Every so often you read something that opens the door to new thinking.
For me, recently, it was a piece by Alexandra Chambers of Divergent Genomics called ‘Connective Tissue on a Divergent Spectrum Part One: The Ear and Eye’.1 Her proposition is elegantly simple. We tend to treat the eye and the ear as gateways to the nervous system, which means that when someone struggles with light or sound, we look immediately at the brain: processing, filtering, attention, tolerance. But the eye and the ear are also connective tissue organs, built from the same collagen and elastin and extracellular matrix that give us skin, ligaments and joints. Light passes through a cornea before it becomes a signal. Sound is carried by a membrane, a chain of tiny bones, ligaments and fluid before a single nerve fires. If that tissue varies from person to person, then the signal arriving at the brain may already be different, before processing it even begins.
Reviewing the hypothesis
I read around Chambers’ claims, and some of what she’s drawing on is better established than most people realise.
The overlap between neurodivergence and joint hypermobility has moved well past anecdote. A 2025 systematic review found joint hypermobility in a substantial minority of autistic people, with the figures rising when hypermobility was clinically assessed rather than self-reported,2 and larger cohort studies have found it in around half of autistic and ADHD adults compared with roughly a fifth of the general population.3 Dysautonomia and chronic pain travel with that cluster.3 Something is going on there.
There’s a lovely worked example of her underlying principle in a condition called superior semicircular canal dehiscence, where thinning of bone in the inner ear creates an abnormal ‘third window’. People with it experience hyperacusis, hear their own eye movements, and become dizzy at particular sounds.4 Nobody suggests they are overreacting to noise, because the mechanics of the ear are measurably different, so the sound arriving is measurably different.
Superior semicircular canal dehiscence is a condition in which abnormal thinning of the bone overlying the inner ear’s superior semicircular canal creates a ‘third window’ into the inner ear.4 It produces measurable symptoms — hyperacusis, sound-induced dizziness, even hearing one’s own eye movements — caused entirely by a structural difference in the ear itself, not by how the brain interprets sound. It is offered here as a clear, well-documented example of how connective tissue structure can alter the signal a nervous system receives before any neural processing begins.
The same logic runs through the collagen research on the tectorial membrane in the inner ear,5 and through genetic work linking collagen variants to the biomechanical properties of the cornea.6 Structure shapes signal. That part is not in doubt.
Structure shapes signal. That part is not in doubt.
The research opportunities
What Chambers is proposing goes further than any of that. Nearly all the strong evidence sits inside named syndromes: Marfan, Stickler, classical Ehlers-Danlos.7 The proposal is that the same principles operate across a much wider group of people whose connective tissue differences are subtler and who will never receive a formal diagnosis.
The broad idea that connective tissue matters in neurodivergence already has company in the literature. Eccles and colleagues have proposed a model linking joint hypermobility to proprioceptive difference and emotional dysregulation in neurodivergent people,8 and the ‘Connectivome Theory’ argues that connective tissue variation across multiple body systems may account for part of the autism phenotype, including altered sensitivity to environmental stimuli.9
What appears not to have been tested, as far as I can establish (Google Scholar search, cross-checked via Consensus and Perplexity), is Chambers’ specific proposition: that the eye and the ear, as connective tissue organs, shape visual and auditory input before it reaches the brain at all. That is a narrower and more testable claim than the general one, and it is arguably the most useful thing about the article. Studies could take the form of participant groups stratified by hypermobility rather than by diagnosis, objective measures of light discomfort and speech-in-noise performance sitting alongside connective tissue assessment, with imaging to correlate subjective measures with objective measures.
Why should you care if you’re not an academic or researcher?
We don’t need a hypothesis to be proven to use the new idea as a lens through which to view various problems, and sometimes using a different lens can help us come up with support approaches that work. Let us consider neurodivergent children. A child who can’t bear the fluorescent lights in a classroom might get described as withdrawn, or present as unable to focus and apply themself to school work. A child who covers their ears and won’t go into the hall may be perceived as oppositional. Auditory fatigue by mid-afternoon can look a great deal like poor attention; visual fatigue, when an eye test shows a child can see clearly, may be missed entirely. These descriptions shape how we respond to and support children, and follow them into their file and their support plan. A new lens on such problems can inform approaches to support.
