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Been saying this for years, feels vindicating. I’m ADD and I’ve been wondering about the possibility of autism, every time I try to look into the symptoms it seems wildly varied, poorly defined and vastly misunderstood. At least with ADHD/ADD you can blame the blood ghosts and do a cocaine about it.
So if autism is a broader term that includes multiple conditions shouldn’t we stop using it and start using the names of the actual conditions? Isn’t it basically like hysteria which was split into epilepsy, dissociative disorders, personality disorders and so on?
IMO, as a ‘high-functioning autist’:
Yes.
The field of psychology is constantly redefining things based on ever shifting subjective analysis of behavioral patterns, and uh, being someone who very much prefers concrete, consistent, definable rules and categories, logically followable mechanistic processes…
Fucking yes, please, be more accurate and precise in a more objective way, based on far superior amethodology, fucking please.
They do for many, but sometimes I think they don’t know exactly what or it could be multiple things which is why it’s the Autism Spectrum and it’s easier to say they are “on the spectrum” or “autistic” if you can’t pinpoint exactly what.
Copy pasting some sections of my own comments from similar discussions over the last month or so:
IRT Folinic Acid as a ‘treatment’ for Autism:
…there are early preliminary studies indicating that this may be a way of alliviating some of the effecfs of non-syndromic ASD.
https://pmc.ncbi.nlm.nih.gov/articles/PMC5794882/
Non-syndromic ASD is essentially nonverbal, nonresponsive ASD.
… There are many autistic people and kids who are not non-syndromic, an ASD diagnosis does not even require this kind of behavior.
Further, the proposed mechanism of action in using folinic acid to ‘treat’ autism is that it acts upon an abnormal level of folate blockers…
While it is true that ASD folks tend to have more of these folate blockers than non ASD folks…
Many of them do not.
Generally speaking, abnormal folate pathways… appear to be called Cerebral Folate Disorder (CFD) by this Dr. Frye who seems to be spearheading this line of research.
So… this would arguably be an identifiable subtype or subcomponent of ASD, that has an actual, physically identifiable (and seemingly potentially treatable) aspect to it, caused by a known cluster of genetic mutations, which themselves cause… basically, your neural pathways in your brain to just literally be different from those without the genetic mutation cluster.
Of course, epigenetics, to what extent and under what conditions genes actually express themselves is a complicating factor here.
Nurture can change how your Nature works, at a fundamental level.
More general commentary on the idea of Autism subtypes/conponents:
There is an emerging, but far from totally agreed on and fully explained… view, that, well, autistic brains, or at least certain potential subclasses of autistic brains… actually do have physically distinct brain chemistry and activity patterns than non autistic brains.
Basically, more and more actual genes and gene clusters are being identified, and at least some of those are being found to alter brain neurochemistry in measurable and mechanistically understood ways that nobody seems to have even known were possible before.
There could possibly thus be a propsensity toward an actually physically different reaction to many kinds of drugs from at least some autists.
But this is also fairly confusing because what is … currently being called ‘Autism Spectrum Disorder’ via psychological diagnosis… well, some autistic people have some of these mutations, some have all of them, some have none.
So… its far from fully understood, but it may be the case that in 5 or 10 years, Autism ends up being actually subclassed partially based on genetics and epigenetics, beyond just based on a description of behavioral patterns.
The analysis, published last week in the journal Nature, showed that children diagnosed before the age of 6 were more likely to have behavioral difficulties—such as problems with social interaction—from an early age. In contrast, those diagnosed after the age of 10 were more likely to experience social and behavioral difficulties during adolescence.
So if you have behavioral problems early, you’re more likely to get diagnosed early, when you have behavioral difficulties later, you’re more likely to get diagnosed later.
The phrasing here seems to want to imply a reverse causal relationship, but I’m pretty sure the conclusion here is that kids don’t get tested for autism before they display autism-like behaviour.
As for the actual causes of autism, I recently read that the genetic and family is about 60-90% of the causes, making it by far the biggest cause, and not environmental factors like RFK likes to suggest. But it’s not a single gene, it might be other stuff, and it’s not an on/off thing but a big pile of factors that add up.
But there are also environmental factors that do have an impact. Not vaccines or Tylenol, but some kinds of pesticides, for example. Maybe that’s something RFK could focus on.
Its more than a tautology, you are oversimplifying.
Or, well, as always with writings on or about science aimed at a general audience… the writers are oversimplifying, always read the paper.
https://www.nature.com/articles/s41586-025-09542-6
What they are describing is that those diagnosed early have a different behavioral psychological profile, different set of observed behaviors, than those diagnosed later.
They are saying that ASD has roughly two different sets of distinguishable behavioral profiles, and one of those sets is so obvious it tends to get diagnosed early, and another set is less obvious such that it tends to get diagnosed later.
