I think there is really something to the fundamental axis of autism vs schizophrenia being understimulation vs overstimulation. Autistics are understimulated and so never get used to high levels of stimulation and are easily overwhelmed by them, but on the other hand have a quiet working environment inside their heads that's useful for intellectual work. Schizophrenics are overstimulated and so learn to pull complex patterns out of noisy data, but then end up also finding a lot of patterns that aren't really there.
I have no intelligent insights into any of these phenomenon. I just want to say they are very interesting and I intend them a topic of conversation among smart people at dinner parties soon.
1) A lot of ASD symptoms are secondary or tertiary from "real ASD genes/phenotypes" - specifically, they are the end of a chain of dominoes emanating from some other thing 'directly caused' by the ASD-causing genes.
2) Congential blindness, via a different pathway, tends to knock over such an early domino, and thus ends up propagating outward into the symptoms knocked over
Like, to throw out a random sounds-good-story to illustrate perhaps what I might mean - suppose that not making eye contact in some critical range makes some brain-development thing go wonky in a small set of ways.
Someone with ASD might find not make that eye contact because (like myself) looking at someone's eyes feels overwhelming (it's... sensorily overwhelming in a similar way to looking at the sun, except without that particular searing eye-pain).
Someone born unable to see doesn't get the same eye contact because they can't see the eyes in the first place.
Both would then end up with the same brain-effects of not having that eye contact.
I am a fan of the model of autism as a disorder of prediction, especially since recently Pawan Sinha measured some features which haven't been looked at before of motor impairment and sensory habituation impairment, are very much like his model predicted 6 years ago.
I feel it can be combined with Scott's and others' writing into a picture that autism and schizophrenia may be both disorders of "how much weight to put on top down priors", with autism defaulting to "too little" and schizophrenia to "too much".
Going on this model, it makes sense that vision during early childhood development is super important for calibrating your prediction machinery. If you literally can't see sensory input coming, you'll accept that the world is entirely unpredictable. That will lead to both 'passive' symptoms of autism (e.g. motor or sensory overload problems), and adaptive symptoms (like stimming or echolalia, which according to the prediction model are simply ways in which the child can create predictable sensory input in an otherwise scarily unpredictable world).
That said, this is a post-hoc justification and I don't know what I would have said if you asked me in advance whether blind kids are likelier to have ASD, so I will try hard to not update on this evidence.
Lacan's theories provide an interesting angle on these questions.
In Lacan, the ego (sense of self) arises from the child's visual field when the child identifies with an external object, such as its reflection, to provide an artificial unity to the chaos of bodily experience. So how does this sense of self arise for the blind child? Somehow the child would have to make object identifications with 'objects' constituted via a different sense, not the visual field. That seems worth exploring on its own.
The blind child would still be able to attain subjectivity, distinct from the ego or self, which arises in the linguistic field where we re-place and re-present ourselves with a signifier which can be recognized in the social realm. We alienate ourselves in language so we can traffic in symbols, and this 'I' in the linguistic field creates 'the subject.' Psychotics (schizophrenics) arises when this entrance into the linguistic field fails, and the psychotic ends up identifying too closely with language. There isn't enough of an alienation, so language starts to "speak them," in a manner of speaking. Hence the weirdly chaotic, incoherent, and boundless creativity of psychotic speech.
A potential fall out of my rambling -- how does the lack of sight contribute to not developing schizophrenia? Does sight somehow contribute to the potential failure to enter language successfully? Or, what if psychosis and autism are actually manifestations of the same structural phenomenon, but the lack of sight causes that failure to manifest as autism in one who is blind but manifest as schizophrenia in the one who possess sight? Super interesting topic that deserves further exploration from a psychoanalytic perspective.
I'm kind of curious how this interacts with aphantasia. It may be too hard to study, or I don't know how to look for studies about it, but anecdotally, I have total aphantasia, and I've worried on numerous occasions that my mind indulges in bouts of paranoia and "magical thinking" of the kind that is described by diagnostic criteria for schizophrenia. But ultimately, it seems like my ability to "roll to disbelieve" these things like intrusive thoughts, delusions, paranoid suspicions about conspiracies against me, etc, is pretty strong. They show up, I sometimes get tripped up by them briefly, but I notice it and dismiss the thoughts as "crazy" or "nonsense" rather than believe them strongly.
And then also, I notice that there's a really weird split between whether people immediately peg me as autistic. I've never been formally diagnosed, but seem to have a number of incidental traits (difficulty "tuning out" stimuli, preference for direct and explicit communication more than is considered "normal" or even "socially appropriate" in some contexts) that would seem to indicate being at least mildly fitting the description. I especially seem to have trouble intuitively grasping social norms about framing information in a way that will upset people, and I notice that the way people describe this to me (especially the people who get the most upset) sounds a lot like what I feel like when I notice intrusive thoughts. People have told me that I've said something that gave them really terrible imagery they can't get out of their heads, which I have a hard time understanding, not just because I don't literally get visual imagery, but also because it's easy for me to dismiss upsetting thoughts when they're not tethered to an unpleasant reality I actually have to deal with, much like I can disbelieve thoughts I come to think are delusional. I don't think people are just being overly sensitive, this really does seem to be a significant difference in how we process information, which is most stark with people who describe their mental processes as involving a lot of vivid visualization
This leads me to wonder whether a visual processing mode is just kind of inherently harder to dismiss. If your brain went to all the trouble of producing some imagery for you, it seems to me from the outside that this might make those thoughts associated with the imagery "stickier" in a way, harder to treat as meaningless or not change other beliefs to accomodate
Historically, it's been noticed that sensory deprivation helps bipolar mania as well. Here is a short story from 110 years ago mentioning this in passing
> He awoke at night. Everything was still; from the large neighboring room could be heard the breathing of the sleeping inmates. Somewhere from afar sounded a strange, monotonous voice. It was that of a patient conversing with himself in a dark room; and from the top floor—the women's department—a hoarse contralto was singing a wild song. The patient listened to these sounds. He felt a terrible weakness in all his organs; his neck pained him frightfully.
> "Where am I? What is the matter with me?" were the thoughts that came into his head, and suddenly, with an unusual vividness, there appeared before him the events of the past month, and he understood that he was ill and the nature of his illness. A whole row of disconnected thoughts, words and actions came into his memory, causing him to shudder in his entire body. "But this is ended, thank God, this is done," he muttered, and fell asleep again.
Perhaps sensory deprivation can help both over-sensitive and under-sensitive people by serving as a "turn it off, then turn it back on again" fix for the brain? There's always a certain amount of filtering to perception - noticing smaller and smaller sensations when they're the only things happening, or becoming numb to things in an active, crowded environment - like turning a volume dial to the comfortable level. When moving from no stimulation to a normal amount of stimulation, the brain might naturally "turn the dial" to a neurotypical level, and then whatever makes you autistic or schizophrenic gradually changes the dial to a different number.
Think of somebody with a messed-up sleep schedule. They're stressed out and exhausted, but in spite of being exhausted still can't sleep at a regular time! Then they go on a nice, relaxing vacation in an isolated valley off the grid, with sunset and sunrise their only clock. Their sleep schedule heals and they start to feel normal again. Emerging back to regular life, they're still well-rested and happy for a while, but it doesn't last - daily stress, a cup of coffee in the afternoon, late-night Netflix - gradually they become the same exhausted insomniac as before the vacation. If the things that make you autistic or schizophrenic work like caffeine and stress in this metaphor - gradual damage that builds up until you're in a maladaptive state - then "autism" and "schizophrenia" could be attractor states in the machinery of sensory processing. Sensory deprivation tanks are like the off-the-grid vacation, completely cutting you off from the damaging influence. There's no sensory processing failure with no senses to process. It doesn't matter whether you were going to process it too much or not enough, as long as the "reset" puts you substantially closer to normal - in the same way that the off-the-grid vacation fixes the insomniac's sleep schedule whether they were sleeping too soon in the day or too late before leaving for the valley.
I can't tell you how valuable it is for someone like you to discuss these issues with so much humility. I don't have to tell you how often people online promote themselves as experts while the real experts are the first to say that the answers aren't always clear. I have two kids with psychiatric issues and we love their doc because she is so transparent about how difficult it can be to find successful approaches to their issues.
