Homeostasis across the blood brain barrier makes me suspect trivial approaches to boosting glutamate won't work. But this even begs the question if boosting available glutamate would be the right thing.
There are perverse consequences in brain chemistry and signalling: flooding a brain deficient in glutamate processing receptors with glutamate may not help, it may overload pathways and cause hindrance, not compensation.
Signs like this may be consequential, or related but not causal, or may simply turn out to be wrong.
IF a small sample effect turns out to be indicative of a larger property, and IF it's shown to be causal and IF remeditation involves boosting blood borne glutamate or precursors is 3 stacked IF.
IF its detectable in a young brain it could be diagnostic.
IF its detectable in a young brain and amenable to gene therapy and IF it's causative then treatment would be useful.
IF excess glutamate is not a problem and dietary supplemented sources cross the blood brain barrier and don't trip over homeostasis then it's possibly worth exploring.
(Not a scientist, not a biologist)
squirrel 3 hours ago [-]
It seems you are assuming that because the majority of people have a certain quantity of glutamate receptors, that they are the healthy ones and that we should be trying to bring autistic people up to that level. Is that right?
Why not consider the opposite, that the most beneficial quantity of glutamate receptors could be somewhere below the typical amount? If that were true, then we could try to help others reduce their glutamate receptor level to become healthier and more successful (and a little more autistic).
If we found, say, an association between a lower level of neurological characteristic X and concert-level piano skill, then those who aspire to play that instrument at an elite level might try to decrease X. The fact that most of us are rubbish piano players would not be evidence that lower levels of X are harmful, but very much the opposite.
ggm 2 hours ago [-]
You're absolutely right that assumption was implicit. The answer was written totally in that framework. I'm not here to say what's right or wrong in determining something about people who lie outside of normal in these things, or what normal means.
So what I wrote should be read with a "if it is held to be a condition which deserved remediation or avoidance of it's manifestation" attached.
Most medical conditions are couched in this sense, that a deficit or departure from the normal is a problem. In matters of brain chemistry it pays to be more nuanced.
roywiggins 9 hours ago [-]
"many neurodivergent people aren’t hindered by autism"
This is more or less not true. If it doesn't hinder a person in any aspect of their life, they don't fit the DSM-V criteria for a diagnosis.
(Many neurodivergent people aren't hindered by autism because they have some other neurodivergence, but that's a different issue with this sentence)
gizmo686 3 hours ago [-]
There is a map-territory problem here.
There is some underlying reality to what autism is, even if we do not have a good understanding of it; and even if turns out to be multiple unrelated things that happen to have similar symptoms.
Of the people with those actual conditions, it seems entirely plausible that some will not be hindered.
The authors of the DSM-V needed to create a diagnostic criteria for a condition that they do not understand, and for which no objective test is known. Further, their objective was designing something useful in a clinical setting. Giving those constraints, saying "if it is not a problem, we don't care about it" is entirely reasonable; despite not being reflective of the underlying reality.
rmoriz 2 hours ago [-]
That‘s why we have so many late diagnosed. People who are on the spectrum but were able to mask or were just lucky until luck runs out. Then it becomes a problem and a diagnosis. I knew I am different as long as I can remember. It was obvious in Kindergarten and also in every type of school and later in work. I‘m an old millennial and nobody was trained back then in the 80/90s. Before it became a diagnosis and before awareness started to rise, people unalived them, died homeless or in prisons/wards.
squirrel 3 hours ago [-]
As I commented in another thread, there's no a priori reason to believe that the "average" glutamate receptor level is the "right" one. Isn't it possible that there are:
1. "Normal" people with a level of glutamate receptors at 10, say, on a scale I'm inventing for this example
2. "Autistic" (according to the DSM) people with a level of, say, 5, who are hindered by the effects of being at this level
3. "A little bit autistic" people at a level of, say, 8, who aren't hindered and don't meet the DSM criteria, but in fact actually benefit from the effects of being at this level
Some "normals" might then want to inhibit their glutamate receptors somewhat to get the benefits of being at an 8 or a 9 on my made-up scale.
literalAardvark 12 minutes ago [-]
Perhaps. But remember that this is a very complex 3D structure with varying receptor densities, it's not "The Glutamate Level", it's some neural network areas with higher or lower excitability connected to other neural networks.
Just like with ADHD it's likely that medication will at best have limited effectiveness and many side effects.
Perhaps your thinking on this lacks grey areas. A healthy percentage of extremely successful people in computing are referred to as “on the spectrum” - are these people helped by having some of the aspects of autism or hindered by it? Why do we need to have a diagnosis for people to have aspects of this pathology?
boltzmann-brain 7 hours ago [-]
I think the point was that the colloquial use of "on the spectrum" is incorrect, as is a majority of layperson derived psychiatrical diagnosing.
andy_ppp 5 hours ago [-]
Are you really saying most people can’t discern autistic spectrum behaviour in their peers?
literalAardvark 7 minutes ago [-]
Clinical autism and clinical ADHD are notoriously difficult to diagnose in adults. In some countries it's even illegal to prescribe stims unless there's a childhood ADHD diagnostic.
