Misophonia may have a meaningful genetic component. The evidence comes from multiple directions: family patterns, heritability research, and genome-wide association work that has reported a possible gene variant.

The TENM2 Gene

In a genome-wide association study (GWAS) using data from 23andMe participants, researchers identified a significant association between misophonia and a variant called rs2937573, located near the TENM2 gene.

TENM2 (Teneurin Transmembrane Protein 2) plays a role in neural development, brain connectivity, and the formation of synaptic connections. That makes it an interesting lead, especially because many people first notice misophonia during childhood or early adolescence.

The TENM2 variant association with misophonia reached genome-wide significance in a 23andMe dataset, making it an important early genetic lead. It still needs replication before it should be treated as settled.

The finding does not mean that TENM2 "causes" misophonia. Genes rarely work that way. What it suggests is that variations in this gene may influence how certain neural pathways develop, potentially predisposing some people to the atypical auditory-emotional connectivity that characterises the condition.

Genetic Correlations

The same GWAS research examined genetic correlations between misophonia and other conditions. The findings are useful, but they should be read as early association signals:

  • Tinnitus: Significant positive correlation, suggesting overlapping neural mechanisms
  • PTSD: Genetic correlation, consistent with shared hypervigilance pathways
  • Depression: Positive correlation, supporting the observed co-occurrence
  • Anxiety disorders: Correlation, consistent with overlapping autonomic dysregulation
"The genetic architecture of misophonia suggests it is not a purely sensory disorder, nor a purely psychiatric one. It occupies a space between the two." — Research summary, 2023 GWAS paper

These correlations do not mean misophonia is the same as PTSD or depression. They mean the conditions share some underlying genetic risk factors. Which may help explain why people with misophonia often experience co-occurring anxiety, and why treatments targeting the autonomic nervous system show promise across all of them.

Familial Patterns

Long before genetic research began, clinicians noticed that misophonia clusters in families. Studies have documented:

  • First-degree relatives (parents, siblings) of people with misophonia have elevated rates of the condition
  • Family members often share similar trigger categories (chewing vs. breathing vs. sniffling) even when raised separately
  • Some family patterns suggest inheritance may matter, but the exact inheritance model is not settled
Some researchers have proposed specific inheritance models for misophonia, but these remain hypotheses pending larger family and genetic studies.

Shared Genetics or Shared Environment?

The clustering of misophonia in families raises an important question: is it genetics, or is it simply that children learn from a parent who models extreme distress at certain sounds?

Both factors likely play a role. Twin studies (including data from the UK Biobank) suggest that genetic factors account for a meaningful portion of misophonia heritability, even after controlling for shared household environment.

But shared environment matters too. A child who grows up watching a parent become distressed at sounds may develop heightened vigilance toward those same sounds. The neural pathways for salience detection are shaped by both genes and experience.

What Genetics Does Not Explain

Genetics is not destiny. Many people with the TENM2 variant may never develop clinically significant misophonia. Many people with severe misophonia may not carry the variant. Genes set a disposition; experience, environment, and nervous system history write the story.

What the genetic research does, powerfully and importantly, is support the idea that misophonia is not a learned preference, cultural habit, or choice. It appears to have biological contributors, while still being shaped by experience, environment, and nervous system history.

The Clinical Implications

Understanding the genetic basis of misophonia has practical implications:

  • It gives skeptical healthcare providers and family members another reason to take the condition seriously
  • It may open pathways for more targeted biological research
  • It may eventually help with early identification in at-risk children
  • It places misophonia closer to neurodevelopmental and sensory-processing research conversations

The research is still early. But the direction is clear enough to matter: misophonia is not weakness. It is an embodied pattern with biological, developmental, and lived components.

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Evidence trail

Sources

These sources orient the public research layer. Thriving with Misophonia is lived-experience education and peer support, not diagnosis, treatment, or medical advice.

  • 0123andMe GWAS study - rs2937573 and TENM2 gene association with misophonia.
  • 02Fayzullina et al. - TENM2 gene association and familial patterns.
  • 03UK Biobank twin study data on misophonia heritability.
  • 04Kumar et al. (2017). The Brain Basis for Misophonia. Current Biology.
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