I'm not a doc myself but I have picked up a lot from the parental sidelines, and I can't name a more informative site than yours.
I'm hoping the genes from my schizophrenic father are sorta balanced out by the high functioning autism-ish genes from my mother. So far so good. I'm in the richest 1% and never hallucinated anything.
So, a common-to-the-point-of-there-being-tiktok-videos-about-it talking point is that we autists notice _different_ things in social settings, and that this often violates expectations about what knowledge/information about mental states is public knowledge.
This makes people deeply uncomfortable, consistently. Which makes us uncomfortable, and prone to doing odd things to try to… not cause that.
Obviously there are a multitude of different ways it can play out, but this resonates with me.
The diametrical model of autism and schizophrenia is complete nonsense. I can't say I'm surprised, because autism research has suffered from a truly appalling lack of rigor for the last eighty years, but I'm disappointed to see Scott fall for it. A few counterarguments:
Autism becomes apparent in early childhood. Schizophrenia rarely becomes apparent before adolescence. And yes, I know there are certain personality traits that appear much earlier and can increase the risk of schizophrenia. A Slate Star Codex article I'm too lazy to look for linked to the experience of recovered psychotic Peter Chadwick, who described his "problematic hardware tendencies": narrow attentional beam, poor context processing resulting in social awkwardness, little ability to integrate thought and feeling, chronic anxiety and threat sensitivity. I would hardly describe those traits as the opposite of autism.
Some of the genes that increase autism risk also increase schizophrenia risk. I recently read "Hidden Valley Road," about a family with twelve children, six of whom were schizophrenic. Every member of the family who was tested had a gene associated with schizophrenia, autism, and bipolar disorder. One of the neurotypical family members went on to have a child with sensory processing disorder.
Schizophrenia can in some cases be medicated. There is no medication that can treat autism. Taking antipsychotics won't make a neurotypical autistic, and taking hallucinogens won't make an autistic neurotypical. (Source: I once hallucinated vividly as an uncommon Ativan side effect, and remained autistic the entire time.)
Not all autistics are oversensitive. Some are undersensitive. Some - probably the majority - are oversensitive and undersensitive in different areas. I'm sure you've heard of autistics who scream when touched, but barely react to actual injuries.
Also, this is a bit of a digression, but I'm sick of seeing autism described as a social disorder. People only think that because of a combination of the double empathy problem - empathizing with people who are different from you is hard, and if everyone is different from you, your inherent human shittiness will be more obvious - and terrible research that involves putting kids through highly artificial lab situations and assuming they'll react to real-world situations the same way. There's the Sally-Anne test, which trips up autistic kids and non-native speakers alike with its confusing sentence structures (and which a significant minority of autistic kids pass, but neurotypicals never mention that because it would get in the way of their sweeping generalizations). The "Reading the Mind in the Eyes" test, which ignores the minor detail that real people aren't static black-and-white photographs of actors' eyeballs with multiple choice options floating around them. Various tests that involve making kids watch a cartoon of a square shoving a triangle, or whatever, and treat the child as socially defective when he correctly states that squares don't have motives. Meanwhile, I'm part of the minority of autistics who actually do lack empathy, but I'm good enough with language and familiar enough with acting and storytelling conventions to pass most of these tests with flying colors. When will people realize that genuine empathy isn't something that can be tested in a lab?
If you talk about schizofrenia, know that these are people with halucation problems (chronic psychosis) AND are treated with poison, see for example zyprexa here: https://pubchem.ncbi.nlm.nih.gov/compound/Olanzapine The symptoms you see are not of schizofrenic people but of schizofrenic people treated with poison.
1a. The blindness-SZ thing is much less clear than it's popularly reported. The actual papers on it will freely shrug and say "Yeah, our evidence for this is pretty weak and heavily supplemented by anecdata". That's not to say it's not true -- it's probably at least adjacent to truth, because the "this should be a common enough comorbidity that the anecdata would be much less certain" argument is pretty strong (but see 1b). The big thing that gives pause here, though, is that much of both the data and anecdata is from parts of the world where two things are true: congenital blindness is very rare, and SZ is generally a disabling chronic illness causing lifelong medical dependency. In the parts of the world where congenital blindness is much more common, the association between SZ and long-term contact with medical frameworks is much weaker, and a lot of people can easily be "lost to follow-up".
1b: No one at all has bothered to look at (though one group, as far as I can tell, has bothered to complain that no one is looking at) by far the single most important thing you would want to look at for this hypothesis: whether blind people are less *schizotypal* than the general population. There's little good excuse at this point to look at SZ as a random thing that Just Happens Sometimes in neurotypical young adults rather than as a semi-common [progression/adaptation] in a common neurodivergence that may or may not be clinically relevant before, but, well, here we are. Whether blind people are less schizotypal or not is the absolute core of the blindness-SZ speculation, and it has completely different consequences for whether this is likely to be a real effect, what it theoretically means, what it might clinically mean, etc.
2a. "Some people are diagnosed with both schizophrenia and autism" is one way of saying it. Another way of saying it is that about 8-15% of autistic adults fit SZ criteria in meta-analyses and as many as 40% in some individual studies. That is, that the risk is about the same as having an SZ parent (and in some samples to having *two* SZ parents). When I corner imprinted-brain/diametrical types and ask them to explain this, I tend to get some stammering about how high-functioning autism is akshully super misdiagnosed and none of those people were ever autistic at all. I am very sympathetic to explanations of weird shit that just look like "yeah, autism diagnosis is atrocious" (see below), but I think this requires much more bullet-biting than any of those parties actually think through; if you assume as in genpop that there are 2-3 people fitting schizotypal PD criteria for each person fitting schizophrenia criteria, you quickly ring up numbers where you'd just have to shrug and go "Yeah, high-functioning autism basically doesn't exist and it's all misdiagnosed schizotypes". I don't think this accurately represents the schizo-autistic spectra range -- even if I bite the bullet on myself and go "those can't overlap, I was always just schizotypal and there's some purely schizospec explanation for my autism-specific characteristics", I've certainly met people who are clearly and entirely on the other one. If you *don't* force yourself to bite really bad bullets for thought experiments just because they're common in pop-psych, I am definitely confident in the existence of distinct spectrum edges *and* their overlap.
2b. Has anyone sat down and read the schizotypal PD criteria? Or talked to a schizotypal person? I can't imagine doing that and coming away with the takeaway that these are unimaginably different, mutually exclusive conditions. Imprinted-brain/diametrical claims about the schizospec consistently strike me as written by people who have no clue at all what the schizospec is and how people on it act, especially when those people are not floridly schizophrenic. (There is still not much better excuse for a "schizospec but only full-blown SZ and everything else is vaguely backfilled" model than an "autism but only the most severe forms of autism and everything else is vaguely backfilled" model.)
2c. The autism-SZ associations are even stronger in childhood-onset SZ, which is generally conceptualised as a more "core" form of the neurotype that digs more directly at the neurological things going on underneath. Most children with COS fit PDD criteria premorbidly, and a substantial proportion fit full autistic criteria.
3. Routing around to the opposite end of Screwy Diagnosis: I've read a lot on autism diagnosis with pre-existing substantial disability in other fields, whether sensory, cognitive, motor, or otherwise. I've come to the conclusion I don't trust any such study as far as I can throw it. The children fitting ASD criteria here were more disabled on just about every axis, which is the case in ~every such sample; as long as ASD continues to essentially supplant intellectual disability alone as the diagnosis of choice for people fitting the latter criteria, I can't look at the sample characteristics here and go "Yes, this is clearly, obviously getting at a neurotype more complex than 'people with low birth rates, cerebral palsy, more signs of underlying brain damage, and lower socioeconomic status are more disabled than people without those characteristics'".
4. Until earlier this year, the Wikipedia article for the imprinted brain hypothesis -- that is, the first thing any random reader was likely to encounter researching this topic -- was a glowing hagiography with a fuckoff-huge table correlating random primary studies that didn't say the things they were represented as saying at all to the hallowed hypothesis cast down by angels, and featuring huge positive block quotes about this revolutionary new theory that was extremely true and about to rewrite psychiatry from the ground up. It looked like that for ten years. It no longer looks like that. I'm looking forward to seeing the long-term consequences.
Unrelated, and I don't have access to the article, but couldn't the low prevalence of smoking in autistic people also be caused by the effects of lower ability to socialize, not just (or even necessarily) biology?
