I had severe issues as a kid with both my head and brain size (which well, still haunts me today, this big head, hehe), but I never got that autism diagnostic, or actively looked for a doctor for it.
A doctor wanted to operate my brain as a baby, but my mother didn't let it, and in the end, it was the right choice as it had a meaningful chance of my death.
I also struggled with language at first, and I went to many years of speech therapy, but eventually, it got better. My learning rate with languages is definitely not the best, but I still speak three languages after a good amount of effort and can communicate effectively.
It also gave me plenty of advantages; I always scored pretty high on IQ tests and had very good long-term memory.
Because I don't buy this narrative from the article or in medical research that there are two kinds of autism. In my opinion, there's only one, and that one has SEVERE conditions; I had a relative who had autism, and it was complicated for both the person and their parents. To me, this seems like a naming issue like software engineers do, who struggle to name an abstraction correctly, and after three years, that abstraction means everything.
Having a different kind of brain wiring isn't some sort of sickness or anomaly. All brains are very different, just like your toes. When you compare them to others, you'll see quite a few differences.
I think there's a communication issue with regards to how a syndrome is portrayed in non-technical media. And it doesn't get any better when we replace "syndrome" with "condition" or "spectrum disorder" or what have you.
A syndrome is just a description of what a black box looks like to us from the outside. We collect different outward expressions (symptoms) and give some sort of statistical baseline - e.g. a certain collection of symptoms clusters together in 70% of cases. In the case of psychological/neurological syndromes - our most poorly understood black boxes - we then create tests which are effectively subjective surveys, aggrandized Turing Tests. And to complete the picture, we also try to cluster with regard to treatment - assuming that if X modality treats Y cases well, those Y cases are all of the same syndrome.
All this is to say that while there might be one "source insult" that creates most of what we cluster as Autism, it is extremely unlikely. There are probably multiple different insults that create multiple conditions that we crudely cluster under the same Autistic umbrella. It is useless to try and define what is the "true" Autism - we need to understand the underlying mechanism first - maybe then we can give whatever we do understand better its own name.
As to why we are quick to label, I'll just say that in my country, as a child psychiatrist put it to me - before the mid-90s parents were angry with him when he made the autistic diagnosis, a trend that was then abruptly reversed and parents started to demand he label their neurodivergent kids autistic, even if he didn't find the diagnosis to be accurate. What changed? The country started to give disability benefits to parents with autistic children.
1) One big change is the recognition that Autism, regardless of particular definition, responds to therapeutic attempts much more effectively in early childhood, rather than later.
2) Much of the effective work is around "functioning" -- if you can't speak, well, an "autism" diagnosis is going to change what's attempted in response, but the goal is still going to be to get a kid to be able to speak. That's much easier when a child is still 2 or 3.
> Because I don't buy this narrative from the article or in medical research that there are two kinds of autism.
I'd like to preface this by saying I don't feel strongly about the naming issue in either direction.
Initially I figured the authors were using the word "Autism" as used in DSM-5, where it's a blanket term for a range of conditions. But, their repeated assertion of "two types" of autism doesn't line up with that theory: DSM-5 defines three levels, not two.
They definitely aren't using the DSM-IV definition of Autism (the stricter definition that you prefer), and they also aren't following the taxonomy laid out in DSM-5. Where did their definition of Autism come from?
Was it implied that their two-level model was derived from the results of their tests? If so, I missed that part. They mention a correlation between brain overgrowth and severity of symptoms, but they don't mention a clear separation in the test data that would justify classification into two distinct groups.
I understand that DSM isn't gospel, but if they're going to make up their own taxonomy, they should provide some rationale for it.
> narrative from the article or in medical research that there are two kinds of autism. In my opinion, there's only one, and that one has SEVERE conditions
I'm not sure that's a narrative? In fact quite the opposite, currently anything from the 'different kind of brain wiring' you mention through to the 'SEVERE conditions' that you acknowledge as autism are all seen as varying aspects and varying degrees of the same underlying difference. Once you get more acquainted with the less dramatic forms of autism there are significant commonalities.
That said, however well-founded the reasons for merging Asperger's Syndrome with the umbrella Autism Spectrum Disorder, I do feel we've lost some nuance in the process. There definitely seems to be a qualitative difference between "person who's a bit different and struggles with some aspects of life, but may be exceptional in others" and "person who's severely impaired and will never be able to navigate life on their own (even if exceptional in others)." Having shorthand terms to identify the two independently was useful.
I fully agree. The amount of people that have “minor” autism and get upset at people looking for a cure is huge, for instance.
