Who I am
Hi! I’m Alia.
A physician who has cared for autistic humans in the ER, often on their worst days, and a mom in a beautiful neurodiverse family. I want to change how our culture – especially our western medical culture – understands autism.
Why I’m here
Even decades into large shifts in how culture understands neurodiversity, we’ve still — in our research, in our textbooks, in our own predictive minds — defined autism first as a disorder. A social communication disorder, a neurodevelopmental disorder, a disorder of restricted and repetitive interests. It’s not that the challenges those describe aren’t real — many autistic people do face significant disability — but as a definition they are drastically incomplete.
It goes back to the old parable of the elephant: one hand on the trunk, another on the ear, another on a leg, each certain it has the whole animal. Defining autism through a deficit-based lens is like feeling the trunk, noticing it’s like a snake, and running off to prove how snake-like it is. And more than that, to reduce what is human in that way isolates and harms autistic people. For many of us, our simple error was that somewhere along the way, we forgot we were using a lens in the first place.
It’s time for a new lens.
The lens
Autism is a neurotype.
Autism is a difference in how we attend – notice, process and respond – to the world around us and the world within us. From the very beginning, that difference shapes how the senses integrate and how development unfolds. It carries certain strengths and certain challenges, and for some, significant disability.
But isn’t autism already defined by the DSM?
Yes, and the diagnosis matters. It opens doors to support.
Clinicians diagnose people with autism in much the same way they make other diagnoses. They compare patient data – symptoms, lab results, images – against established standards for physiological and psychological health. Any deviation from these norms can be interpreted as a potential indicator of disease or disorder. This is the foundation of medicine. It was the core of my medical education.
But autism, like the other diagnoses in the DSM, is different. Appendicitis is an inflamed appendix. A heart attack is a blocked artery. Autism isn’t diagnosed by an underlying pathology at all. It is diagnosed by its traits.
That’s true of the whole manual, not just autism. In 2013, the director of the US National Institute of Mental Health said DSM diagnoses rest on agreement about clusters of symptoms, not on objective measures, and the institute began funding research that looks underneath the categories.
Autism researchers are doing the same. As the diagnosis has widened, measured differences between autistic and non-autistic groups have been shrinking. And in 2025, two large studies found that people who share the label can differ in their genetics and in how their development unfolds.
The DSM describes some of what autism looks like, but not what it is.
Further reading: NIMH and the DSM (2013) · Rødgaard et al., JAMA Psychiatry (2019) · Litman et al., Nature Genetics (2025) · Zhang et al., Nature (2025)
This lens is built by weaving together three strands of theoretical work: monotropism, predictive processing and allostasis. I bring years of deep scientific research, lived experience and a mind that can turn a web of chaos into something that resembles a line.
Or at least I try to.
Warmly, Alia
Autism and ADHD as neurotypes
What’s a neurotype?
A neurotype is a kind of mind: a stable pattern in how a nervous system notices, processes and responds. We all have one. Autism and ADHD are two of them. A neurotype isn’t a diagnosis and isn’t a deficit, though it can come with both. It’s the shape of the mind that everything else happens inside of.
Wait, are you talking about ADHD too?
Yes, because the science already does. The diagnostic manual doesn’t define autism or ADHD by what’s happening in the brain. Each is a cluster of observed behaviors that tend to travel together, drawn up by committee and revised every edition. The boundaries between clusters are decisions, not discoveries. Until 2013, the manual didn’t allow a person to be diagnosed with both; the overlap was so obvious that the rule was dropped. Today, somewhere between a third and two-thirds of autistic people also meet criteria for ADHD, depending on the study, and ADHD is the most common co-occurring diagnosis in autism. Twin and family studies show the two share a large part of their genetic risk, and they share many of the same features: differences in attention regulation, executive function, sensory processing and emotional regulation. Clinicians increasingly describe them as overlapping presentations rather than separate conditions, and the people who first described monotropism noted from the start that ADHD attention looks monotropic too.