Adults have been socialised to mask the more problematic behaviours, and they can also be unaware that what they're doing is masking: they can believe that everyone struggles like that.
vosper 4 hours ago [-]
To the level of a clinical diagnosis, yeah it seems quite likely to me that most people can’t discern autistic spectrum behaviour in their peers. I bet most people couldn't even accurately say what those behaviours would be.
andy_ppp 3 hours ago [-]
Definitely nobody in this thread struggling to see the grey areas and wanting to make sure everything is very cleanly defined, as if it’s difficult for them to deal with situations that are outside of rigorously defined clinical diagnostic criteria, for example… BTW just to be crystal clear - I’m obviously making a silly joke here it’s not intended to be serious :-D
TheOtherHobbes 2 hours ago [-]
"On the spectrum" has more or less become code for "introverted, obsessive, socially inept, and a little scary."
That can certainly be a syndrome, but the official DSM definition of autism is not based on those criteria.
Clinical autism tends to be much harsher in its presentation.
6 hours ago [-]
tiberriver256 9 hours ago [-]
Maybe they meant neurodivergent as a broader category? Like "some people are neurodivergent but don't have autism"
That would be a bit weird though...
EDIT: Neurodivergent is very much a broader category. What I meant would be weird is to state the obvious... Very much sounded like they were trying to say some people with autism may not want to get "cured" but using the wrong words
3836293648 7 hours ago [-]
Neurodivergent doesn't mean autistic. There are tonnes on non-autistic neurodivergent people. All the dyslexics, ADHDers and so on
RobotToaster 52 minutes ago [-]
Almost all of those conditions include some kind of hinderance in their definition though.
The only possible exception I can think of is synaesthesia.
LoganDark 1 hours ago [-]
> This is more or less not true. If it doesn't hinder a person in any aspect of their life, they don't fit the DSM-V criteria for a diagnosis.
You're confusing autism itself with Autism Spectrum Disorder. Autism Spectrum Disorder indeed has to do with difficulties ("deficits" / "impairment"). Autism itself on the other paw is a physical, quantifiable difference in neural architecture. Autistic people think and work differently, whether they have been diagnosed with Autism Spectrum Disorder or not.
It's also worth noting that autism is not the only neurodivergence, it's just the most widely known one (IIRC).
For reference, my copy of the DSM-5 states the following diagnostic criteria for Autism Spectrum Disorder: (sub-items elided)
> A. Persistent deficits in social communication and social interaction across multiple contexts, as manifested by the following, currently or by history (examples are illustrative, not exhaustive; see text): [...]
> B. Restricted, repetitive patterns of behavior, interests, or activities, as manifested by at least two of the following, currently or by history (examples are illustrative, not exhaustive; see text): [...]
> Symptoms must be present in the early developmental period (but may not become fully manifest until social demands exceed limited capacities, or may be masked by learned strategies in later life).
> D. Symptoms cause clinically significant impairment in social, occupational, or other important
areas of current functioning.
> E. These disturbances are not better explained by intellectual disability (intellectual developmental disorder) or global developmental delay. Intellectual disability and autism spectrum disorder frequently co-occur; to make comorbid diagnoses of autism spectrum disorder and intellectual disability, social communication should be below that expected for general developmental level.
wizzwizz4 9 hours ago [-]
The DSM-V criteria are not a good description of the natural category, and most people don't actually use them. They are, at best, a vague gesture in the direction of the natural category. The ICD-11 criteria (6A02) are better, but are still contradicted by, for instance, studies evidencing the double-empathy problem. Trained psychologists know which diagnostic criteria to take literally, and which to interpret according to the understanding of the authors.
roywiggins 8 hours ago [-]
If someone doesn't have any deficits or impairments at all then they won't qualify under ICD-11 either:
"Deficits are sufficiently severe to cause impairment in personal, family, social, educational, occupational or other important areas of functioning..."
wizzwizz4 8 hours ago [-]
Virtually none of the definitions in the ICD or DSM are entirely correct: that doesn't mean they're not useful. For example, you stop meeting the literal diagnostic criteria of many conditions if they're being treated adequately, but that doesn't mean you no longer have those conditions. Someone on antiretrovirals with no detectable HIV viral load still has HIV, and still needs to take the antiretrovirals. No competent doctor would diagnose them as "cured". Yet, they would not meet the diagnostic criteria described in the ICD-11:
> A case of HIV infection is defined as an individual with HIV infection irrespective of clinical stage including severe or stage 4 clinical disease (also known as AIDS) confirmed by laboratory criteria according to country definitions and requirements.
and rarely they may never have met these criteria. This is HN, so a computer analogy might be more helpful: ask a non-technical friend to read through some of the POSIX.1-2024 spec, then ask them to explain the signal handling, or the openat error codes. They will totally misunderstand it, because the POSIX specs are not actually clear: their purpose is to jog the memory of the expert reader, and describe the details they might have forgotten, not to provide a complete and accurate description suitable for teaching.
