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.
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.
(Edit: pointless confrontational passage excised. Thanks for the criticism.)
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.
> 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 metabotropic glutamate receptor subtype 5 (mGlu5) is involved in the central mechanism of action of paracetamol (acetaminophen), where the bioactive metabolite AM404 activates the TRPV1 channel–mGlu5 receptor–PLC–DAGL–CB1 receptor signaling cascade in the periaqueductal grey, contributing to its analgesic effect.
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.
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?
> 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.
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.
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.
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)
That would be a bit weird though...
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.
"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.
(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.
> 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
Wish I could read the paper.
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.
> 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.
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!