While they seem hesitant to use the terminology of saying ‘there may be two fairly distinct subtypes of autism’, likely because they want to emphasize that more research needs to be done, they do not want to lead to people making rash an non nuanced conclusions… that basically is what they are saying, that there appear to be distinct genetic profiles that produce observably different ‘kinds’ of autism.
They ran a battery of statstical meta analysis on different genomes and behavioral profiles of Autists, and this chart I think summarizes it best:
(Those bars are 95% confidence intervals)
Two, fairly distinct behavioral/neurodevelopmental/phenotypical profiles, that also go along with two, fairly distinct underlying genomic profiles.
Scientists concluded this in the 1990s, and then had to produce yet another study to unequivocally state it again after every time someone claimed to have found the “cause”.
This is part of the reason it was re-named ASD in the first place; it describes a set of atypical neurological development symptoms, not an identifiable state of being. Kind of like “cancer” describes an atypical cellular reproductive state, not a pathogen attacking your cells. Both can be caused by many different factors or combination of factors.
Of course, with ASD, it doesn’t even mean there’s anything particularly wrong most of the time; just atypical, resulting in a person whose thoughts are weighted differently than historically typical, with less interpretation of social cues and a greater ability to focus.
This seems similar to the phenomenon where antidepressants are only effective for about 15% of patients. The benefit is large for those who benefit. For the rest, they’re no better than placebo, suggesting the drugs treat one of several causes for the syndrome known as depression.
with less interpretation of social cues and a greater ability to focus.
“ability to focus” is more accurately described as “tendency to focus”. “ability to focus” connotes control over focus, which… from lived experience and what I’ve read, just isn’t generally true. Autistic inertia – the inability to defocus and then focus on a new context – is very real. Autism is a neurodevelopmental disorder not just because of an ignorance of social cues but because of how rigid, inflexible patterns of behavior often interfere with daily life.
Autist here:
Yeah, describing it as simply ‘greater’ or ‘lesser’ ability to control or maintain focus is… well, too simplistic.
I can, when it comes to task, hyperfocus on something like writing a piece of complex code / software, try to solve a real world engineering problem, do a comprehensive data analysis of some topic, write a chapter of a novel… I can hyperfocus on that for a solid day or week or month, and I have to actively remind myself to do things like eat and sleep regularly, because I know I tend to get obsessively focused on ‘the task’.
Shifting to another task, another very different … realm of thinking, or way of thinking, is often very jarring and exhausting.
But on the flip side, when socializing, people tend to say I am scatter brained, overwhelming, because I just flow all the way through my entire chain of concept associations to end up with a resulting… thing I am trying to say.
Sort of like how modern agentic AI has an ‘explain its thinking process’ mode.
Thats just the default for me, its all an explicit, conscious train of thought.
For me, summarizing that chain of thought into just a resultant ‘thing to say’ is the difficult part, that I get worse at the more mentally exhausted I am.
Also, I would say most, not all, but most autists… its not that we are inattentive to or ignorant of social cues.
Its that neurotypicals tend to process social cues mostly subconsciously, whereas autists tend to process social cues mostly consciously…
… and that most neurotypicals actually all have widely variable, inconsistent and imprecise standards by which they judge and perform social cues, but most of them are unaware of this, to the point that they are overly confident that everyone has the same rubric and understanding of social cues as they do, when this very obviously is not the case.
So, this confuses/overwhelms many/most autists, because they are presented with an inconsistent and variable ruleset, and then also told that this ruleset is consistent and invariable.
Neurotypicals will often get angry/rude/frustrated/overwhelmed when you try to break this down and explain this to them, presumably because they largely are not aware of / do not have this explicit, conscious thought process, and tend to interperet being asked to formulate it in consistent, precise detail just as a rude, unreasonable thing to ask for.
Basically, imo, NTs use a fuzzy, fast, less accurate, mostly unconscious heuristic to evaluate and perform social cues, and they tend to be very confident they are doing this correctly…
… whereas Autists tend to logically and consciously go through an entire evaluation system, which is more robust and thorough in that its basically a discrete series of probabilistic associations, but this is all much slower, much more ‘computationally costly’ to perform.
So, when an Autist is oversocialized, under too much pressure to perform socially, they can get overwhelmed and then either basically shutdown or freak out.
This also works, imo, to explain why Autists tend to take longer to initially learn socialization cues and concepts… because they are having to build a much more conscious, step by step evaluation model of all possible micro/macro expressions, tonal shifts, inflexions, vocab choices, all possibly relevant context, etc, and this can often be much more difficult to establish when Neurotypicals are nearly entirely unaware of or dismissive of their own inconsistencies and variability when it comes to those things.
