Researchers discover molecular difference in autistic brains

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.

> boosting glutamate won't work.

You would not want to boost glutamate. It's the opposite. You want to reduce glutamate and/or increase GABA. The problem is overexcitation, not underexcitation.

The reason the number of receptors might be low in the first place is downregulation from too much glutamate.

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.

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.

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.

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.

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.

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.

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

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?

> 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.

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.

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.

Whenever you measure two different groups, you find a difference. Can it be solely ascribed to the one variable? Doubtful. You would have to match the groups for all possible contributing factors, and here not even the basic demographics have been matched? Another statistical effect for the irreproducibility bin.

>It’s only one apple

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.

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.

A lot of people in the corresponding Reddit threads claim that NAC (N-Acetyl Cysteine) might help.

The paper is concerned mainly with one of several glutamate receptor subtypes.

Meta comment - what a weird comment to downvote. I am expressing curiosity in good faith after reading the article, with a fairly logical follow up. What is the point of commenting in this community if it's primarily cynicism and negativity?

That quote is over the top. Given the imbalance between groups it is also embarrassing to read.

Which autism? There are four: https://www.medrxiv.org/content/10.1101/2024.08.15.24312078v...

My impression is this article and research that generalizes across the entire spectrum is not very useful.

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.