Auditory fatigue by mid-afternoon looks a great deal like poor attention; visual fatigue, when an eye test shows a child can see clearly, may be missed entirely.
This is why I so strongly advocate an integrative multi-disciplinary approach to understanding and supporting neurodivergence. Imagine a soundboard with a hundred slider switches that together determine the sound. Most of the help offered to a struggling child adjusts one switch, maybe two or three, and hopes for the best. The value of work like Chambers’ article is that it points at switches nobody was checking. And yes, it creates research questions that open the door to potentially really useful research, but even before that research is done, it gives us a new lens through which to consider problems and to approach understanding and supporting our kids.
If you’re working in this territory, whether from genomics, audiology, education, neuropsychology, or your own lived experience, I’d be glad to hear from you. And if you'd like a more person take on sensory sensitivity, hypermobility, neurodivergence, and parenting, you might enjoy this post on Medium.
Illumin-Ed’s work is educational and developmental. Nothing here is diagnosis, treatment or medical advice, and anyone with concerns about their own health or their child’s should take them to an appropriately qualified professional.
- Chambers, A. (2026, January 21). The eye and ear: Connective tissue organs on a divergent spectrum. Neurotopia CIC. theneurotopiaproject.co.uk
- Baeza-Velasco, C., Vergne, J., Poli, M., Kalisch, L., & Calati, R. (2025). Autism in the context of joint hypermobility, hypermobility spectrum disorders, and Ehlers-Danlos syndromes: A systematic review and prevalence meta-analyses. Autism, 29, 1939–1958. doi:10.1177/13623613251328059
- Csecs, J. L. L., Iodice, V., Rae, C. L., Brooke, A., Simmons, R., Quadt, L., Savage, G. K., Dowell, N. G., Prowse, F., Themelis, K., Mathias, C. J., Critchley, H. D., & Eccles, J. A. (2022). Joint hypermobility links neurodivergence to dysautonomia and pain. Frontiers in Psychiatry, 12, 786916. doi:10.3389/fpsyt.2021.786916
- Ward, B. K., Carey, J. P., & Minor, L. B. (2017). Superior canal dehiscence syndrome: Lessons from the first 20 years. Frontiers in Neurology, 8, 177. doi:10.3389/fneur.2017.00177
- Masaki, K., Gu, J. W., Ghaffari, R., Chan, G., Smith, R. J. H., Freeman, D. M., & Aranyosi, A. J. (2009). Col11a2 deletion reveals the molecular basis for tectorial membrane mechanical anisotropy. Biophysical Journal, 96, 4717–4724. doi:10.1016/j.bpj.2009.02.056
- Lu, Y., Vitart, V., Burdon, K. P., Khor, C. C., Bykhovskaya, Y., Mirshahi, A., Hewitt, A. W., Koehn, D., Hysi, P. G., Ramdas, W. D., Zeller, T., Vithana, E. N., Cornes, B. K., Tay, W.-T., Tai, E. S., Cheng, C.-Y., Liu, J., Foo, J.-N., Saw, S. M., … Young, T. L. (2013). Genome-wide association analyses identify multiple loci associated with central corneal thickness and keratoconus. Nature Genetics, 45, 155–163. doi:10.1038/ng.2506
- Asif, M. I., Kalra, N., Sharma, N., Jain, N., Sharma, M., & Sinha, R. (2023). Connective tissue disorders and eye: A review and recent updates. Indian Journal of Ophthalmology, 71, 2385–2398. doi:10.4103/IJO.IJO_286_22
- Eccles, J. A., Quadt, L., Garfinkel, S. N., & Critchley, H. D. (2024). A model linking emotional dysregulation in neurodivergent people to the proprioceptive impact of joint hypermobility. Philosophical Transactions of the Royal Society B, 379(1908), 20230247. doi:10.1098/rstb.2023.0247
- Zoccante, L., Ciceri, M. L., Gozzi, L. A., Di Gennaro, G., & Zerman, N. (2022). The ‘Connectivome Theory’: A new model to understand autism spectrum disorders. Frontiers in Psychiatry, 12, 794516. doi:10.3389/fpsyt.2021.794516