I was born with one eye. I also believe I am slightly autistic. I am a schizoid personality but the relationship between schizoid and schizophrenia is not conclusive. I can relate a lot to this post and the comments. For me it is a chicken and egg thing as in are some of the things mentioned in the post and comments biology i.e. a result of my partial blindness and other genetic issues or did my lack of socialization due to my self consciousness of having a prosthetic eye as a child contribute to my schizoidness, autism, sensitivities, etc. As a child it was obvious that I had a prosthetic eye so I was teased and bullied a lot. Also my parents both worked in the evenings so I was not socialized much as a child. Fully adult it is much less obvious as my prosthetic eye, eye lid, etc look no different than my good eye. Even without my birth defect I have always felt different. So did my partial blindness contribute to my autism and schizoid personality? Yes but having studied a considerable amount of neuroscience I believe it is also in my innate biology not necessarily hereditary. I also think it is partially due to birth trauma and prenatal environment as my mother had a difficult pregnancy. So again genes and environment. Like the rest of us it is a combination of factors that made me who I am. Thanks again for this post it help me understand myself a bit more even at 62 years old.
Just spit-balling, but I wonder how schizophrenics, autistics and the blind experience inner speech the same or differently. Might the inner voice as a focal point be probative?
About schizophrenics' heavy smoking: Knew some researchers 20 yrs ago who believed the smoking was actually driven by one of the med side effects of the drugs most commonly given then for schizophrenia -- akasthisia. Nicotine apparently gives some relief from akasthisia. Don't know whether this theory has held up, though.
wonder if its possible that autism is at its core a kind of sensory overactivation. That the brain dedicates too much effort to processes most automate away. This for me would explain the pathological rationality, as well as the correlation with blindness (as blindness would require a heightened sensitivity of the remaining senses).
Epistemic status: speculative (as in: I'm a mechanical engineer and read papers on predictive processing as a hobby, let's wait for some sane people to weigh in on this)
We don't know what autism actually is, but predictive processing (PP) offers some theories. Yon and Frith 2021 explain that "characteristics of autism (e.g., a preference for stable and repetitive environments) can be cast as an consequence of overly-strong beliefs about the precision of incoming evidence - where every fluctuation in our sensory system seems to signal the need to change our models of the environment (i.e., the world seems unstable)." (1). The causal direction is not really clear to me, maybe high expected sensory precision leads to bad generalization capabilities and strong reliance on bottom-up sensory input, maybe it's the other way around? Beren Millidge's master thesis (2017) has a theory on a potential neural basis for Autistic Spectrum Disorders: "It argues that the observed pattern of long-range underconnectivity and local overconnectivity observed in ASD, when instantiated in a predictive processing framework, will lead to impoverished high level regions and lower-level regions which down-weight prior information coming from above and prioritise incoming immediate sensory information. This pattern is hypothesised to result in many behaviours recognised in autism such as sensory hy- persensitivity, a local, detailed-oriented processing style, and a preference towards predictable behaviours and routines." (2)
I'm even more confused on the schizophrenia side of the story. The best discussion I've seen so far is (3), which ties PP and the diametric model together and compares schizotypy to an underfitting strategy in machine learning: "One of the downsides of the generalization function of positive schizotypy is apophenia. It is considered the predisposition to false positives: if you have noisy data and you want to see a pattern in the data, you need to be giving a low weight to sensory input - that's the only way you're going to find the line of best fit. The downside: well, you're also going to sometimes see patterns that aren't actually there. You're essentially imposing your assumptions onto the data and you're imposing your model onto the world." (I'm not so happy with this source here, I just don't have anything better right now)
Now I don't see any way of looking at the theory above and coming up with a prediction of low schizophrenia and high autism rates for blind people. So let's push our luck and see if we at least in retrospect fit this together and come up with a few follow-up predictions.
I'd be really surprised if autism leads to blindness. Let's try to reverse the causal arrow: could blindness lead to autism? I'm not sure either, but to get the ideas started: there's an ongoing discussion of how exactly the brain learns in young children. Think of it as a nature vs nurture question: either you provide a genetically encoded brain for an infant (e.g. for animals who can walk right from day one) or you only provide some brain infrastructure and have the system learn on it's own (e.g. cats that fail to see horizontal stripes if they don't encounter them in the first weeks of life). There's some plausibility the human brain might be similar, especially when brain regions are missing at birth with the brain routing around this issue. Soooo maybe, by being blind, the brain reuses the area intended for visual processing and this kinda shifts the whole brain balance to a higher-autism structure?
You can find both links to the source papers and some discussion on r/predictiveprocessing:
Scott sez: “Maybe blindness makes children seem more autistic in some boring, mechanical sense? Like maybe if you can’t read other people’s body language or even consistently know where they are, it’s hard to be social and so you don’t interact with other people and that seems autistic to people trying to diagnose you?”
Here’s a proposal for how blindness could make children actually be more autistic in a real and interesting sense: Their inability to see what other people are doing, and especially their inability to see faces, results in their having a very substantially impoverished feed of information about people and the rest of the world. They suffer from a sort of cognitive malnutrition that causes autistic-like stunted and abnormal development in many areas; or produces full-on autism.
Babies are wired to pay attention to faces: Even as newborns they are especially attentive to faces, and they become able to recognize their caregivers very early, at about 2 months I believe. The responses they see on faces are crucial data to them, and if their caregiver suddenly goes deadpan they become desperate and disorganized (Still Face Experiment, https://www.youtube.com/watch?v=apzXGEbZht0). As they learn to navigate the world, the facial expressions of observers are important data for them (Visual Cliff Experiment, https://www.youtube.com/watch?v=p6cqNhHrMJA). The approval, disapproval, fear or even just friendly interest they see on the faces around them gives them information and probably also makes the explorations more satisfying. And of course babies and toddlers don’t just see faces looking at them with various expressions, they also see people with faces they recognize doing all kinds of stuff. Maybe the interpersonal data about visually recognizable people — what the people did, how they looked at me when I did this and that — even forms the framework on which hangs all the rest of the what people learn about how things work. Even if it does not, it must be very important.
Consider the situation of a blind baby: She lives perpetually in the Still Face Experiment. She navigates life’s visual cliffs without being able to see whether her caregiver is enthusiastic or terrified. She toddles around without the benefit of seeing smiling and interested faces observing her. She never gets to see anybody else do anything at all. It doesn’t seem terribly surprising to me that growing up with this very impoverished feed of info about one’s own actions and about life in general leads to social deficits and also deficits in using the body, using objects, activity level, flexibility, adaptability etc. Of course, caregivers can mitigate the damage by staying in touch with the young child via other channels — touch, speech, etc. Still, if we are born wired to tune into faces and to use them as a portal to learning everything else, it may not be possible to make up the visual-interpersonal shortfall via other channels. That shortfall could account for the high-frequency of autistic-like traits even in blind kids who are not actually autistic.
What does this theory have to say about sighted babies who develop into autistic children? Well, maybe they are born with something wrong with the face-processing parts of their brain. Maybe they are born without the wiring that makes them interested in faces, good at recognizing different people, naturally predisposed to be highly responsive to affective displays on the faces of others, naturally interested in the activities of facially recognizable others.
And about that Hobson and Bishop paper: Yeah, it’s really blurry-minded. My theory, above, may or may not have been what they were trying to get at. I did wonder, after reading it, why they had not examined the literature on the development of infants blind from birth. There must be a substantial body of research, and also a bunch of stuff out there, not all of it wrong-headed, about how to foster the development of blind babies. For them not to have incorporated any of this info into their study seems sort of — well, impoverished and rigid, if not frankly autistic. We should not make that mistake ourselves.
Wow. Too much new information for me. One silly question. Is someone working on a drug/thing that replaces smoking for schizophrenics so they don't incur the downside cancer risk of smoking? (As a x-smoker, cigs are both a drug and a thing to do. I sometimes miss the 'thing to do' part of smoking.)
More trivia from what I'm currently reading: 'Visually impaired people usually have more sensitive photoreceptors, which react very sensitively to every slight change in light. This is also one reason why depression (seasonal affective disorder, or SAD), a condition that is linked to, among other things, disturbed melatonin production, affects them three times as often.'