(Edit: pointless confrontational passage excised. Thanks for the criticism.)
tibbar 8 hours ago [-]
This bit:
> Are you a trained psychologist?
seems a bit confrontational, unless you yourself are a trained psychologist, in which case it would seem fitting to volunteer those credentials along with this challenge.
ribosometronome 7 hours ago [-]
Why is someone on HIV antivirals if no test ever confirmed them to have HIV? Presumably, they were confirmed as having HIV and have reduced its load to beneath detectable levels but that doesn't erase the previous confirmation.
I think that's all an aside, though, if not the ICD (as suggested by another poster) or the DSM definition initially used, which definition is correct?
OP, I think, is clearly harkening back to a previous post on HN (article at: https://www.psychiatrymargins.com/p/autisms-confusing-cousin...) by a professional discussing that the public often misunderstands and ignores key aspects of the definition. This seems rather a bit like you pointing out laypeople might read and not understand what they got out of the POSIX.1-2024 spec. Except it seems you're suggesting instead that the layperson understanding is correct.
ACow_Adonis 8 hours ago [-]
But going by the strict notion of DSM-V criteria of providing a hindrance, we hit the somewhat problematic definition whereby a person can have autism at one point in their life (when it hinders them in a context), moves into another point or context in their life (where it does not) and therefore they do not or would not meet the criteria for having autism if they sought a diagnosis at that point in time, and then move back into another point or context in their life where it hinders them and so now they meet the criteria and presumably have autism again.
Now, needless to say, this is not how anyone actually thinks about psychiatric or psychological issues in practice, especially with conditions such as autism, and just highlights the relative absurdity of some of the diagnostic metrics, practices and definitions.
What we tend to do is tie the diagnosis of autism to the individual identity and assume that it is a consistent category and applicative diagnosis that stays with a person over time because it is biological. We know, of course, that this is despite not having any working biological test for it, and diagnosing it via environmental and behavioural contexts. And don't even get me started on tying in diagnosis of aspergers/autistic individuals with broadly differing abilities and performance metrics on a range of metrics under the one condition such that the non-verbals and low-functioning side of neurotypicals get lumped in with the high iq and hyper-verbal high-functioning aspergers as having the same related condition even though neurotypicals are closer to the non-verbals and low-iqs on the same metrics and scores.
The entire field and classification system, along with the popular way of thinking about the condition is, if i might editorialise, an absolute mess.
RobotToaster 44 minutes ago [-]
A person without legs does not stop being disabled because they have no need or desire to walk. The fact remains that should they need or desire to walk in the future the hinderance will still very much exist.
A similar example could be made of someone with gluten intolerance. If they do not eat foods that contain gluten they are still gluten intolerant. They are however still disabled by needing to stay in that situation.
roywiggins 7 hours ago [-]
Being reliant on a particular life situation does strike me as a hindrance in and of itself. Maybe more of a macro limitation than a day-to-day one, but a reasonable definition could encompass that, too.
fallingfrog 7 hours ago [-]
The autism itself, depending on the person, is often less of a problem than societal expectations. For example- in a world where everyone was red/green colorblind, such a condition would not be considered a handicap. And in a world where everyone was autistic, many things would be different.
Society punishes us severely for not being able to see the difference between red and green, to use that metaphor. And they seem to expect that if they punished us just a little harder, we would suddenly become normal. Thats the big problem. Non conforming behavior is always treated as a crime or offense on some level, but we cannot conform, and therefore must adjust to a life of endless punishment doled out by both authorities and peers.
Its quite difficult to go through life that way without developing a negative self image. This goes for people with autism, adhd and other types of neurodivergence.
hiddencost 5 hours ago [-]
Buddy. If you're building your world view around the DSM you're in serious trouble.
The only people who take the DSM seriously are insurance agents and charlatans.
zmmmmm 7 hours ago [-]
It's an interesting finding but important to note they are making no claim about causality. In fact, an explicit future question is whether changes in these receptors is present at onset or if it's a result of living with Autism.
Neurons specifically increase / decrease receptor density in response to environmental factors, eg: use of SSRI's. Any excess of neurotransmitter would likely lead to reduction in receptor density as part of the response. So the story can be as much about an excess of neurotransmitter as it is about depletion of the receptor.
Perhaps the main story here is they can use EEGs as a proxy for measuring this effect so they don't need to put people through PET scans to do wider studies.
ear7h 11 hours ago [-]
N=32 and
> We want to start creating a developmental story and start understanding whether the things that we’re seeing are the root of autism or a neurological consequence of having had autism your whole life
jmward01 10 hours ago [-]
Yeah, how many studies are done a year? Random chance is the #1 explanation with that small of a sample size. It doesn't take a degree in stats say that the next thing that needs to be done is to replicate the study a few times before making any claims or searching for any publicity. This subject is so emotional for the families involved that publicizing without more confirmation is a bit irresponsible especially if it is easy to do follow-up studies.
jfengel 9 hours ago [-]
Follow-up studies cost money, and you don't get any of that if you don't publish.
jmward01 8 hours ago [-]
Agreed. Publish, but don't publicize. My remarks were aimed at the article, not the paper. This sounds like a promising, very initial, study that needs a lot more data before making claims about having found anything. Qualified headlines like 'Early study hints at..' Or 'Initial research potentially shows a promising....' would be better but even then a study with this little data should be very cautiously approached by any type of science reporting. More than mentioning it in passing as promising is probably not warranted until the n value is a lot higher and involves other teams and other methods.
robwwilliams 6 hours ago [-]
The reduction of mGluR5 was reported 10 years ago in postmortem tissue.
doi: 10.1016/j.bbi.2015.05.009
slashdave 10 hours ago [-]
It's a university press release. Hyperbole in practice.