Imagine we each explore the world with a beam — a flashlight. Whatever falls inside the beam gets noticed, processed, and responded to. Whatever falls outside it goes unnoticed.
That beam is attention. We can focus it narrow and bright, or spread it dim and wide, but the lumens — the energy available — stay the same. And the quality of the light — steady or flickering, calm or driven by fear — shapes how we feel about what we see.
For all of us, how attention is shaped, where it goes, and how long it stays is first an instinct: pulled toward what matters to us, and away from what we don’t yet have the capacity to face.
Change how you pay attention and you change everything that follows.
How layers of memory, context and meaning are added.
How emotion, empathy and awareness are constructed.
How we understand ourselves, our world and those around us.
How learning and development unfold.
The theory of monotropism
“A way of thinking about autism not as a set of deficits, but as a different, more focused strategy for using attention.” — monotropism.org
Monotropism is often reduced to “autistic people can’t multitask.” That misses the idea. It’s more like one web, one experience, one channel at a time. The foundation of monotropic theory is the relationship: the gravitational pull between what the nervous system flags as important or interesting and the processing resources that follow. In autism, that pull is stronger.
Monotropic attention is pulled into a narrow, bright beam
Details and connections inside the beam are fully processed, and attention stays there until that processing is complete. Outside the beam, the world goes quiet.
Polytropic attention spreads into a wide, soft light
Many things are held in view at once, each a little lit, and attention flows easily between them. Small details blend into the whole.
Monotropic processing brings certain strengths, like deep focus, pattern-finding and noticing what others miss. And certain challenges, like overwhelm, burnout and inflammation, especially when autistic thinkers exist in environments and systems that weren’t built for their processing style.
Polytropic processing brings its own strengths, like flexibility, breadth and the ability to track many things at once. And its own challenges, like jumping to conclusions, overly broad assumptions, and a tendency to see what it expects to see rather than what is actually there.
The world needs both types of thinkers.
The research behind monotropism
Monotropism was first described by Dinah Murray, Mike Lesser and Wenn Lawson in 2005, and has been carried forward largely by autistic researchers. Attention is a limited resource. Monotropic minds concentrate it in a few places at a time, deeply; polytropic minds spread it across many. Many autistic traits follow from how attention is distributed.
Read: Murray, Lesser & Lawson (2005), Autism · monotropism.org: papers, talks and the Monotropism Questionnaire
The sensory processing lens
Monotropic minds construct monotropic experiences.
But to understand that (and why environments that force monotropic minds to maintain broad or rapidly shifting attention to stay safe cause harm), first you have to understand how the human mind constructs experience.
Concept 1Constructing experience from the sensory system up is bottom-up processing.
Think of it like this: your mind lives inside a black box (we call that box a skull). It doesn’t see images like a camera; it constructs them. Light hits sensory receptors in the eye, the receptors convert it into electrical impulses, nerve cells carry those impulses to the brain, and the brain assembles them into an image. But construction doesn’t stop there. Our mind adds layers of context and significance to not just construct an image, but also tell us what that image means and how we feel about it.
Construction like this happens in all our senses: the senses that deliver information from the outside world (exteroception) and the senses that deliver information about the inside world (interoception). What’s interoception?
Interoception is the sense of the body’s inside: heartbeat, breath, hunger, temperature, the stretch of the gut, the tension in a muscle. It is the raw material the mind uses to build feelings.
Concept 2Bottom-up processing is expensive.
Everything the body does, including constructing experience and preparing our body to respond to it, consumes resources. Resources are the things our cells need to perform their basic functions. In the simplest terms, resources are things like glucose (sugar), oxygen, water and ATP (the cellular currency).
The work of processing the sensory world from the bottom-up requires a massive amount of cellular energy, and not only because of the processing energy required to build the layers of meaning. Because the work of that processing doesn’t just happen in the mind, it also happens in the body. The mind doesn’t just construct an image, it constructs a whole-body response to it: a new set of motor and visceromotor commands to tighten these muscles, speed the heart, release glucose, ready the immune system.