Scott, are you aware of Dehaene's theory that schizophrenia is caused by an impaired consciousness? More precisely, because the threshold for perception to become conscious is higher than in neurotypicals? The difference is ridiculously strong, e.g. here:
Perhaps cutting away a large part of perception makes it easier for other perceptions to propagate to consciousness, because there are less competitors.
I am not sure how this relates to an axis schizophrenia-autism, but Clark's theory from "Surfing Uncertainty" is that autism is caused by too much error signal propagating upwards. Or rather, by too low thresholds for error signals to propagate upwards, so that it happens all the time.
Oversimplifying, perhaps schizophrenics are people with too little consciousness, while autistics are people with too much consciousness.
Adding a neuroscience viewpoint on sensory deprivation:
One effect of the day/sleep cycle is that synapses become on average stronger during daytime, and become weaker (go back to baseline?) during sleep. The homeostatic theory of sleep says that this is one of the reasons for sleep.
Sensory deprivation has the same effect. Your synapse strengths become weaker during sensory deprivation. At least some studies claim that.
There are lots of theories of autism and schizophrenia where signal strengths play a role, so this invites endless speculations on the interplay between sleep/sensory deprivation/signal strength/autism/schizophrenia.
I see a lot of comments here about blindfolding, sleep, sensory deprivation. Has anyone ever tried anesthesia? There is no clearer analog of just turning if off and back on again for the human brain. Is it considered too dangerous to be used outside of surgery where it is absolutely necessary? Surely, it isn't more dangerous than electroshock therapy. Is it just no history of collaboration between psychiatrists and anesthesiologists?
I don't nearly have the means in terms of domain knowledge or journal access to do a real lit review, but a web search seems to indicate there are potentially dangerous interactions between anesthesia and antipsychotic drugs. I can't quickly find any indication of whether anyone has ever tried to use anesthesia as an actual treatment *before* the patient has a lifelong history of taking antipsychotics. I suppose one problem is this would be extremely expensive compared to things like electrocuting or blindfolding a person.
I have a relative who experiences Intense Imagery Movements (IIM; https://pubmed.ncbi.nlm.nih.gov/26561043/). Because of frequent stimming, he was checked out for autism by a neurologist as a toddler. He's definitely not on the spectrum and actually is quite empathetic and insightful about others' emotional states. Nevertheless, as he's grown older, we've noted many autism-adjacencies and similar sensitivities. For instance, he has deep sensitivities to various sounds and tactile experiences.
The idea that there are constellations of related neurological conditions that manifest differently makes a lot of sense IMHO.
Also I wonder if the congenitally deaf have higher rates of schizophrenia. I had 3 deaf patients on decanoates at our clinic, and none just there for depression/anxiety. Though maybe deaf people with depression/schizophrenia go to places staffed with people who use sign language.
As an autistic person, this is possibly relevant: Until I was fifteen or so, I would walk around the house blindfolded (or with my eyes shut tight) quite often, as a way to relax. I never knew any other autistic people to ask if they did something similar, but I'd be interested to find out!
On a related note - I've thought about the possibility of treating auditory hallucinations in schizophrenia patients using some sort of sensory substitution (see https://eagleman.com/science/sensory-substitution/ - he even has a TED talk!). Maybe having something vibrate when speech is recognized would help patients recognize hallucinated speech as such, and eventually something something predictive coding would lead to having weaker beliefs regarding inner speech. It might also be interesting to think of utilizing some form of sensory substitution in autistic people
The levels of melatonin depend strongly on the visual cues, that blind people lack. I wasn't able to get a full picture of how melatonin levels fluctuate in blind vs non-blind people, but there surely is a difference, that's probably most pronounced when it comes to rare, non-standard situation: let's say staying in a brightly lit room long past sunset would create a strong deviation in melatonin cycle in non-blind person but not in a blind person.
The dopaminergic theory of schizophrenia is far from a complete explanation. In fact it can be posed that D2 antagonists simply mask the disease as they largely don't revert schizophrenics to normal functioning.
The alternative theory of schizophrenia involves glutamate receptors. Now, there is a multitude of interactions between melatonin and glutaminergic system in the brain and it's hard to tell which interaction, if any, would explain the lack of schizophrenia in patients that aren't strongly affected by light, ie. for example blind people.
One potential link is that melatonin is a potent neuroprotector in cases of glutaminergic excitotoxicity. So one hypothesis here can be that non-blind people are at risk of being exposed to bright light and consequently having low levels of melatonin. And then in the case of increased glutamate secretion they wouldn't be protected from excitoxicity and subsequent death of certain neurons.
I'm far for claiming that this particular hypothesis has much chance of turning true. But I have a fairly strong belief in that melatonin and glutamate are strongly implicated in the biological basis of schizophrenia.
Intuitively, it looks to me (someone with zero expertise in the matter) like schizophrenia is a deficit of recursive processing in the brain relative to the amount of sensory input, and autism is an excess of the same. Consider what we might expect for different amounts of recursive processing versus sensory input:
(1) Too little recursion: inability to stay on topic (which looks like disorganized thought and lack of concentration), inadequate processing of thoughts (which looks like failure to distinguish between thoughts, impressions, and reality) and too direct translation of sense data into action (which looks like lack of internal motivation in unstimulating environments but flighty, compulsive behavior in stimulating ones)
(2) Low-ish but healthy amounts of recursion being handled well: somewhat reduced processing of thoughts (which looks like an intuitive or artistic style), reduced constraints the brain is trying to satisfy (which looks like uninhibitedness, confidence, and creativity), relative quickness changing topics in a conversation, relatively more effort put into finding or creating a stimulating environment
(3) Normal amounts of recursion - most folk (the baseline for comparison)
(4) High-ish but healthy amounts of recursion being handled well: somewhat increased processing of thoughts (which looks like an analytical or rational style), increased constraints the brain is trying to satisfy (which looks like inhibitions, awkwardness, and uncreativity), relative slowness moving on to new topics in a conversation, relatively less effort put into finding or creating a stimulating environment
(5) Too much recursion: leading to cyclic bodily motions, getting stuck on a topic obsessively, sometimes failing to respond to external stimuli, and sometimes experiencing painful sensory feedback analogous to a microphone screech.
I'd expect sensory deprivation to help people at (5) mainly by preventing the painful sensory feedback, maybe also thereby letting them relax and spare thought to control their other symptoms, and to help people at (1) mainly by making internal motivation the "loudest" remaining input, giving them a chance to focus.
A big chunk of the brain is dedicated to processing vision, so maybe congenitally blind people can re-purpose enough of that they all have enough processing capacity to spare, keeping them out of group (1).
TBH, the reason this account comes to mind is because of the effects of cannabis. Google tells me cannabis probably helps autists and definitely makes schizophrenia worse. From a (4)-ish starting point, cannabis makes me feel like much of my working memory has been turned off, and as a result I get reduced ability to concentrate, a more intuitive/less rational style, fewer inhibitions and more creativity, and even twinges of paranoid ideation that feel like my insecurities getting a free pass to invade my brain instead of being quashed as obviously unjustified.
Have people tried asking schizophrenics to wear blindfolds 12 hours a day?
I think there is really something to the fundamental axis of autism vs schizophrenia being understimulation vs overstimulation. Autistics are understimulated and so never get used to high levels of stimulation and are easily overwhelmed by them, but on the other hand have a quiet working environment inside their heads that's useful for intellectual work. Schizophrenics are overstimulated and so learn to pull complex patterns out of noisy data, but then end up also finding a lot of patterns that aren't really there.
How do we know there's not some boring allele that increases rates of both congenital blindness and autism?
I have no intelligent insights into any of these phenomenon. I just want to say they are very interesting and I intend them a topic of conversation among smart people at dinner parties soon.
My conjecture is that:
1) A lot of ASD symptoms are secondary or tertiary from "real ASD genes/phenotypes" - specifically, they are the end of a chain of dominoes emanating from some other thing 'directly caused' by the ASD-causing genes.
2) Congential blindness, via a different pathway, tends to knock over such an early domino, and thus ends up propagating outward into the symptoms knocked over
Like, to throw out a random sounds-good-story to illustrate perhaps what I might mean - suppose that not making eye contact in some critical range makes some brain-development thing go wonky in a small set of ways.