Wish I could read the paper.
robwwilliams 7 hours ago [-]
Classic academic public relations piece. Not bad but more fluff than insight. Authors often have to grin and bear this PR machine, praying peers will forgive them their trespasses.
But here there’s a basic design flaw. This is a study of 16 ASD cases and 16 neurotypical controls. Small sample sizes like this require careful matching. The problem: the autistic subjects are 100% White but controls are 37.5% White. That imbalance can’t be waved away with statistics or Jedi mind tricks. Recruiting matched neurotypicals would have been straightforward.
One other issue is high heterogeneity within the two groups. In their Figure 1 (sorry behind a paywall), 4 - 6 of the autistic individuals have low mGlu5 levels across all regions. Two or three neurotypicals have high levels. Are these distributions actually normal, or are subgroups driving effects? It would help to know whether the participants’ GRM5 genotypes were informative wrt these subgroups. They weren’t checked.
rapjr9 7 hours ago [-]
“We have found this really important, never-before-understood difference in autism that is meaningful, has implications for intervention, and can help us understand autism in a more concrete way than we ever have before,”
So we might be able to make all the non-autistic people autistic? What would the world be like if everyone was mildly autistic?
My impression is this article and research that generalizes across the entire spectrum is not very useful.
robwwilliams 6 hours ago [-]
That quote is over the top. Given the imbalance between groups it is also embarrassing to read.
LoganDark 44 minutes ago [-]
I hope emerging research that divides the autism spectrum into four phenotypes[0] eventually gets recognized and incorporated into research like this. I still believe comparing the entire spectrum at once is the wrong approach, especially since the variants of autism express so differently.
As an example: I'm autistic and I learn inside-out, building larger new concepts out of smaller existing ones; those with Asperger's on the other paw, learn outside-in instead, breaking down larger existing concepts into smaller new ones; both are part of the "autism spectrum", but differ very fundamentally.
Given that the origin of "autism" is simply "thinking that differs from usual", there's no evidence that there is a single underlying cause to find, nor that generalizations across the entire spectrum will reveal much of anything other than coincidence.
I believe we need to individualize new research to the variants that we now know exist, because otherwise we will continue to all-but erase anything that isn't common to the entire spectrum.
Interesting indeed. Does such a finding suggest any worthwhile easy-to-try 'treatments' that may help alleviate symptoms?
I don't know much about the biochemistry here, I assume this is not something like GABA that can be directly supplemented. But maybe there are precursor nutritional and supplemental substances that can help these people upregulate how much of the glutamate molecule in question the body can produce.
GoatInGrey 9 hours ago [-]
Unless you can get the blastocyst and fetus to take supplements, any treatment would be attempting to undo the effects that have already taken place.
For now, your best options are ESDM, occupational therapy, modified CBT, ABA, or neurofeedback, depending on your circumstances and presentation. Except for neurofeedback, these are behavioral approaches, so the architectural and neural activity variations aren't directly addressed.
zmmmmm 7 hours ago [-]
Receptors quite readily remodel in response to external factors. It is one of the things antidepressants do.
To me it's kind of the biggest red flag here, if it's really about receptors then autism should be far more plastic than it is currently defined to be (which is kind of silly since at the moment any sign of plasticity puts you outside one of the hard criteria for an autism diagnosis - so almost definitionally, it can't be the answer).
wizzwizz4 11 hours ago [-]
There isn't enough information to start doing that. Consider: UV exposure results in sunburn, cellular damage, and increased skin pigmentation. We have medication that reduces skin pigmentation. Should we give it to people who experience chronic sunburn?
esseph 10 hours ago [-]
The third paragraph:
> Now, a new study in The American Journal of Psychiatry has found that brains of autistic people have fewer of a specific kind of receptor for glutamate, the most common excitatory neurotransmitter in the brain. The reduced availability of these receptors may be associated with various characteristics linked to autism.
Reduce receptors. This might suggest a _developmental_ or genetic link. Think of this more like "height" or a particular "facial feature" of a person.
joshcsimmons 9 hours ago [-]
Very interesting - wonder when this will be cost effective for testing!
ziofill 5 hours ago [-]
Someone needs to tell RFK Jr -_-
8 hours ago [-]
8 hours ago [-]
Uptrenda 9 hours ago [-]
can we use this to detect all the tiktok normies who are now claiming they have autism to be spedcal? that is the question.
Edit: HNs love to "steel man" every argument, just not my elegant shit posts. Hey, what gives? Here is the extended argument then. Modern psychiatric circles are complaining about a trend of patients that are basically using information online to fake psychiatric disorders. It's based on whatever is "fashionable" in the moment. In the past it was "multiple personality disorder" (contested -- most dont think it exists.) Today its autism and ADHD.