And the body’s new state (the faster heart, the tightened gut) arrives back at the brain as interoception, the raw material for the next round. Mind and body are one loop, and every turn of the loop draws on the same energy budget.
Concept 3Top-down (predictive) processing is an energy-saving strategy.
The mind’s first job is to ensure we have enough resources available to find threats and respond to them. And predictive processing is one of its best resource-conserving (allostasis-protecting) strategies. What is allostasis?
Allostasis is the body’s way of staying stable by changing ahead of time. Instead of waiting to drift out of balance and then correcting, the brain predicts what the body will need next (glucose, oxygen, heart rate, attention) and arranges it in advance, so there is always something in reserve for the next demand.
It works like this: the mind doesn’t only sense, process and respond to the world. It predicts. In every moment, before the light waves hit the retina or the sound waves hit the eardrum, the brain has already made its best guess at what will land next and sent that guess, that prediction, down to the cells of the body. Before the sensory information even hits the receptor, the body has already done the visceromotor and deep cellular work to prepare for it. Let that settle a moment.
When your mind anticipates the next word of a written sentence, that guess doesn’t just live in the mind. It actually creates that experience in the cells at the back of your eyes, and if the sentence carries emotional significance, it shifts the visceromotor experience in the body to generate the felt experience. And it does all that in the instant before the sensory experience lands.
You hear your name across a noisy room. Your ears received the same sound as everyone else’s; your prediction picked it out. You reach the bottom of the stairs and your foot drops through a step that isn’t there: the lurch is your body meeting a prediction, not a stair. The smell of a hospital corridor tightens your stomach before you have thought a single thought. Your phone buzzes in your pocket and it hasn’t.
Try this. Look at this picture and, just at a glance, try to make meaning of it:
Once you’ve seen it, you can’t unsee it. That’s your mind relying on the prediction (top-down processing) rather than repeating the energy-consumptive work of building it from scratch: sorting through every possibility (what could this be? what could it mean? how should I feel about it?) and trying to find one that fits.
Top-down (predictive) processing is cheap: it conserves processing energy for other tasks. If you already know what to expect, the work has already been done. There is nothing more to learn. Bottom-up processing, constructing from the sensory system up, requires far more processing energy.
How does that save energy? Only sensory information that is significantly different from the prediction makes it through.
Concept 4All minds construct experience using a combination of top-down predictive processing and bottom-up sensory processing.
How I put it together
Monotropism × HIPPEA × Allostatic load
Monotropic attention guides development.
Where attention goes, strength and sensitivity take root
Our neurobiology (our neurotype) changes how we pay attention, and how we pay attention shapes and builds our neurobiology. When attention is pulled deep into one channel at a time, the senses may learn to work together differently. Some channels can be built richly while others are left under-built, or easily overwhelmed.
Read more: how attention builds the developing brain
London taxi drivers are the classic example. To earn their licence, they spend years memorizing roughly 25,000 streets. Brain scans show they end up with a larger posterior hippocampus, the part of the brain that maps space. And when trainees were followed over time, the growth appeared only in those who qualified. What we attend to, over and over, is what the brain builds. That’s neuroplasticity. Tell me more.
Neuroplasticity is the brain’s ability to change its own structure in response to what it does. Connections that are used repeatedly get stronger and faster; connections that go unused are pruned away. The pattern is often summed up as “neurons that fire together, wire together.” It happens throughout life, but it is fastest in early childhood, when the brain is forming and trimming connections at an enormous rate. So what a young mind attends to, over and over, is quite literally what it builds.
Read: Maguire et al. (2000), PNAS · Woollett & Maguire (2011), Current Biology
And what is most intriguing about considering autism as a difference in how we attend to the world is that those differences likely start long before any autistic traits develop. See the research.