Someone with ASD might find not make that eye contact because (like myself) looking at someone's eyes feels overwhelming (it's... sensorily overwhelming in a similar way to looking at the sun, except without that particular searing eye-pain).
Someone born unable to see doesn't get the same eye contact because they can't see the eyes in the first place.
Both would then end up with the same brain-effects of not having that eye contact.
Schizophrenia is a disease that causes one to find social patterns where none exist.
Autism is a disease that inhibits one from finding social patterns that are obvious to others.
I am a fan of the model of autism as a disorder of prediction, especially since recently Pawan Sinha measured some features which haven't been looked at before of motor impairment and sensory habituation impairment, are very much like his model predicted 6 years ago.
https://www.pnas.org/content/111/42/15220
I feel it can be combined with Scott's and others' writing into a picture that autism and schizophrenia may be both disorders of "how much weight to put on top down priors", with autism defaulting to "too little" and schizophrenia to "too much".
Going on this model, it makes sense that vision during early childhood development is super important for calibrating your prediction machinery. If you literally can't see sensory input coming, you'll accept that the world is entirely unpredictable. That will lead to both 'passive' symptoms of autism (e.g. motor or sensory overload problems), and adaptive symptoms (like stimming or echolalia, which according to the prediction model are simply ways in which the child can create predictable sensory input in an otherwise scarily unpredictable world).
That said, this is a post-hoc justification and I don't know what I would have said if you asked me in advance whether blind kids are likelier to have ASD, so I will try hard to not update on this evidence.
Lacan's theories provide an interesting angle on these questions.
In Lacan, the ego (sense of self) arises from the child's visual field when the child identifies with an external object, such as its reflection, to provide an artificial unity to the chaos of bodily experience. So how does this sense of self arise for the blind child? Somehow the child would have to make object identifications with 'objects' constituted via a different sense, not the visual field. That seems worth exploring on its own.
The blind child would still be able to attain subjectivity, distinct from the ego or self, which arises in the linguistic field where we re-place and re-present ourselves with a signifier which can be recognized in the social realm. We alienate ourselves in language so we can traffic in symbols, and this 'I' in the linguistic field creates 'the subject.' Psychotics (schizophrenics) arises when this entrance into the linguistic field fails, and the psychotic ends up identifying too closely with language. There isn't enough of an alienation, so language starts to "speak them," in a manner of speaking. Hence the weirdly chaotic, incoherent, and boundless creativity of psychotic speech.
A potential fall out of my rambling -- how does the lack of sight contribute to not developing schizophrenia? Does sight somehow contribute to the potential failure to enter language successfully? Or, what if psychosis and autism are actually manifestations of the same structural phenomenon, but the lack of sight causes that failure to manifest as autism in one who is blind but manifest as schizophrenia in the one who possess sight? Super interesting topic that deserves further exploration from a psychoanalytic perspective.
A bit off topic but related in the sense of “Hmm, that’s interesting”
James Fadiman’s micro dosing site says that people who are red green color blind should not micro dose.
“People with colorblindness report lasting visual distortions from microdosing”
https://sites.google.com/view/microdosingpsychedelics/faq-on-microdosing
So this may be a dumb question, but I take from all this that Schizophrenia and Autism is never diagnosed in the same person either?
> more likely to get autism
Why does this seem like weird phrasing to me? It feels like it should say "more likely to have autism", but I'm not really sure why.
Scott,
This website says that schizophrenia rates may be three times higher than normal in autistic people.
https://www.spectrumnews.org/news/schizophrenia-prevalence-may-threefold-higher-people-autism/
Is the spectrum model, where Autism lies on one end and Schizophrenia on the other, fundamentally misleading?
I'm kind of curious how this interacts with aphantasia. It may be too hard to study, or I don't know how to look for studies about it, but anecdotally, I have total aphantasia, and I've worried on numerous occasions that my mind indulges in bouts of paranoia and "magical thinking" of the kind that is described by diagnostic criteria for schizophrenia. But ultimately, it seems like my ability to "roll to disbelieve" these things like intrusive thoughts, delusions, paranoid suspicions about conspiracies against me, etc, is pretty strong. They show up, I sometimes get tripped up by them briefly, but I notice it and dismiss the thoughts as "crazy" or "nonsense" rather than believe them strongly.
And then also, I notice that there's a really weird split between whether people immediately peg me as autistic. I've never been formally diagnosed, but seem to have a number of incidental traits (difficulty "tuning out" stimuli, preference for direct and explicit communication more than is considered "normal" or even "socially appropriate" in some contexts) that would seem to indicate being at least mildly fitting the description. I especially seem to have trouble intuitively grasping social norms about framing information in a way that will upset people, and I notice that the way people describe this to me (especially the people who get the most upset) sounds a lot like what I feel like when I notice intrusive thoughts. People have told me that I've said something that gave them really terrible imagery they can't get out of their heads, which I have a hard time understanding, not just because I don't literally get visual imagery, but also because it's easy for me to dismiss upsetting thoughts when they're not tethered to an unpleasant reality I actually have to deal with, much like I can disbelieve thoughts I come to think are delusional. I don't think people are just being overly sensitive, this really does seem to be a significant difference in how we process information, which is most stark with people who describe their mental processes as involving a lot of vivid visualization
This leads me to wonder whether a visual processing mode is just kind of inherently harder to dismiss. If your brain went to all the trouble of producing some imagery for you, it seems to me from the outside that this might make those thoughts associated with the imagery "stickier" in a way, harder to treat as meaningless or not change other beliefs to accomodate
Historically, it's been noticed that sensory deprivation helps bipolar mania as well. Here is a short story from 110 years ago mentioning this in passing
https://en.wikisource.org/wiki/A_Red_Flower (a beautiful if sad read, well worth it).
> He awoke at night. Everything was still; from the large neighboring room could be heard the breathing of the sleeping inmates. Somewhere from afar sounded a strange, monotonous voice. It was that of a patient conversing with himself in a dark room; and from the top floor—the women's department—a hoarse contralto was singing a wild song. The patient listened to these sounds. He felt a terrible weakness in all his organs; his neck pained him frightfully.
> "Where am I? What is the matter with me?" were the thoughts that came into his head, and suddenly, with an unusual vividness, there appeared before him the events of the past month, and he understood that he was ill and the nature of his illness. A whole row of disconnected thoughts, words and actions came into his memory, causing him to shudder in his entire body. "But this is ended, thank God, this is done," he muttered, and fell asleep again.
Perhaps sensory deprivation can help both over-sensitive and under-sensitive people by serving as a "turn it off, then turn it back on again" fix for the brain? There's always a certain amount of filtering to perception - noticing smaller and smaller sensations when they're the only things happening, or becoming numb to things in an active, crowded environment - like turning a volume dial to the comfortable level. When moving from no stimulation to a normal amount of stimulation, the brain might naturally "turn the dial" to a neurotypical level, and then whatever makes you autistic or schizophrenic gradually changes the dial to a different number.
Think of somebody with a messed-up sleep schedule. They're stressed out and exhausted, but in spite of being exhausted still can't sleep at a regular time! Then they go on a nice, relaxing vacation in an isolated valley off the grid, with sunset and sunrise their only clock. Their sleep schedule heals and they start to feel normal again. Emerging back to regular life, they're still well-rested and happy for a while, but it doesn't last - daily stress, a cup of coffee in the afternoon, late-night Netflix - gradually they become the same exhausted insomniac as before the vacation. If the things that make you autistic or schizophrenic work like caffeine and stress in this metaphor - gradual damage that builds up until you're in a maladaptive state - then "autism" and "schizophrenia" could be attractor states in the machinery of sensory processing. Sensory deprivation tanks are like the off-the-grid vacation, completely cutting you off from the damaging influence. There's no sensory processing failure with no senses to process. It doesn't matter whether you were going to process it too much or not enough, as long as the "reset" puts you substantially closer to normal - in the same way that the off-the-grid vacation fixes the insomniac's sleep schedule whether they were sleeping too soon in the day or too late before leaving for the valley.
"Still, as far as we can tell that’s not it."
I can't tell you how valuable it is for someone like you to discuss these issues with so much humility. I don't have to tell you how often people online promote themselves as experts while the real experts are the first to say that the answers aren't always clear. I have two kids with psychiatric issues and we love their doc because she is so transparent about how difficult it can be to find successful approaches to their issues.
