©Alexandra Chambers | Neurotopia CIC | January 2026
All research is available for PDF digital download on: https://studio.buymeacoffee.com/extras and all money goes directly to Neurotopia CIC to fund further research, thank you.
Sensory overload is often described as a quirk of perception or a flaw in neurological filtering. However, when you stop treating the brain as the sole source of experience, and look instead at the tissues that receive sensory input, a much clearer – and more nuanced – picture begins to emerge.
Both the eye and the ear are connective tissue-based sensory organs. They are not passive receivers, nor are they uniform across the population. Their structure – and by extension, their sensitivity – is shaped by collagen, elastin, extracellular matrix proteins, and their genetic regulation. When these underlying frameworks vary, so does the experience of the world.
This matters – especially for divergent populations – because it means sensory overwhelm is not just “how your brain works.” It’s also how your body is built.
Connective Tissue Genes are a Spectrum too
Connective tissue variation isn’t binary. It’s not only diagnosable syndromes like Ehlers-Danlos or Marfan. It exists on a spectrum of expression, influenced by:
Genomic variants in collagen, ECM, methylation, and redox pathways.
Epigenetic signalling during development
Levels of introgressed DNA (such as introgressed Neanderthal variants affecting immune and tissue architecture).
The result is wide-ranging presentations:
Some individuals show full syndromic features (e.g. hypermobility, mitral valve prolapse, translucent skin).
Others have subtle (yet impactful) connective tissue fragility, manifesting only through sensory experiences: light aversion, ear pressure, chronic fatigue, or GI issues.
What’s dismissed as “sensory sensitivity” is often a visible consequence of this hidden, spectrum-level connective tissue divergence.
The Eye: Light-Sensing Collagen
The eye is constructed from multiple collagen-rich structures:
Cornea, sclera, and iris – composed of collagen types I, III, and V.
Zonular fibres – suspended by fibrillin (FBN1), vulnerable in Marfan-type spectrums.
Retina and Bruch’s membrane – dependent on ECM integrity for light handling.
Lens capsule – collagen-structured and prone to oxidative stiffening.
When these structures are looser, irregular, or structurally fragile:
Light scatters unpredictably.
Contrast sensitivity and buffering decline
The retina becomes overexposed, sending a chaotic signal to the brain.
The individual experiences photophobia, migraines, or visual snow – misdiagnosed as anxiety or “screen intolerance”.
These aren’t perception disorders. They are connective tissue divergences with sensory consequences.
The Ear: Sound-Conducting Collagen
The ear also depends heavily on connective tissue:
Tympanic membrane (eardrum) – radial collagen layers regulate vibration.
Middle ear ligaments and ossicles – controlled by elastin and collagen tension.
Tensor tympani and stapedius muscles – modulate sound pressure, anchored in connective tissue.
Cochlea and basilar membrane – collagen stiffness tunes frequency response.
Vestibular labyrinth – balance relies on collagen-structured compartments and fluid pressure.
When this system is divergent:
Sound is poorly buffered or excessively amplified.
The body cannot modulate loudness or sharpness.
Balance may be disrupted by sound-induced vestibular shifts.
The person may experience hyperacusis, sound-triggered pain, dizziness, or auditory fatigue.
The issue is in the collagen matrix that receives and transmits the sound.
The Sensory Cascade: From Structure to Overload
Whether it’s light through the eye or sound through the ear, the pathway is the same:
Genomic variation → Connective tissue divergence → Altered structural interface → Distorted input signal → Neurological overload → Misdiagnosis interpreted under a behavioural lens.
This leads to a cascade of misinterpretations:
Light sensitivity becomes “social withdrawal”
Sound intolerance becomes “oppositional behaviour”.
Painful environments become “meltdowns” or “attention problems”.
All while the actual biology – collagen type, tissue tension, sensory load thresholds – is never examined.
Suppression of Genomic and Physiological Divergence
This physiology is not unknown; it is simply rarely diagnosed and omitted from diagnostic frameworks.
Why?
Because recognising tissue-level divergence as a root cause of sensory overwhelm would:
Undermine purely behavioural models of autism, ADHD, and SPD.
Require cross-disciplinary thinking in medicine.
Expose massive underdiagnosis of connective tissue variation in children and adults.
Challenge pharmaceutical and psychiatric dominance over divergent care.
It is easier to label the child, medicate the adult, or design a behavioural plan – than it is to admit that the tissues of divergent bodies are different, and that those differences are biomechanically valid.
The Missing Integration
It is time to stop asking “why are they so sensitive?”
and start asking:
What is the structural condition of the organs receiving that input?
This changes everything – not just for treatment, but for how we understand divergence itself. These aren’t behavioural issues; they are biofabric differences, and they deserve to be recognised, and supported.
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