For them they’re just a little bit different, and they wouldn’t want to be someone else. They don’t realize there are people like my cousin that needs to live in a group home because he’s almost non-verbal.
I think this is a really good way to put it. It feels like there's a rush to label and self-diagnose which ultimately results in a ton of pathologization of relatively normal behaviors. That is: "normal" as in we expect to see some diversity of behavior. Maybe less labeling would lead to more acceptance and understanding, which seems after all to be one of the goals...
Judging by how things go at my kids' school, it's quite the opposite. I and several of my friends have neurodivergent kids. The kids are quite open about it at school, and generally don't pathologize it at all. It's a huge difference from the traumatic childhood I experienced, where I was undiagnosed and also openly bullied for being a little bit weird.
If I may get a bit direct, if you believe that the move toward classifying some things as spectrum disorders, and neurodiversity in general, is about pathologizing the range of human behavior, I'd encourage you to spend some more time looking into it.
"I had a childhood health complication that was somewhat similar to this, therefore I am very well suited to comment on something that affected a relative that is not in my immediate family."
I have a son who is on the spectrum, he is often assumed to be neuro-typical by people he doesn't spend a lot of time with. He is "high functioning", but is still vastly different to his peers with issues that I don't think anyone would categorise as "severe", but the impact on him emotionally and our family unit as a whole is severe and pervasive.
To be clear, I am not offended or upset, I just feel that you need to be made aware that you are deeply ignorant on a topic that is only a blip in your world.
We have a son, nearly five now, who matches this description. He has, in my amateur opinion, severe sensory processing issues. He is extremely highly strung, prone to meltdowns at the drop of a hat, has trouble regulating, focusing, and so on. He is only young, so it all may change, but he is behind in micro and gross motor skills, behind in writing because of this, and is almost impossible to help because any time he senses a hint that he isn't perfect he shuts down, eventually with a meltdown if pressed. A meltdown for him involves spinning around on the floor, hitting himself over and over. He calms himself by going into a dark space and sucking on a comforter.
And yet, in social environments, if he is kept stimulated and has a lot of positive attention, you would never guess at this other side and we feel that people look at us strangely when we mention how hard our family life is. The ironic thing is I'm sitting in my home office right now and I can hear him having a meltdown outside as my wife is trying to keep him entertained.
It causes huge issues for us, and we've been having a difficult time keeping things together as a family. My wife and my relationship has suffered a lot.
PS. We have another son, two years old, who is just a typical child. Challenging at times, but otherwise fine. So it's not like we did anything different.
Females store fat on ass and hips first, males on the gut first. Not only, but primarily first. Once these regions get to a point, fat accumulates all over.
Kids are indeed fatter in the West, just as adults are.
I think it's just selection bias for women with fat asses. Baby got back came out in 1992, and remained popular for quite sometime. It puts the people most influenced by it right around the age on having first graders. And of course it didn't stand alone, lots of music and popular culture focused much more heavily on ass at that point. Previously almost all focus had been on being skinny with "alert" breasts.
After reading the whole thing, I am bit worried about all the logical leaps and this just being a weird mashup of ideas that don't make much sense.
That being said, as a person that is mildly on ASD spectrum I was bit intrigued by the hypothesis of higher lactate orinted energy production in autistics. It would match two of my lifelong problems, having strong exhaustion (food coma) after eating high carbs and having similar reaction to even short (5min) high-intensity workouts. I had to adapt by avoiding large doses of carbs and focusing more on resistance training with large pauses inbetween.
I am baffled how some of my friends can eat a mountain of white rice or workout hard for hour and be completely fine after.
>”Now that Courchesne and Muotri have established that brain overgrowth begins in the womb, they hope to pinpoint its cause, in a bid to develop a therapy that might ease intellectual and social functioning for those with the condition.”
There is a slight difference between “beginning in the womb” snd beginning in some odd organoid derived from blood cells.
Autism research imho tends to be flaky and this type of press release does not help.
They had a neurotypical control group, their effect size is massive, and clearly separates the autistic group from the control group. They reject the null hypothesis that there is no difference between the groups, and argue from literature for an alternative hypothesis. What's the problem?
There's a step left out, which is how they know that what happens in the BCO models also happens in real brains in developing fetuses. That might be context known from previous research, but it isn't explained in the linked article, as far as I can see.
I did not see information on the ancestry of the 9-10 ASD toddlers or on the even fewer neurotypical controls. May have missed this.