Why is this bad? Because there's a limited number of resources available to help these disabled individuals. And it really doesn't help them out much when the the spokesmen for their illness don't even have the illness. You should look at the diagnostic increases for autism in Australia. "In 2022 there were 290,900 Autistic Australians, a 41.8% increase from the 205,200 in 2018" Now, does +41 percent reflect a capability increase in diagnosis ability? Or (more likely) does it reflect trends in people seeking out the diagnosis.
Keep in mind getting diagnosed with autism in Australia comes with considerable benefits. You get bux from cennolink for life. Potentially people come to clean your house for you (yes really). There are organisations to improve your quality of life that will even make allowances for things like buying you a gaming PC if thats what it means for you or cooking meals for you. There are also allowances in scholastic capacities like additional test time, longer periods to do assignments, and on and on. You're basically set for life in Australia if you get an autism diagnosis which people share how to do on TikTok.
So yeah, that's the context for my post. I'm seeing many people now faking this illness and I think its messed up.
ijustwork 10 hours ago [-]
[flagged]
mapontosevenths 9 hours ago [-]
This was studied because it sounds reasonable on paper and several small studies showed a small link.
However, they did a very large cohort study with hundreds of thousands of subjects. The link completely disappears when genetics are accounted for via sibling pairs.[0]
It took almost two whole minutes of Googling for me to disprove this nonsense. Which shows that RFK did less than 2 minutes worth of research before panicking the world.
I will say that this study presented a major challenge to the tylenol hypothesis. To my mind, there is still a remote possibility that the tylenol hypotehsis might just be relevant to a smaller subset of autistic individuals...but I am coming from the general outlook of believing autism needs to be subtyped when looking at etiology.
mapontosevenths 8 hours ago [-]
Personally, I very much agree. I feel that while the idea of a spectrum wasn't a mistake, it was only a start.
api 9 hours ago [-]
But did you check the vibes?
mapontosevenths 8 hours ago [-]
I did, but I'm on the spectrum so I failed the vibe check. ;)
tomerico 9 hours ago [-]
Didn’t whole internet get angry for Trump’s administration publishing a warning that Tylenol during pregnancy may cause autosim?
MangoToupe 9 hours ago [-]
Can you explain the logical leap you're making here? Unless this is RFK Jr we're talking to, you're comparing two wildly different contexts.
ijustwork 9 hours ago [-]
.
MangoToupe 9 hours ago [-]
The logical leap
ijustwork 9 hours ago [-]
.
mapontosevenths 9 hours ago [-]
Anything claimed without evidence can be dismissed without evidence.
perching_aix 9 hours ago [-]
> propaganda mouthpieces
Bit rich coming from a sockpuppet account created 57 minutes ago...
- exclusively commenting on this thread
- uncritically addressing it from a very specific angle
- mentioning specific things that sound related while not actually connecting them to the overall story with the same rigor
...isn't it?
ijustwork 10 hours ago [-]
.
diydsp 9 hours ago [-]
The vaccine autism hoax is traced back to one specific discredired researcher:
It would also be interesting if there's no link to be found.
lez 10 hours ago [-]
[flagged]
tiberriver256 9 hours ago [-]
16 "autistic brains" were scanned and they are thinking this applies generally to all people with autism?
Shows how shockingly unaware even researchers are on how broad and nonspecific the diagnosis of autism is...
Were these 16 people hypo or hyper sensitive? Which of their five senses were involved? All? Some? Were some senses hyper and others hypo?
Need to start with categorization and specificity before we can make meaningful progress in research
SubiculumCode 9 hours ago [-]
I have not read the paper as I am traveling, but just in case your opinion is based on the news article, let's not confuse that reporting with the actual research.claims or the actual views held by the scientists involved. This was likely a paper demonstrating the technique in preparation of a more comprehensive study.
tiberriver256 8 hours ago [-]
The full paper isn't open so I can only read the abstract, method and results.
The part I take issue with:
"lower brain-wide mGlu5 availability may represent a molecular mechanism underlying altered excitatory neurotransmission that has the potential to stratify the heterogeneous autism phenotype."
Seems like the very premise is flawed, though. Searching for a single global identifier for autism would be like if we spent research time trying to find a single global identifier for cancer. Noble effort... Way harder than spending effort on subcategorization into "lung" and "heart" cancers and working on research for detection of those subtypes.
The only good categorization we have in autism now is severity.
The anecdote I always like to share is Temple Grandin.
She was hyper-sensitive to auditory and tactile senses. The cause for this hypersensitivity was cerebellar abnormalities in her brain. Right now, someone who is hypo-sensitive to sound and touch because of different cerebellar development will also be put in the same bucket diagnostically speaking. There's not gonna be any universal way to detect that though...
To quote her directly:
"It would be my number one research priority, but one of the problems we’ve got on studying this, is that one person may have visual sensitivity, another one touch sensitivities, another one, auditory sensitivities. And when you study these, you got to separate them out. You can’t just mix them all together."
https://www.sensoryfriendly.net/podcast/understanding-my-aut...