Tsang, Green, Liu et al. (2024), Communications Biology. Scanned 53 sleeping six-week-olds. Infants with an autistic older sibling already showed a different pattern of salience-network connectivity (the network that flags what matters and directs resources toward it) than infants with no family history. Read the study →
Jones & Klin (2013), Nature. Tracked eye-gaze in infants from 2 months of age. In those later diagnosed, attention to other people’s eyes was present at first, then declined between 2 and 6 months. Read the study →
Emerson, Adams, Nishino et al. (2017), Science Translational Medicine. Scanned six-month-olds with a family history of autism and used their connectivity patterns to predict, with high accuracy, which of them would be diagnosed autistic at age two. Read the study →
Hazlett, Gu, Munsell et al. (2017), Nature. Followed 106 infants with an autistic older sibling. Those later diagnosed showed faster growth of the brain’s surface area between 6 and 12 months, before any behavioural signs, and a model built on those scans predicted diagnosis at 24 months with high accuracy. Read the study →
Wolff, Gu, Gerig et al. (2012), American Journal of Psychiatry. Scanned 92 infants with a family history at 6, 12 and 24 months. The white-matter pathways connecting brain regions were already developing differently at 6 months in those later diagnosed. Read the study →
- 6 weekssalience-network differences visible on imaging
- 2–6 monthsattention to eyes declines in infants later diagnosed
- 6 monthswhite-matter and connectivity patterns predict a later diagnosis
- 6–12 monthsfaster growth of the brain’s surface area
- 2 yearstraits emerge
In infancy and early childhood, when neuroplasticity is at its greatest, attention doesn’t just accompany development—it drives it. For a monotropic mind, what fascinates is a strong current. The circuits that receive the most early attention can become both a mind’s greatest strengths and its most easily overwhelmed channels. Each child shares the same monotropic pull, but the focus of their early attention differs—sculpting neural pathways that lead to uniquely developing minds.
Explore a similar theory: Intense World Theory
Henry and Kamila Markram’s Intense World Theory (2007) proposes that autistic brains are hyper-reactive and hyper-plastic: local circuits respond more strongly, learn faster and remember more. The result is a world that is perceived, felt and remembered too intensely, and a mind that retreats into what is predictable to cope.
It fits this lens. The world may feel too intense because of too much prediction error. It remains a hypothesis, but it points to the same place: strengths and sensitivities growing from the same circuits.
Read: Markram, Rinaldi & Markram (2007), Frontiers in Neuroscience
Deep and narrow attention → deep and narrow predictions → more prediction error → allostatic overload
Deep, narrow attention builds detailed, precise predictions, which means more prediction error and more bottom-up processing demands. The constant, energy-consuming work of bottom-up sensory processing leaves the mind and body in a constant state of allostatic overload.
What is allostatic overload?
Allostasis is how the brain regulates the body by anticipating its needs and meeting them before they arise. Neuroscientist Lisa Feldman Barrett calls the brain’s running account of those resources the body budget. Every demand is an expense. When demands are brief and followed by recovery, the budget rebalances. When they pile up without enough recovery, the body stays in a state of allostatic overload, and the costs accumulate as wear and tear on the cardiovascular, metabolic and immune systems.
Cells throughout the body respond to a stressed body budget by conserving, and often that conservation comes at the cost of cellular cleanup. Cellular waste accumulates, and the immune system responds with inflammation. The inflammatory patterns we see in many autistic people – gut, skin, joint and lung inflammation, and neuroinflammation – may be the downstream cost of that stress.
Read: Sterling (2012), Physiology & Behavior · Barrett & Simmons (2015), Nature Reviews Neuroscience · Kleckner et al. (2017), Nature Human Behaviour
Are you saying that deep focus drains the body budget?
No, not exactly. This is where it gets tricky. Autistic thinkers often find deep focus restful. Inside the tunnel, attention narrows and processing resources pour into one thing, so the stimuli outside it go unnoticed. Fewer channels to process means less prediction error, and less to pay for.
But that only works when what lies outside the tunnel is safe: safe for the senses, and safe emotionally. A child can’t zoom in at school unless their teacher makes it safe to miss what’s happening outside the beam, both in the room and in the world of judgment and emotion. Deep focus in a safe space restores. Deep focus held while bracing for the next interruption doesn’t.