As for large putative effect sizes this is often due to subtle batch processing differences between cases and controls. Where they all processed by the same tech in an interleaved way? All stored in the same way over this very long duration study? Authors do discuss batch controls but with single digit sample sizes I regard statistics as fundamentally unreliable.
I am also not convinced by the claim of any over-proliferation of neurons in autism during development. It is certainly a highly controversial result. See notes above by “subiculum…” and the Li et al paper he cites.
I don’t understand your complaint. The conclusion of the paper says this: “By embryogenesis, the biological bases of two subtypes of ASD social and brain development—profound autism and mild autism—are already present and measurable and involve dysregulated cell proliferation and accelerated neurogenesis and growth.” It is correct to describe that as “established that brain overgrowth begins in the womb”.
It seems you have an issue with that the researchers reached this conclusion from experiments with what you call “some odd organoid derived from blood cells”. I’m not an expert so I wouldn’t know if that is a valid way to make the conclusion but once they do it seems the summary in the article is correct.
What do you feel is wrong with the article and what do you feel is flaky with the research?
This growth pattern has been documented pretty well? I used to teach it in undergrad courses.
Autism spectrum issues are associated with overgrowth and then deceleration more than normal. This seems like a hyperexperimental version of it. Still interesting and good to see corroborating evidence, also useful as a model for therapies and other things.
Th predominant view in the field has been that there is early cerebral overgrowth followed by either normalization or regression of brain volume in adolescence. However, this conclusion is based on cross-sectional comparisons. This means, they look at different people at different ages, and make inferences on developmental trajectories based on these cross-sectional, age-related patterns. While this is often a starting point, cross-sectional research can suffer from sampling biases.
A huge weakness in autism neuroimaging research is the un-representativeness of
their samples. Nearly a third of individuals with autism have severe intellectual impairments (IQ's < 70) yet represent less than 1% of neuroimaging samples. Individuals with other immense behavioral, sensory and language challenges are also rarely make it through the rigors of imaging protocols.
A rare exception has been imaging research that performed brain imaging in very young children during natural sleep. and thus can hold still enough for quality MRI images to be acquired. This has allowed imaging of autistic children aged 2-6 years to include autism over a whole range of severities, challenges, and intellectual abilities.
This presents a problem though. The research that suggested there is brain overgrowth in early childhood sampled from a wide range of autism phenotypes and severities, while the normalization evidence in adolescents and adults came from autistic participants with normal ranged IQs and less severe challenges, a clear cross-sectional sampling bias that threatens the validity of the overgrowth normalization story.
Moreover, research indicated that disproportionate brain size in autism was associated with slower intellectual improvements with development.
I and my colleagues thus hypothesized that the discrepancy would be removed if we can follow the same children from childhood into adolescence longitudinally. Using a number of behavioral techniques and a lots of care and dedication, our team managed to acquire brain data in a broad spectrum of autism phenotypes and severity levels from early childhood into early adolescence.
Our conclusion: Longitudinal evidence does not support the notion that early brain overgrowth is followed by volumetric regression, at least from early to late childhood.
I used to joke to myself that I was the next step in evolution, home sapiens superior. I was aware enough no to provoke my classmates though ;)
But, I wonder if it is at all related to Neanderthal lineages. They had bigger brains and were basically autists: the species. Since we are a bastard of them and early Sapiens, maybe some of us present with more of their genome than others?
blaming Neanderthals for most things is a gross over-simplification and misdirects reader's attention towards genetics. While there is some humour to it, I would be cautious of giving into unwarranted fixation towards genetics, as we no longer live in the world where it needs to be defended against Lamarckism and like.
I posit that the "runtime environment" i.e. epigentics, among other things, has a far traceable cause than the smidge of related species. The nature and consequences of autism land me to believe that it's more likely a consequence of a compiler error, although shoddy source code could be a secondary/compounding cause for it. Take Down's Syndrome as an prime example of genetic disorder, and it becomes clear why such categorization does not work for autism: autism is too broad, it describes the effect rather than cause, and I'd argue that autism is far less debilitating (pronounced) and definitely not inherited.
Also macrocephaly is significantly more common in autistic people than the general population (that is, macrocephaly is a head circumference at the 97th percentile or higher, but ~20% of autistic people have it).
Overgrowth is a normal process in the development of the fetal brain. It is followed by a reorganization, which means the pruning and migration of neurons to the right locations in the brain.
Readit News
A doctor wanted to operate my brain as a baby, but my mother didn't let it, and in the end, it was the right choice as it had a meaningful chance of my death.