SubiculumCode 8 hours ago [-]
I would say that as an autism researcher whose focus is in finding autism subgroups that I doubt that any specific receptor differences will not apply to the whole spectrum, probably just to one or several subsets
tiberriver256 8 hours ago [-]
So glad to hear research is being done in that area.
I'm a dad of two autistic boys who I think would be very different categories. I have friends whose child isn't really autistic, they have a much more rare and specific diagnosis but it's so rare it's hard to get supports so they got him diagnosed as autistic because that criteria is so broad almost anyone can qualify.
Thank you for your work!
Rendered at 10:40:03 GMT+0000 (Coordinated Universal Time) with Vercel.
There are perverse consequences in brain chemistry and signalling: flooding a brain deficient in glutamate processing receptors with glutamate may not help, it may overload pathways and cause hindrance, not compensation.
Signs like this may be consequential, or related but not causal, or may simply turn out to be wrong.
IF a small sample effect turns out to be indicative of a larger property, and IF it's shown to be causal and IF remeditation involves boosting blood borne glutamate or precursors is 3 stacked IF.
IF its detectable in a young brain it could be diagnostic.
IF its detectable in a young brain and amenable to gene therapy and IF it's causative then treatment would be useful.
IF excess glutamate is not a problem and dietary supplemented sources cross the blood brain barrier and don't trip over homeostasis then it's possibly worth exploring.
(Not a scientist, not a biologist)
Why not consider the opposite, that the most beneficial quantity of glutamate receptors could be somewhere below the typical amount? If that were true, then we could try to help others reduce their glutamate receptor level to become healthier and more successful (and a little more autistic).
If we found, say, an association between a lower level of neurological characteristic X and concert-level piano skill, then those who aspire to play that instrument at an elite level might try to decrease X. The fact that most of us are rubbish piano players would not be evidence that lower levels of X are harmful, but very much the opposite.
So what I wrote should be read with a "if it is held to be a condition which deserved remediation or avoidance of it's manifestation" attached.
Most medical conditions are couched in this sense, that a deficit or departure from the normal is a problem. In matters of brain chemistry it pays to be more nuanced.
This is more or less not true. If it doesn't hinder a person in any aspect of their life, they don't fit the DSM-V criteria for a diagnosis.
(Many neurodivergent people aren't hindered by autism because they have some other neurodivergence, but that's a different issue with this sentence)
There is some underlying reality to what autism is, even if we do not have a good understanding of it; and even if turns out to be multiple unrelated things that happen to have similar symptoms.
Of the people with those actual conditions, it seems entirely plausible that some will not be hindered.
The authors of the DSM-V needed to create a diagnostic criteria for a condition that they do not understand, and for which no objective test is known. Further, their objective was designing something useful in a clinical setting. Giving those constraints, saying "if it is not a problem, we don't care about it" is entirely reasonable; despite not being reflective of the underlying reality.
1. "Normal" people with a level of glutamate receptors at 10, say, on a scale I'm inventing for this example
2. "Autistic" (according to the DSM) people with a level of, say, 5, who are hindered by the effects of being at this level
3. "A little bit autistic" people at a level of, say, 8, who aren't hindered and don't meet the DSM criteria, but in fact actually benefit from the effects of being at this level
Some "normals" might then want to inhibit their glutamate receptors somewhat to get the benefits of being at an 8 or a 9 on my made-up scale.
Just like with ADHD it's likely that medication will at best have limited effectiveness and many side effects.
Adults have been socialised to mask the more problematic behaviours, and they can also be unaware that what they're doing is masking: they can believe that everyone struggles like that.
That can certainly be a syndrome, but the official DSM definition of autism is not based on those criteria.
Clinical autism tends to be much harsher in its presentation.
That would be a bit weird though...
EDIT: Neurodivergent is very much a broader category. What I meant would be weird is to state the obvious... Very much sounded like they were trying to say some people with autism may not want to get "cured" but using the wrong words
The only possible exception I can think of is synaesthesia.
You're confusing autism itself with Autism Spectrum Disorder. Autism Spectrum Disorder indeed has to do with difficulties ("deficits" / "impairment"). Autism itself on the other paw is a physical, quantifiable difference in neural architecture. Autistic people think and work differently, whether they have been diagnosed with Autism Spectrum Disorder or not.
It's also worth noting that autism is not the only neurodivergence, it's just the most widely known one (IIRC).
For reference, my copy of the DSM-5 states the following diagnostic criteria for Autism Spectrum Disorder: (sub-items elided)
> A. Persistent deficits in social communication and social interaction across multiple contexts, as manifested by the following, currently or by history (examples are illustrative, not exhaustive; see text): [...]
> B. Restricted, repetitive patterns of behavior, interests, or activities, as manifested by at least two of the following, currently or by history (examples are illustrative, not exhaustive; see text): [...]
> Symptoms must be present in the early developmental period (but may not become fully manifest until social demands exceed limited capacities, or may be masked by learned strategies in later life).
> D. Symptoms cause clinically significant impairment in social, occupational, or other important areas of current functioning.
