© Alexandra Chambers | Neurotopia CIC | December 2025
The recent study from Yale (linked at the bottom of the post) claiming that autistic adults have reduced mGlu5 receptor availability may feel like a breakthrough to some. However, it’s another fragment in a long trail of fragmented science.
For decades, autistic people have been used as subjects in studies that isolate a single brain receptor, a lone circuit, or a narrow behavioural pattern – and then project these isolated features back onto the person as if they define the whole. What this study does is no different: it measures lower mGlu5 availability in autistic adults using PET imaging, and then subtly implies that this may be a key factor in autism itself.
This is exactly the kind of reductionist framing that needs to stop.
The Problem with Pathologising Pieces
mGlu5 is a glutamate receptor – a regulator of excitatory signalling in the brain. It’s part of the larger ecosystem that balances stimulation and inhibition, often referred to as the E/I (excitation/inhibition) balance. This is not new information to those in functional health; glutamate sensitivity is part of the autistic experience. This presents in a variety of ways such as sensory overload and migraines to anxiety, sleep disturbance, and digestive issues.
So why is this being reported like a revelation?
Because mainstream neuroscience continues to operate as if each molecular finding is a potential cause, rather than a consequence or corollary of a divergent developmental trajectory. They find a downstream marker – a receptor change, a structural difference, a brainwave pattern – and then treat it like it’s the origin or a key to pathology. It isn’t.
This mode of thinking is not only scientifically lazy; it’s deeply misleading.
Glutamate Sensitivity is not a Defect
Reduced mGlu5 availability does not mean “dysfunction” in the way the word is used. It may be:
A protective (epigenetic) downregulation after years of glutamate overexposure.
A reflection of genetic differences in excitatory set-point.
Or a compensatory adaptation in the context of a more sensitive and perceptive neurotype.
What it absolutely is not, is evidence of a broken brain.
A Jigsaw of Correlations
There’s an irony here that many autistic people will recognise: for years, autism was symbolised by a jigsaw puzzle piece (some people still use it) – an icon many now reject due to its history. In a strange way, that symbol has come full circle, because researchers are continuously doing just that: pulling out disconnected “pieces” of the divergent profile and treating them like they represent the whole picture.
Glutamate receptors.
Brain volumes.
White matter lesions.
Eye-tracking patterns.
Collagen.
Repetitive behaviours.
Gastro.
Genetics.
Inflammation.
Mitochondria.
Every study picks up a new piece of the jigsaw and the author(s) hold it up in silo looking for the explanation. It never is; because neurodivergence isn’t a jigsaw – it’s a living system.
It is not a condition to be solved or assembled. It is a full-body, full-brain, genetically influenced, environmentally modulated way of being.
When researchers ignore that, when they chase markers as if they are causes, they not only miss the forest for the trees – they flatten the dignity of those they claim to study.
We need a new scientific paradigm that treats neurodivergence not as a list of broken parts but as a coherent, adaptive system shaped by both biology and context.
That means:
Stopping the reflex to pathologise every difference.
Abandoning causality-chasing in downstream measurements.
Studying divergence as an integrated systemic configuration in need of systemic support.
And listening to those who live it, not just imaging their brains.
The reduced mGlu5 availability is a meaningful piece of data, but it is not causal. It does not require ‘targeted therapeutics’ aside from cessation or reduction of glutamate/MSG (Monosodium Glutamate) containing medical interventions.
MSG (Monosodium Glutamate) Is Officially Listed in several pharmaceutical interventions including FluMist:
“Non-medicinal ingredients: Arginine hydrochloride, dibasic potassium phosphate, gelatin hydrolysate (porcine Type A), gentamicin (a trace residual), monobasic potassium phosphate, monosodium glutamate, ovalbumin (a trace residual), and sucrose.”
Monosodium glutamate is a formally declared excipient in FluMist (live attenuated influenza vaccine, administered intranasally).
Even though FluMist is a nasal spray, not an injection, its route of administration is still highly invasive neurologically:
The olfactory nerve pathway provides direct access to the central nervous system (CNS):
Unlike ingestion (which goes through the GI tract), intranasal delivery bypasses the blood-brain barrier.
This route is used intentionally in pharmacology to deliver drugs into the CNS.
For divergent individuals with glutamate sensitivity, impaired GABA balance, or connective tissue-related BBB permeability, this raises significant risk.
Monosodium glutamate is a known excitotoxin in susceptible terrain:
It can overstimulate NMDA and AMPA glutamate receptors, particularly in the limbic system and hypothalamus.
In animal studies, neonatal intranasal MSG administration has been used to induce excitotoxic brain damage.
For individuals with GAD1/GAD2, GRIN2B, MTHFR, SLC1A1, or other terrain-impairing variants, this can trigger a neuro-inflammatory or neurotoxic response.
FluMist may be Especially Risky for:
Neurodivergents.
People with glutamate-related migraines, seizures, or sensory overload.
Anyone with connective tissue divergence, BBB vulnerability, mast cell activation, or mitochondrial fragility.
Summary
MSG is present in FluMist, this is verified by the official leaflet.
FluMist is delivered via the nose, meaning direct brain exposure is possible through the olfactory pathway (a vulnerable route for divergents); this is non-trivial.
Until researchers begin acknowledging divergent biology and treating divergence as more than the sum of its receptor levels, they will continue to chase pieces and never see the real picture.
#divergentgenomicsbyneurotopia#neurodiversity#orthomolecularmedicine#science#neurodivergent#adhd#connectivetissue#autism#divergent#metabolism#glutamate#monosodiumglutamate#sensitivity#environmental
Link to Study: https://psychiatryonline.org/doi/10.1176/appi.ajp.20241084