I also struggled with language at first, and I went to many years of speech therapy, but eventually, it got better. My learning rate with languages is definitely not the best, but I still speak three languages after a good amount of effort and can communicate effectively.
It also gave me plenty of advantages; I always scored pretty high on IQ tests and had very good long-term memory.
Because I don't buy this narrative from the article or in medical research that there are two kinds of autism. In my opinion, there's only one, and that one has SEVERE conditions; I had a relative who had autism, and it was complicated for both the person and their parents. To me, this seems like a naming issue like software engineers do, who struggle to name an abstraction correctly, and after three years, that abstraction means everything.
Having a different kind of brain wiring isn't some sort of sickness or anomaly. All brains are very different, just like your toes. When you compare them to others, you'll see quite a few differences.
All this is to say that while there might be one "source insult" that creates most of what we cluster as Autism, it is extremely unlikely. There are probably multiple different insults that create multiple conditions that we crudely cluster under the same Autistic umbrella. It is useless to try and define what is the "true" Autism - we need to understand the underlying mechanism first - maybe then we can give whatever we do understand better its own name.
As to why we are quick to label, I'll just say that in my country, as a child psychiatrist put it to me - before the mid-90s parents were angry with him when he made the autistic diagnosis, a trend that was then abruptly reversed and parents started to demand he label their neurodivergent kids autistic, even if he didn't find the diagnosis to be accurate. What changed? The country started to give disability benefits to parents with autistic children.
1) One big change is the recognition that Autism, regardless of particular definition, responds to therapeutic attempts much more effectively in early childhood, rather than later.
2) Much of the effective work is around "functioning" -- if you can't speak, well, an "autism" diagnosis is going to change what's attempted in response, but the goal is still going to be to get a kid to be able to speak. That's much easier when a child is still 2 or 3.
I'd like to preface this by saying I don't feel strongly about the naming issue in either direction.
Initially I figured the authors were using the word "Autism" as used in DSM-5, where it's a blanket term for a range of conditions. But, their repeated assertion of "two types" of autism doesn't line up with that theory: DSM-5 defines three levels, not two.
They definitely aren't using the DSM-IV definition of Autism (the stricter definition that you prefer), and they also aren't following the taxonomy laid out in DSM-5. Where did their definition of Autism come from?
Was it implied that their two-level model was derived from the results of their tests? If so, I missed that part. They mention a correlation between brain overgrowth and severity of symptoms, but they don't mention a clear separation in the test data that would justify classification into two distinct groups.
I understand that DSM isn't gospel, but if they're going to make up their own taxonomy, they should provide some rationale for it.
I'm not sure that's a narrative? In fact quite the opposite, currently anything from the 'different kind of brain wiring' you mention through to the 'SEVERE conditions' that you acknowledge as autism are all seen as varying aspects and varying degrees of the same underlying difference. Once you get more acquainted with the less dramatic forms of autism there are significant commonalities.
That said, however well-founded the reasons for merging Asperger's Syndrome with the umbrella Autism Spectrum Disorder, I do feel we've lost some nuance in the process. There definitely seems to be a qualitative difference between "person who's a bit different and struggles with some aspects of life, but may be exceptional in others" and "person who's severely impaired and will never be able to navigate life on their own (even if exceptional in others)." Having shorthand terms to identify the two independently was useful.
For them they’re just a little bit different, and they wouldn’t want to be someone else. They don’t realize there are people like my cousin that needs to live in a group home because he’s almost non-verbal.
If I may get a bit direct, if you believe that the move toward classifying some things as spectrum disorders, and neurodiversity in general, is about pathologizing the range of human behavior, I'd encourage you to spend some more time looking into it.
I have a son who is on the spectrum, he is often assumed to be neuro-typical by people he doesn't spend a lot of time with. He is "high functioning", but is still vastly different to his peers with issues that I don't think anyone would categorise as "severe", but the impact on him emotionally and our family unit as a whole is severe and pervasive.
To be clear, I am not offended or upset, I just feel that you need to be made aware that you are deeply ignorant on a topic that is only a blip in your world.
And yet, in social environments, if he is kept stimulated and has a lot of positive attention, you would never guess at this other side and we feel that people look at us strangely when we mention how hard our family life is. The ironic thing is I'm sitting in my home office right now and I can hear him having a meltdown outside as my wife is trying to keep him entertained.
It causes huge issues for us, and we've been having a difficult time keeping things together as a family. My wife and my relationship has suffered a lot.
PS. We have another son, two years old, who is just a typical child. Challenging at times, but otherwise fine. So it's not like we did anything different.
https://www.tinygnomes.com/qwiki.cgi?mode=previewSynd&uuid=B...