I'm not a doc myself but I have picked up a lot from the parental sidelines, and I can't name a more informative site than yours.
I'm hoping the genes from my schizophrenic father are sorta balanced out by the high functioning autism-ish genes from my mother. So far so good. I'm in the richest 1% and never hallucinated anything.
So, a common-to-the-point-of-there-being-tiktok-videos-about-it talking point is that we autists notice _different_ things in social settings, and that this often violates expectations about what knowledge/information about mental states is public knowledge.
This makes people deeply uncomfortable, consistently. Which makes us uncomfortable, and prone to doing odd things to try to… not cause that.
Obviously there are a multitude of different ways it can play out, but this resonates with me.
The diametrical model of autism and schizophrenia is complete nonsense. I can't say I'm surprised, because autism research has suffered from a truly appalling lack of rigor for the last eighty years, but I'm disappointed to see Scott fall for it. A few counterarguments:
Autism becomes apparent in early childhood. Schizophrenia rarely becomes apparent before adolescence. And yes, I know there are certain personality traits that appear much earlier and can increase the risk of schizophrenia. A Slate Star Codex article I'm too lazy to look for linked to the experience of recovered psychotic Peter Chadwick, who described his "problematic hardware tendencies": narrow attentional beam, poor context processing resulting in social awkwardness, little ability to integrate thought and feeling, chronic anxiety and threat sensitivity. I would hardly describe those traits as the opposite of autism.
Some of the genes that increase autism risk also increase schizophrenia risk. I recently read "Hidden Valley Road," about a family with twelve children, six of whom were schizophrenic. Every member of the family who was tested had a gene associated with schizophrenia, autism, and bipolar disorder. One of the neurotypical family members went on to have a child with sensory processing disorder.
Schizophrenia can in some cases be medicated. There is no medication that can treat autism. Taking antipsychotics won't make a neurotypical autistic, and taking hallucinogens won't make an autistic neurotypical. (Source: I once hallucinated vividly as an uncommon Ativan side effect, and remained autistic the entire time.)
Not all autistics are oversensitive. Some are undersensitive. Some - probably the majority - are oversensitive and undersensitive in different areas. I'm sure you've heard of autistics who scream when touched, but barely react to actual injuries.
Also, this is a bit of a digression, but I'm sick of seeing autism described as a social disorder. People only think that because of a combination of the double empathy problem - empathizing with people who are different from you is hard, and if everyone is different from you, your inherent human shittiness will be more obvious - and terrible research that involves putting kids through highly artificial lab situations and assuming they'll react to real-world situations the same way. There's the Sally-Anne test, which trips up autistic kids and non-native speakers alike with its confusing sentence structures (and which a significant minority of autistic kids pass, but neurotypicals never mention that because it would get in the way of their sweeping generalizations). The "Reading the Mind in the Eyes" test, which ignores the minor detail that real people aren't static black-and-white photographs of actors' eyeballs with multiple choice options floating around them. Various tests that involve making kids watch a cartoon of a square shoving a triangle, or whatever, and treat the child as socially defective when he correctly states that squares don't have motives. Meanwhile, I'm part of the minority of autistics who actually do lack empathy, but I'm good enough with language and familiar enough with acting and storytelling conventions to pass most of these tests with flying colors. When will people realize that genuine empathy isn't something that can be tested in a lab?
If you talk about schizofrenia, know that these are people with halucation problems (chronic psychosis) AND are treated with poison, see for example zyprexa here: https://pubchem.ncbi.nlm.nih.gov/compound/Olanzapine The symptoms you see are not of schizofrenic people but of schizofrenic people treated with poison.
Thoughts, roughly itemized:
1a. The blindness-SZ thing is much less clear than it's popularly reported. The actual papers on it will freely shrug and say "Yeah, our evidence for this is pretty weak and heavily supplemented by anecdata". That's not to say it's not true -- it's probably at least adjacent to truth, because the "this should be a common enough comorbidity that the anecdata would be much less certain" argument is pretty strong (but see 1b). The big thing that gives pause here, though, is that much of both the data and anecdata is from parts of the world where two things are true: congenital blindness is very rare, and SZ is generally a disabling chronic illness causing lifelong medical dependency. In the parts of the world where congenital blindness is much more common, the association between SZ and long-term contact with medical frameworks is much weaker, and a lot of people can easily be "lost to follow-up".
1b: No one at all has bothered to look at (though one group, as far as I can tell, has bothered to complain that no one is looking at) by far the single most important thing you would want to look at for this hypothesis: whether blind people are less *schizotypal* than the general population. There's little good excuse at this point to look at SZ as a random thing that Just Happens Sometimes in neurotypical young adults rather than as a semi-common [progression/adaptation] in a common neurodivergence that may or may not be clinically relevant before, but, well, here we are. Whether blind people are less schizotypal or not is the absolute core of the blindness-SZ speculation, and it has completely different consequences for whether this is likely to be a real effect, what it theoretically means, what it might clinically mean, etc.
2a. "Some people are diagnosed with both schizophrenia and autism" is one way of saying it. Another way of saying it is that about 8-15% of autistic adults fit SZ criteria in meta-analyses and as many as 40% in some individual studies. That is, that the risk is about the same as having an SZ parent (and in some samples to having *two* SZ parents). When I corner imprinted-brain/diametrical types and ask them to explain this, I tend to get some stammering about how high-functioning autism is akshully super misdiagnosed and none of those people were ever autistic at all. I am very sympathetic to explanations of weird shit that just look like "yeah, autism diagnosis is atrocious" (see below), but I think this requires much more bullet-biting than any of those parties actually think through; if you assume as in genpop that there are 2-3 people fitting schizotypal PD criteria for each person fitting schizophrenia criteria, you quickly ring up numbers where you'd just have to shrug and go "Yeah, high-functioning autism basically doesn't exist and it's all misdiagnosed schizotypes". I don't think this accurately represents the schizo-autistic spectra range -- even if I bite the bullet on myself and go "those can't overlap, I was always just schizotypal and there's some purely schizospec explanation for my autism-specific characteristics", I've certainly met people who are clearly and entirely on the other one. If you *don't* force yourself to bite really bad bullets for thought experiments just because they're common in pop-psych, I am definitely confident in the existence of distinct spectrum edges *and* their overlap.
2b. Has anyone sat down and read the schizotypal PD criteria? Or talked to a schizotypal person? I can't imagine doing that and coming away with the takeaway that these are unimaginably different, mutually exclusive conditions. Imprinted-brain/diametrical claims about the schizospec consistently strike me as written by people who have no clue at all what the schizospec is and how people on it act, especially when those people are not floridly schizophrenic. (There is still not much better excuse for a "schizospec but only full-blown SZ and everything else is vaguely backfilled" model than an "autism but only the most severe forms of autism and everything else is vaguely backfilled" model.)
2c. The autism-SZ associations are even stronger in childhood-onset SZ, which is generally conceptualised as a more "core" form of the neurotype that digs more directly at the neurological things going on underneath. Most children with COS fit PDD criteria premorbidly, and a substantial proportion fit full autistic criteria.
3. Routing around to the opposite end of Screwy Diagnosis: I've read a lot on autism diagnosis with pre-existing substantial disability in other fields, whether sensory, cognitive, motor, or otherwise. I've come to the conclusion I don't trust any such study as far as I can throw it. The children fitting ASD criteria here were more disabled on just about every axis, which is the case in ~every such sample; as long as ASD continues to essentially supplant intellectual disability alone as the diagnosis of choice for people fitting the latter criteria, I can't look at the sample characteristics here and go "Yes, this is clearly, obviously getting at a neurotype more complex than 'people with low birth rates, cerebral palsy, more signs of underlying brain damage, and lower socioeconomic status are more disabled than people without those characteristics'".
4. Until earlier this year, the Wikipedia article for the imprinted brain hypothesis -- that is, the first thing any random reader was likely to encounter researching this topic -- was a glowing hagiography with a fuckoff-huge table correlating random primary studies that didn't say the things they were represented as saying at all to the hallowed hypothesis cast down by angels, and featuring huge positive block quotes about this revolutionary new theory that was extremely true and about to rewrite psychiatry from the ground up. It looked like that for ten years. It no longer looks like that. I'm looking forward to seeing the long-term consequences.