> E. These disturbances are not better explained by intellectual disability (intellectual developmental disorder) or global developmental delay. Intellectual disability and autism spectrum disorder frequently co-occur; to make comorbid diagnoses of autism spectrum disorder and intellectual disability, social communication should be below that expected for general developmental level.
"Deficits are sufficiently severe to cause impairment in personal, family, social, educational, occupational or other important areas of functioning..."
> A case of HIV infection is defined as an individual with HIV infection irrespective of clinical stage including severe or stage 4 clinical disease (also known as AIDS) confirmed by laboratory criteria according to country definitions and requirements.
and rarely they may never have met these criteria. This is HN, so a computer analogy might be more helpful: ask a non-technical friend to read through some of the POSIX.1-2024 spec, then ask them to explain the signal handling, or the openat error codes. They will totally misunderstand it, because the POSIX specs are not actually clear: their purpose is to jog the memory of the expert reader, and describe the details they might have forgotten, not to provide a complete and accurate description suitable for teaching.
(Edit: pointless confrontational passage excised. Thanks for the criticism.)
> Are you a trained psychologist?
seems a bit confrontational, unless you yourself are a trained psychologist, in which case it would seem fitting to volunteer those credentials along with this challenge.
I think that's all an aside, though, if not the ICD (as suggested by another poster) or the DSM definition initially used, which definition is correct?
OP, I think, is clearly harkening back to a previous post on HN (article at: https://www.psychiatrymargins.com/p/autisms-confusing-cousin...) by a professional discussing that the public often misunderstands and ignores key aspects of the definition. This seems rather a bit like you pointing out laypeople might read and not understand what they got out of the POSIX.1-2024 spec. Except it seems you're suggesting instead that the layperson understanding is correct.
Now, needless to say, this is not how anyone actually thinks about psychiatric or psychological issues in practice, especially with conditions such as autism, and just highlights the relative absurdity of some of the diagnostic metrics, practices and definitions.
What we tend to do is tie the diagnosis of autism to the individual identity and assume that it is a consistent category and applicative diagnosis that stays with a person over time because it is biological. We know, of course, that this is despite not having any working biological test for it, and diagnosing it via environmental and behavioural contexts. And don't even get me started on tying in diagnosis of aspergers/autistic individuals with broadly differing abilities and performance metrics on a range of metrics under the one condition such that the non-verbals and low-functioning side of neurotypicals get lumped in with the high iq and hyper-verbal high-functioning aspergers as having the same related condition even though neurotypicals are closer to the non-verbals and low-iqs on the same metrics and scores.
The entire field and classification system, along with the popular way of thinking about the condition is, if i might editorialise, an absolute mess.
A similar example could be made of someone with gluten intolerance. If they do not eat foods that contain gluten they are still gluten intolerant. They are however still disabled by needing to stay in that situation.
Society punishes us severely for not being able to see the difference between red and green, to use that metaphor. And they seem to expect that if they punished us just a little harder, we would suddenly become normal. Thats the big problem. Non conforming behavior is always treated as a crime or offense on some level, but we cannot conform, and therefore must adjust to a life of endless punishment doled out by both authorities and peers.
Its quite difficult to go through life that way without developing a negative self image. This goes for people with autism, adhd and other types of neurodivergence.
The only people who take the DSM seriously are insurance agents and charlatans.
Neurons specifically increase / decrease receptor density in response to environmental factors, eg: use of SSRI's. Any excess of neurotransmitter would likely lead to reduction in receptor density as part of the response. So the story can be as much about an excess of neurotransmitter as it is about depletion of the receptor.
Perhaps the main story here is they can use EEGs as a proxy for measuring this effect so they don't need to put people through PET scans to do wider studies.
> We want to start creating a developmental story and start understanding whether the things that we’re seeing are the root of autism or a neurological consequence of having had autism your whole life
doi: 10.1016/j.bbi.2015.05.009
Wish I could read the paper.
But here there’s a basic design flaw. This is a study of 16 ASD cases and 16 neurotypical controls. Small sample sizes like this require careful matching. The problem: the autistic subjects are 100% White but controls are 37.5% White. That imbalance can’t be waved away with statistics or Jedi mind tricks. Recruiting matched neurotypicals would have been straightforward.
One other issue is high heterogeneity within the two groups. In their Figure 1 (sorry behind a paywall), 4 - 6 of the autistic individuals have low mGlu5 levels across all regions. Two or three neurotypicals have high levels. Are these distributions actually normal, or are subgroups driving effects? It would help to know whether the participants’ GRM5 genotypes were informative wrt these subgroups. They weren’t checked.
So we might be able to make all the non-autistic people autistic? What would the world be like if everyone was mildly autistic?
My impression is this article and research that generalizes across the entire spectrum is not very useful.
As an example: I'm autistic and I learn inside-out, building larger new concepts out of smaller existing ones; those with Asperger's on the other paw, learn outside-in instead, breaking down larger existing concepts into smaller new ones; both are part of the "autism spectrum", but differ very fundamentally.
