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.
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..."
I repeat: “Trained psychologists know which diagnostic criteria to take literally, and which to interpret according to the understanding of the authors.” Are you a trained psychologist? Virtually none of the definitions in the ICD or DSM are entirely correct: that doesn't mean they're not useful.
> 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.
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.
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
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.
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...
"Deficits are sufficiently severe to cause impairment in personal, family, social, educational, occupational or other important areas of functioning..."
> 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.
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 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/