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)
"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)
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
Neurodivergent doesn't mean autistic. There are tonnes on non-autistic neurodivergent people. All the dyslexics, ADHDers and so on
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?
I think the point was that the colloquial use of "on the spectrum" is incorrect, as is a majority of layperson derived psychiatrical diagnosing.
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.
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.
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.
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.
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..."
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.)
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.
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.
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.
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.
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
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.
The reduction of mGluR5 was reported 10 years ago in postmortem tissue.
doi: 10.1016/j.bbi.2015.05.009
Follow-up studies cost money, and you don't get any of that if you don't publish.
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.
It's a university press release. Hyperbole in practice.
Wish I could read the paper.
“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?
That quote is over the top. Given the imbalance between groups it is also embarrassing to read.
Very interesting - wonder when this will be cost effective for testing!
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.
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.
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).
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?
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.
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stop already with the sockpuppet accounts
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
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.
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...
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
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!