We had already known from autopsies that neural density in certain brain regions is much higher among autists.
This is certainly... something
Females store fat on ass and hips first, males on the gut first. Not only, but primarily first. Once these regions get to a point, fat accumulates all over.
Kids are indeed fatter in the West, just as adults are.
That being said, as a person that is mildly on ASD spectrum I was bit intrigued by the hypothesis of higher lactate orinted energy production in autistics. It would match two of my lifelong problems, having strong exhaustion (food coma) after eating high carbs and having similar reaction to even short (5min) high-intensity workouts. I had to adapt by avoiding large doses of carbs and focusing more on resistance training with large pauses inbetween.
I am baffled how some of my friends can eat a mountain of white rice or workout hard for hour and be completely fine after.
>”Now that Courchesne and Muotri have established that brain overgrowth begins in the womb, they hope to pinpoint its cause, in a bid to develop a therapy that might ease intellectual and social functioning for those with the condition.”
There is a slight difference between “beginning in the womb” snd beginning in some odd organoid derived from blood cells.
Autism research imho tends to be flaky and this type of press release does not help.
As for large putative effect sizes this is often due to subtle batch processing differences between cases and controls. Where they all processed by the same tech in an interleaved way? All stored in the same way over this very long duration study? Authors do discuss batch controls but with single digit sample sizes I regard statistics as fundamentally unreliable.
I am also not convinced by the claim of any over-proliferation of neurons in autism during development. It is certainly a highly controversial result. See notes above by “subiculum…” and the Li et al paper he cites.
Deleted Comment
It seems you have an issue with that the researchers reached this conclusion from experiments with what you call “some odd organoid derived from blood cells”. I’m not an expert so I wouldn’t know if that is a valid way to make the conclusion but once they do it seems the summary in the article is correct.
What do you feel is wrong with the article and what do you feel is flaky with the research?
Autism spectrum issues are associated with overgrowth and then deceleration more than normal. This seems like a hyperexperimental version of it. Still interesting and good to see corroborating evidence, also useful as a model for therapies and other things.
A huge weakness in autism neuroimaging research is the un-representativeness of their samples. Nearly a third of individuals with autism have severe intellectual impairments (IQ's < 70) yet represent less than 1% of neuroimaging samples. Individuals with other immense behavioral, sensory and language challenges are also rarely make it through the rigors of imaging protocols.
A rare exception has been imaging research that performed brain imaging in very young children during natural sleep. and thus can hold still enough for quality MRI images to be acquired. This has allowed imaging of autistic children aged 2-6 years to include autism over a whole range of severities, challenges, and intellectual abilities.
This presents a problem though. The research that suggested there is brain overgrowth in early childhood sampled from a wide range of autism phenotypes and severities, while the normalization evidence in adolescents and adults came from autistic participants with normal ranged IQs and less severe challenges, a clear cross-sectional sampling bias that threatens the validity of the overgrowth normalization story. Moreover, research indicated that disproportionate brain size in autism was associated with slower intellectual improvements with development.
I and my colleagues thus hypothesized that the discrepancy would be removed if we can follow the same children from childhood into adolescence longitudinally. Using a number of behavioral techniques and a lots of care and dedication, our team managed to acquire brain data in a broad spectrum of autism phenotypes and severity levels from early childhood into early adolescence.
We reported the results of our study in Biological Psychiatry Lee in 2021. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8089123/ (open access).
Our conclusion: Longitudinal evidence does not support the notion that early brain overgrowth is followed by volumetric regression, at least from early to late childhood.
Deleted Comment
But, I wonder if it is at all related to Neanderthal lineages. They had bigger brains and were basically autists: the species. Since we are a bastard of them and early Sapiens, maybe some of us present with more of their genome than others?
You would also expect autism to be nearly completely absent in Africa, East Asia, and native Oceania and North and South American populations.
I’m not an expert, but I don’t believe any of that is true.
It’s a fun “theory” but it doesn’t survive even casual analysis.
I posit that the "runtime environment" i.e. epigentics, among other things, has a far traceable cause than the smidge of related species. The nature and consequences of autism land me to believe that it's more likely a consequence of a compiler error, although shoddy source code could be a secondary/compounding cause for it. Take Down's Syndrome as an prime example of genetic disorder, and it becomes clear why such categorization does not work for autism: autism is too broad, it describes the effect rather than cause, and I'd argue that autism is far less debilitating (pronounced) and definitely not inherited.