Unrelated, and I don't have access to the article, but couldn't the low prevalence of smoking in autistic people also be caused by the effects of lower ability to socialize, not just (or even necessarily) biology?
Is it possible that Tourette syndrome deserves a place in this constellation?
https://en.wikipedia.org/wiki/Tourette_syndrome
> I don’t know what’s up with the echolalia
Phonological loop things maybe? Caching stuff while you process audio input for more than just the speech?
I was born with one eye. I also believe I am slightly autistic. I am a schizoid personality but the relationship between schizoid and schizophrenia is not conclusive. I can relate a lot to this post and the comments. For me it is a chicken and egg thing as in are some of the things mentioned in the post and comments biology i.e. a result of my partial blindness and other genetic issues or did my lack of socialization due to my self consciousness of having a prosthetic eye as a child contribute to my schizoidness, autism, sensitivities, etc. As a child it was obvious that I had a prosthetic eye so I was teased and bullied a lot. Also my parents both worked in the evenings so I was not socialized much as a child. Fully adult it is much less obvious as my prosthetic eye, eye lid, etc look no different than my good eye. Even without my birth defect I have always felt different. So did my partial blindness contribute to my autism and schizoid personality? Yes but having studied a considerable amount of neuroscience I believe it is also in my innate biology not necessarily hereditary. I also think it is partially due to birth trauma and prenatal environment as my mother had a difficult pregnancy. So again genes and environment. Like the rest of us it is a combination of factors that made me who I am. Thanks again for this post it help me understand myself a bit more even at 62 years old.
Just spit-balling, but I wonder how schizophrenics, autistics and the blind experience inner speech the same or differently. Might the inner voice as a focal point be probative?
About schizophrenics' heavy smoking: Knew some researchers 20 yrs ago who believed the smoking was actually driven by one of the med side effects of the drugs most commonly given then for schizophrenia -- akasthisia. Nicotine apparently gives some relief from akasthisia. Don't know whether this theory has held up, though.
wonder if its possible that autism is at its core a kind of sensory overactivation. That the brain dedicates too much effort to processes most automate away. This for me would explain the pathological rationality, as well as the correlation with blindness (as blindness would require a heightened sensitivity of the remaining senses).
Being a pseudoscientist, I was actually thinking that autism and narcissism were at the respective extremes of introversion and extroversion.
Epistemic status: speculative (as in: I'm a mechanical engineer and read papers on predictive processing as a hobby, let's wait for some sane people to weigh in on this)
We don't know what autism actually is, but predictive processing (PP) offers some theories. Yon and Frith 2021 explain that "characteristics of autism (e.g., a preference for stable and repetitive environments) can be cast as an consequence of overly-strong beliefs about the precision of incoming evidence - where every fluctuation in our sensory system seems to signal the need to change our models of the environment (i.e., the world seems unstable)." (1). The causal direction is not really clear to me, maybe high expected sensory precision leads to bad generalization capabilities and strong reliance on bottom-up sensory input, maybe it's the other way around? Beren Millidge's master thesis (2017) has a theory on a potential neural basis for Autistic Spectrum Disorders: "It argues that the observed pattern of long-range underconnectivity and local overconnectivity observed in ASD, when instantiated in a predictive processing framework, will lead to impoverished high level regions and lower-level regions which down-weight prior information coming from above and prioritise incoming immediate sensory information. This pattern is hypothesised to result in many behaviours recognised in autism such as sensory hy- persensitivity, a local, detailed-oriented processing style, and a preference towards predictable behaviours and routines." (2)
I'm even more confused on the schizophrenia side of the story. The best discussion I've seen so far is (3), which ties PP and the diametric model together and compares schizotypy to an underfitting strategy in machine learning: "One of the downsides of the generalization function of positive schizotypy is apophenia. It is considered the predisposition to false positives: if you have noisy data and you want to see a pattern in the data, you need to be giving a low weight to sensory input - that's the only way you're going to find the line of best fit. The downside: well, you're also going to sometimes see patterns that aren't actually there. You're essentially imposing your assumptions onto the data and you're imposing your model onto the world." (I'm not so happy with this source here, I just don't have anything better right now)
Now I don't see any way of looking at the theory above and coming up with a prediction of low schizophrenia and high autism rates for blind people. So let's push our luck and see if we at least in retrospect fit this together and come up with a few follow-up predictions.
I'd be really surprised if autism leads to blindness. Let's try to reverse the causal arrow: could blindness lead to autism? I'm not sure either, but to get the ideas started: there's an ongoing discussion of how exactly the brain learns in young children. Think of it as a nature vs nurture question: either you provide a genetically encoded brain for an infant (e.g. for animals who can walk right from day one) or you only provide some brain infrastructure and have the system learn on it's own (e.g. cats that fail to see horizontal stripes if they don't encounter them in the first weeks of life). There's some plausibility the human brain might be similar, especially when brain regions are missing at birth with the brain routing around this issue. Soooo maybe, by being blind, the brain reuses the area intended for visual processing and this kinda shifts the whole brain balance to a higher-autism structure?
You can find both links to the source papers and some discussion on r/predictiveprocessing:
(1) https://www.reddit.com/r/PredictiveProcessing/comments/myasvt/precision_and_imprecision_in_the_predictive_brain/
(2) https://www.reddit.com/r/PredictiveProcessing/comments/njv87k/a_predictive_processing_theory_of_autism_a_neural/
(3) https://www.reddit.com/r/PredictiveProcessing/comments/no563j/relevance_realization_predictive_processing/h0omw1k/
Scott sez: “Maybe blindness makes children seem more autistic in some boring, mechanical sense? Like maybe if you can’t read other people’s body language or even consistently know where they are, it’s hard to be social and so you don’t interact with other people and that seems autistic to people trying to diagnose you?”
Here’s a proposal for how blindness could make children actually be more autistic in a real and interesting sense: Their inability to see what other people are doing, and especially their inability to see faces, results in their having a very substantially impoverished feed of information about people and the rest of the world. They suffer from a sort of cognitive malnutrition that causes autistic-like stunted and abnormal development in many areas; or produces full-on autism.
Babies are wired to pay attention to faces: Even as newborns they are especially attentive to faces, and they become able to recognize their caregivers very early, at about 2 months I believe. The responses they see on faces are crucial data to them, and if their caregiver suddenly goes deadpan they become desperate and disorganized (Still Face Experiment, https://www.youtube.com/watch?v=apzXGEbZht0). As they learn to navigate the world, the facial expressions of observers are important data for them (Visual Cliff Experiment, https://www.youtube.com/watch?v=p6cqNhHrMJA). The approval, disapproval, fear or even just friendly interest they see on the faces around them gives them information and probably also makes the explorations more satisfying. And of course babies and toddlers don’t just see faces looking at them with various expressions, they also see people with faces they recognize doing all kinds of stuff. Maybe the interpersonal data about visually recognizable people — what the people did, how they looked at me when I did this and that — even forms the framework on which hangs all the rest of the what people learn about how things work. Even if it does not, it must be very important.
Consider the situation of a blind baby: She lives perpetually in the Still Face Experiment. She navigates life’s visual cliffs without being able to see whether her caregiver is enthusiastic or terrified. She toddles around without the benefit of seeing smiling and interested faces observing her. She never gets to see anybody else do anything at all. It doesn’t seem terribly surprising to me that growing up with this very impoverished feed of info about one’s own actions and about life in general leads to social deficits and also deficits in using the body, using objects, activity level, flexibility, adaptability etc. Of course, caregivers can mitigate the damage by staying in touch with the young child via other channels — touch, speech, etc. Still, if we are born wired to tune into faces and to use them as a portal to learning everything else, it may not be possible to make up the visual-interpersonal shortfall via other channels. That shortfall could account for the high-frequency of autistic-like traits even in blind kids who are not actually autistic.
What does this theory have to say about sighted babies who develop into autistic children? Well, maybe they are born with something wrong with the face-processing parts of their brain. Maybe they are born without the wiring that makes them interested in faces, good at recognizing different people, naturally predisposed to be highly responsive to affective displays on the faces of others, naturally interested in the activities of facially recognizable others.