What is overwhelm, and what is burnout?
Overwhelm is fundamentally a ratio problem. It is the alert that tells us when processing demands have exceeded capacity. That we no longer have enough available resources to manage what comes next.
Attention constricts, locking onto the most immediate demand and dropping everything else. The prefrontal cortex, our most sophisticated and energy-intensive processing center, begins to go offline. The nervous system shifts from flexible, creative, open-ended thinking to something faster and more rigid: react, protect, survive.
And if we don’t listen, the body doesn’t stop sending messages. It sends louder ones.
Burnout is the state of a body budget that has been overdrawn one too many times. In this state, even a small demand will feel like more than the system can bear.
Neuroinflammation interrupts development.
The science here is rapidly advancing, but not yet settled.
Allostatic load doesn’t stay in one place; it shows up wherever the body is spending its budget. In the gut, it can manifest as gastrointestinal distress and food sensitivities. In the lungs, it worsens airway reactivity and slows recovery from illness. In the brain, it can manifest as neuroinflammation—driving brain fog, sensory hypersensitivity, and altering how neural circuits develop.
Chronic allostatic load likely primes the brain, leaving it more vulnerable to each new allostatic hit.
Read more
How does a stressed body budget reach the brain? It starts with chemical priming.
When cognitive and sensory demands outpace energy resources, the body stays locked in survival mode. Stress hormones like cortisol and CRH (corticotropin-releasing hormone) circulate continuously. In acute bursts, cortisol calms inflammation. Held too long, immune cells become resistant to it, putting the entire defense system on a hair-trigger.
The brain’s cellular sculptors
The brain’s resident immune cells, called microglia, serve two roles: they defend tissue against threats, and they sculpt the developing brain by pruning away weak or unused synaptic connections.
In an un-inflamed brain, this pruning creates clean, efficient neural pathways. But microglia are sensitive to signals from mast cells—first-responder immune cells that line the blood-brain barrier and react directly to stress hormones like CRH.
When chronic stress triggers mast cells, microglia abandon their pruning duties and shift into threat-defense mode:
- They may halt essential pruning, leaving sensory circuits hyper-dense, hyper-connected, and overwhelmed by input.
- Or, during acute immune flares, they may become overly aggressive, stripping away newly formed connections and emerging skills—offering a biological mechanism for developmental regressions.
Mast cells carry receptors for stress hormones, including CRH. Stress-activated mast cells can loosen the blood–brain barrier, and stress hormones can prime microglia. Much of this comes from animal studies and the work of Theoharides and colleagues.
Vargas, Nascimbene, Krishnan et al. (2005), Annals of Neurology. Found activated microglia and astroglia, and inflammatory signalling molecules, in brain tissue and spinal fluid from autistic people. Read the study →
Suzuki, Sugihara, Ouchi et al. (2013), JAMA Psychiatry. Used PET imaging to show excessive microglial activation across multiple brain regions in autistic young adults. Read the study →
Paolicelli, Bolasco, Pagani et al. (2011), Science. Showed that microglia prune synapses during normal brain development, and that disrupting them changes how brain circuits mature. Read the study →
Estes & McAllister (2015), Nature Reviews Neuroscience. A review of immune signalling in the brain and body in autism, and how immune activation during development can shape brain wiring. Read the review →
Theoharides, Angelidou, Alysandratos et al. (2012), Biochimica et Biophysica Acta. Proposes that mast cell activation, triggered by allergic, environmental and stress signals, contributes to brain inflammation in autism. Read the paper →
Breon (2026), aliabreonMD. Meet the Mast Cell: what mast cells are, where they live, and why they matter for sensitive bodies. Read the post →
Could the timing, intensity, and location of this inflammatory burden help explain why some autistic nervous systems maintain resilience, while others face profound physical disability, chronic exhaustion, and intense daily barriers?