This also works to explain why Autists are often seen as overly straightforward or blunt: They’re just telling you the result of their attempt to evaluate a social interaction.
And this also explains why almost no NT person I’ve ever met can accurately assess my emotional state / social interaction disposition, yet they almost all are very confident they can do so correctly and precisely.
EDIT
And I will here comment on the meta-irony of all of this, that … any scientist could just ask a ‘high-functioning’ autist to explain how this works, and they could… you know, trust what a person says about how their own thought processes work?
But nope, nope, still we are pathologized as if we are strange, alien, confused and confusing others, not valid sources of information as to how our own minds work, when our whole ‘problem’ is that we are way too aware of how our minds work.
Why do you think PTSD coincides with the later Autism diagnosis group more strongly than the early diagnosis group?
Because we have been saying shit like this our whole lives, and broadly, nobody cares and just makes up whatever explanation or understanding they prefer, which is almost always significantly innacurate/incomplete, so we tend to live lives of constantly being slandered and mocked, rarely being respected as human beings with full agency.
Great so now I’ve been downing Tylenol for no reason?
FUCK!
It says no single thing, so you need to do multiple things, yeah? Get circumcized. 🤷♂️
Think you’re safe as long as you don’t also get a vaccine at the same time.
Here’s the source instead of a paywalled news article https://www.cam.ac.uk/research/news/study-reveals-genetic-and-developmental-differences-in-people-with-earlier-versus-later-autism
And here is just the full open access paper:
Scientists from Cambridge’s Department of Psychiatry found that children diagnosed as autistic earlier in life (typically before six years old) were more likely to show behavioural difficulties from early childhood, such as problems with social interaction.
However, those diagnosed with autism later on in life (in late childhood or beyond) were more likely to experience social and behavioural difficulties during adolescence.
I assume that the paper itself frames this a little differently, because what this is saying is trust there’s a correlation between when traits become noticeable and when people get a diagnosis. Which is what you’d expect. You don’t tend to diagnose people who don’t exhibit the traits required for diagnosis.
But chief US stientists have discovered that it’s all caused by Tylenol!
That’s not true. RFK Jr recently said it was from circumcisions.
If you take tylonol for the soreness after being circumcised you are 100% going to catch the autism.
If you’re smart, you’ll buy Tylenol stock and bank on the rebound.
It’s multiple conditions we group together naively based on surface level symptoms. Same for many disorders.
The type that comes with gender and sexual fluidity, bendyness, ADHD = rccx caused ASD.
Then that will have multiple subtypes based on mutation combination within the rccx module.
(The RCCX module would’ve been excluded from the genetic analysis the report this article is based on - due to its complexity).
Severe/non-verbal ASD is more likely completely unrelated and caused by dendritic abnormalities (reduced or excessive branching, immature spines, disrupted morphology, etc)
You seem to have a more in depth grasp of the precise genetics involved here than I do, what would your opinion be of Dr. Frye’s concept of “Cerebral Folate Disorder” that I mention in another comment?
Here’s a paper from him and his team, he has many though:
https://pmc.ncbi.nlm.nih.gov/articles/PMC5794882/
As best I can tell, he is focused on the non-syndromic, non-verbal, uh, what this recent paper OP is about seems to categorize as ‘early diagnosis autism’.
He’s got a cluster of specific mutations that produce an evidenced, differing neurochemistry in the brain, and apparently a potential treatment for that ‘subypr/component’ as well?
I… don’t agree with his general description of autism as basically only the kind that makes you developmentally delayed, but, if you can get past that… do you think he may be onto something as far as that being an distinct ‘type’ of autism?
Also, apologies if I am using some terms incorrectly or innacurately, I am not a neuroscientist.
In other news: scientists reconfirmed the wheel to be round.
I thought we already knew, it’s a spectrum
The ‘spectrum’ terminology comes about from the field of peychology only being able to attempt to analyze … basically, ‘symptoms’, behavioral profiles, phenotypes, and also the field of psychology constantly changing how it does those analyses as well as categorize observable behaviors into conditions/disorders.
What this new understsnding is pointing toward is that there is an actual, identifiable, genomic variance of mutation clusters that actually explains how differences in that spectrum of ‘symptoms’ actually work, what actually causes which ones.
A spectrum suggests varying degrees of a single condition, and would be compatible with both the hypothesis that all occurrences of this condition share a cause and the hypothesis of multiple causes. So to claim there are multiple causes is different from saying that cases fall on a spectrum. It tells you that multiple conditions can appear the same way, so they get diagnostically grouped together based on symptoms even though the underlying causes, and so the appropriate treatments, can be quite different.
But now it’s a conclusion and presumably a publication that can be referred to.