And about that Hobson and Bishop paper: Yeah, it’s really blurry-minded. My theory, above, may or may not have been what they were trying to get at. I did wonder, after reading it, why they had not examined the literature on the development of infants blind from birth. There must be a substantial body of research, and also a bunch of stuff out there, not all of it wrong-headed, about how to foster the development of blind babies. For them not to have incorporated any of this info into their study seems sort of — well, impoverished and rigid, if not frankly autistic. We should not make that mistake ourselves.
Wow. Too much new information for me. One silly question. Is someone working on a drug/thing that replaces smoking for schizophrenics so they don't incur the downside cancer risk of smoking? (As a x-smoker, cigs are both a drug and a thing to do. I sometimes miss the 'thing to do' part of smoking.)
More trivia from what I'm currently reading: 'Visually impaired people usually have more sensitive photoreceptors, which react very sensitively to every slight change in light. This is also one reason why depression (seasonal affective disorder, or SAD), a condition that is linked to, among other things, disturbed melatonin production, affects them three times as often.'
Source, The Magic of Melatonin by Dr. Fautek and https://doi.org/10.1192/bjp.bp.114.162354.
Scott, are you aware of Dehaene's theory that schizophrenia is caused by an impaired consciousness? More precisely, because the threshold for perception to become conscious is higher than in neurotypicals? The difference is ridiculously strong, e.g. here:
https://www.pnas.org/content/pnas/100/23/13722/F2.large.jpg
Perhaps cutting away a large part of perception makes it easier for other perceptions to propagate to consciousness, because there are less competitors.
I am not sure how this relates to an axis schizophrenia-autism, but Clark's theory from "Surfing Uncertainty" is that autism is caused by too much error signal propagating upwards. Or rather, by too low thresholds for error signals to propagate upwards, so that it happens all the time.
Oversimplifying, perhaps schizophrenics are people with too little consciousness, while autistics are people with too much consciousness.
Adding a neuroscience viewpoint on sensory deprivation:
One effect of the day/sleep cycle is that synapses become on average stronger during daytime, and become weaker (go back to baseline?) during sleep. The homeostatic theory of sleep says that this is one of the reasons for sleep.
Sensory deprivation has the same effect. Your synapse strengths become weaker during sensory deprivation. At least some studies claim that.
There are lots of theories of autism and schizophrenia where signal strengths play a role, so this invites endless speculations on the interplay between sleep/sensory deprivation/signal strength/autism/schizophrenia.
I see a lot of comments here about blindfolding, sleep, sensory deprivation. Has anyone ever tried anesthesia? There is no clearer analog of just turning if off and back on again for the human brain. Is it considered too dangerous to be used outside of surgery where it is absolutely necessary? Surely, it isn't more dangerous than electroshock therapy. Is it just no history of collaboration between psychiatrists and anesthesiologists?
I don't nearly have the means in terms of domain knowledge or journal access to do a real lit review, but a web search seems to indicate there are potentially dangerous interactions between anesthesia and antipsychotic drugs. I can't quickly find any indication of whether anyone has ever tried to use anesthesia as an actual treatment *before* the patient has a lifelong history of taking antipsychotics. I suppose one problem is this would be extremely expensive compared to things like electrocuting or blindfolding a person.
I have a relative who experiences Intense Imagery Movements (IIM; https://pubmed.ncbi.nlm.nih.gov/26561043/). Because of frequent stimming, he was checked out for autism by a neurologist as a toddler. He's definitely not on the spectrum and actually is quite empathetic and insightful about others' emotional states. Nevertheless, as he's grown older, we've noted many autism-adjacencies and similar sensitivities. For instance, he has deep sensitivities to various sounds and tactile experiences.
The idea that there are constellations of related neurological conditions that manifest differently makes a lot of sense IMHO.
Need study with people blinded in infancy. Couldn't make it double blind though.
Also I wonder if the congenitally deaf have higher rates of schizophrenia. I had 3 deaf patients on decanoates at our clinic, and none just there for depression/anxiety. Though maybe deaf people with depression/schizophrenia go to places staffed with people who use sign language.
As an autistic person, this is possibly relevant: Until I was fifteen or so, I would walk around the house blindfolded (or with my eyes shut tight) quite often, as a way to relax. I never knew any other autistic people to ask if they did something similar, but I'd be interested to find out!
On a related note - I've thought about the possibility of treating auditory hallucinations in schizophrenia patients using some sort of sensory substitution (see https://eagleman.com/science/sensory-substitution/ - he even has a TED talk!). Maybe having something vibrate when speech is recognized would help patients recognize hallucinated speech as such, and eventually something something predictive coding would lead to having weaker beliefs regarding inner speech. It might also be interesting to think of utilizing some form of sensory substitution in autistic people
My best shot at this would be: melatonin
The levels of melatonin depend strongly on the visual cues, that blind people lack. I wasn't able to get a full picture of how melatonin levels fluctuate in blind vs non-blind people, but there surely is a difference, that's probably most pronounced when it comes to rare, non-standard situation: let's say staying in a brightly lit room long past sunset would create a strong deviation in melatonin cycle in non-blind person but not in a blind person.
The dopaminergic theory of schizophrenia is far from a complete explanation. In fact it can be posed that D2 antagonists simply mask the disease as they largely don't revert schizophrenics to normal functioning.
The alternative theory of schizophrenia involves glutamate receptors. Now, there is a multitude of interactions between melatonin and glutaminergic system in the brain and it's hard to tell which interaction, if any, would explain the lack of schizophrenia in patients that aren't strongly affected by light, ie. for example blind people.
One potential link is that melatonin is a potent neuroprotector in cases of glutaminergic excitotoxicity. So one hypothesis here can be that non-blind people are at risk of being exposed to bright light and consequently having low levels of melatonin. And then in the case of increased glutamate secretion they wouldn't be protected from excitoxicity and subsequent death of certain neurons.
I'm far for claiming that this particular hypothesis has much chance of turning true. But I have a fairly strong belief in that melatonin and glutamate are strongly implicated in the biological basis of schizophrenia.
Isn't this perfectly explained by sparsity of data resulting in more hesitant tuning of a precision parameter?
Intuitively, it looks to me (someone with zero expertise in the matter) like schizophrenia is a deficit of recursive processing in the brain relative to the amount of sensory input, and autism is an excess of the same. Consider what we might expect for different amounts of recursive processing versus sensory input:
(1) Too little recursion: inability to stay on topic (which looks like disorganized thought and lack of concentration), inadequate processing of thoughts (which looks like failure to distinguish between thoughts, impressions, and reality) and too direct translation of sense data into action (which looks like lack of internal motivation in unstimulating environments but flighty, compulsive behavior in stimulating ones)
(2) Low-ish but healthy amounts of recursion being handled well: somewhat reduced processing of thoughts (which looks like an intuitive or artistic style), reduced constraints the brain is trying to satisfy (which looks like uninhibitedness, confidence, and creativity), relative quickness changing topics in a conversation, relatively more effort put into finding or creating a stimulating environment
(3) Normal amounts of recursion - most folk (the baseline for comparison)
(4) High-ish but healthy amounts of recursion being handled well: somewhat increased processing of thoughts (which looks like an analytical or rational style), increased constraints the brain is trying to satisfy (which looks like inhibitions, awkwardness, and uncreativity), relative slowness moving on to new topics in a conversation, relatively less effort put into finding or creating a stimulating environment
(5) Too much recursion: leading to cyclic bodily motions, getting stuck on a topic obsessively, sometimes failing to respond to external stimuli, and sometimes experiencing painful sensory feedback analogous to a microphone screech.
I'd expect sensory deprivation to help people at (5) mainly by preventing the painful sensory feedback, maybe also thereby letting them relax and spare thought to control their other symptoms, and to help people at (1) mainly by making internal motivation the "loudest" remaining input, giving them a chance to focus.
A big chunk of the brain is dedicated to processing vision, so maybe congenitally blind people can re-purpose enough of that they all have enough processing capacity to spare, keeping them out of group (1).
TBH, the reason this account comes to mind is because of the effects of cannabis. Google tells me cannabis probably helps autists and definitely makes schizophrenia worse. From a (4)-ish starting point, cannabis makes me feel like much of my working memory has been turned off, and as a result I get reduced ability to concentrate, a more intuitive/less rational style, fewer inhibitions and more creativity, and even twinges of paranoid ideation that feel like my insecurities getting a free pass to invade my brain instead of being quashed as obviously unjustified.