Given that the origin of "autism" is simply "thinking that differs from usual", there's no evidence that there is a single underlying cause to find, nor that generalizations across the entire spectrum will reveal much of anything other than coincidence.
I believe we need to individualize new research to the variants that we now know exist, because otherwise we will continue to all-but erase anything that isn't common to the entire spectrum.
[0]: https://www.medrxiv.org/content/10.1101/2024.08.15.24312078v...
I don't know much about the biochemistry here, I assume this is not something like GABA that can be directly supplemented. But maybe there are precursor nutritional and supplemental substances that can help these people upregulate how much of the glutamate molecule in question the body can produce.
For now, your best options are ESDM, occupational therapy, modified CBT, ABA, or neurofeedback, depending on your circumstances and presentation. Except for neurofeedback, these are behavioral approaches, so the architectural and neural activity variations aren't directly addressed.
To me it's kind of the biggest red flag here, if it's really about receptors then autism should be far more plastic than it is currently defined to be (which is kind of silly since at the moment any sign of plasticity puts you outside one of the hard criteria for an autism diagnosis - so almost definitionally, it can't be the answer).
> Now, a new study in The American Journal of Psychiatry has found that brains of autistic people have fewer of a specific kind of receptor for glutamate, the most common excitatory neurotransmitter in the brain. The reduced availability of these receptors may be associated with various characteristics linked to autism.
Reduce receptors. This might suggest a _developmental_ or genetic link. Think of this more like "height" or a particular "facial feature" of a person.
Edit: HNs love to "steel man" every argument, just not my elegant shit posts. Hey, what gives? Here is the extended argument then. Modern psychiatric circles are complaining about a trend of patients that are basically using information online to fake psychiatric disorders. It's based on whatever is "fashionable" in the moment. In the past it was "multiple personality disorder" (contested -- most dont think it exists.) Today its autism and ADHD.
Why is this bad? Because there's a limited number of resources available to help these disabled individuals. And it really doesn't help them out much when the the spokesmen for their illness don't even have the illness. You should look at the diagnostic increases for autism in Australia. "In 2022 there were 290,900 Autistic Australians, a 41.8% increase from the 205,200 in 2018" Now, does +41 percent reflect a capability increase in diagnosis ability? Or (more likely) does it reflect trends in people seeking out the diagnosis.
Keep in mind getting diagnosed with autism in Australia comes with considerable benefits. You get bux from cennolink for life. Potentially people come to clean your house for you (yes really). There are organisations to improve your quality of life that will even make allowances for things like buying you a gaming PC if thats what it means for you or cooking meals for you. There are also allowances in scholastic capacities like additional test time, longer periods to do assignments, and on and on. You're basically set for life in Australia if you get an autism diagnosis which people share how to do on TikTok.
So yeah, that's the context for my post. I'm seeing many people now faking this illness and I think its messed up.
However, they did a very large cohort study with hundreds of thousands of subjects. The link completely disappears when genetics are accounted for via sibling pairs.[0]
It took almost two whole minutes of Googling for me to disprove this nonsense. Which shows that RFK did less than 2 minutes worth of research before panicking the world.
[0] https://jamanetwork.com/journals/jama/fullarticle/2817406
Bit rich coming from a sockpuppet account created 57 minutes ago...
- exclusively commenting on this thread
- uncritically addressing it from a very specific angle
- mentioning specific things that sound related while not actually connecting them to the overall story with the same rigor
...isn't it?
https://time.com/5175704/andrew-wakefield-vaccine-autism/
Shows how shockingly unaware even researchers are on how broad and nonspecific the diagnosis of autism is...
Were these 16 people hypo or hyper sensitive? Which of their five senses were involved? All? Some? Were some senses hyper and others hypo?
Need to start with categorization and specificity before we can make meaningful progress in research
The part I take issue with: "lower brain-wide mGlu5 availability may represent a molecular mechanism underlying altered excitatory neurotransmission that has the potential to stratify the heterogeneous autism phenotype."
Seems like the very premise is flawed, though. Searching for a single global identifier for autism would be like if we spent research time trying to find a single global identifier for cancer. Noble effort... Way harder than spending effort on subcategorization into "lung" and "heart" cancers and working on research for detection of those subtypes.
The only good categorization we have in autism now is severity.
The anecdote I always like to share is Temple Grandin.
She was hyper-sensitive to auditory and tactile senses. The cause for this hypersensitivity was cerebellar abnormalities in her brain. Right now, someone who is hypo-sensitive to sound and touch because of different cerebellar development will also be put in the same bucket diagnostically speaking. There's not gonna be any universal way to detect that though...
To quote her directly:
"It would be my number one research priority, but one of the problems we’ve got on studying this, is that one person may have visual sensitivity, another one touch sensitivities, another one, auditory sensitivities. And when you study these, you got to separate them out. You can’t just mix them all together." https://www.sensoryfriendly.net/podcast/understanding-my-aut...
I'm a dad of two autistic boys who I think would be very different categories. I have friends whose child isn't really autistic, they have a much more rare and specific diagnosis but it's so rare it's hard to get supports so they got him diagnosed as autistic because that criteria is so broad almost anyone can qualify.
Thank you for your work!