Autism

See if it watches the same YouTube video over and over

They used the valproic-acid mouse model of autism spectrum disorder; such mice exhibit reduced social behaviors as a result of being exposed to the anti-epileptic drug valproic acid in the womb.

Just like with autistic humans, you flood them with valproic acid while they are gestating.

/s

https://www.drugs.com/sfx/valproic-acid-side-effects.html

Valproate can impair cognitive development with prenatal exposure and produce major congenital malformations, particularly neural tube defects (eg, spina bifida), and neurodevelopmental disorders.

Basically, drug manufacturers decided that autism is the same thing as chemically lobotomizing and physically deforming the subject in utero, because chemically lobotomized mice are less social.

I wish I was making this up, but I'm not.

https://pmc.ncbi.nlm.nih.gov/articles/PMC4688329/

Autism is a specific disorder in humans, and most of its symptoms can only be approximated by animal models.

VPA induces ASD both in human and animals. The etiological mechanism may involve changes in epigenetic marks, expression level of genetic determinants as well as brain lesion.

Translated: If we give flood mice with valproic acid in utero, they develop brain lesions, which makes them kind of retarded (they literally use mental retardation as a 'common symptom' of autism in the paper) and bad at socializing, therefore that's basically the same as autism.

To apply this directly to humans, when an adult autism diagnosis requires something like a year or two of continuous meeting with a PhD psychologist, is completely bonkers.

Given that the core 'chemical imbalance' model that was the theoretical underpinning for the development of SSRIs has been shown to be at best, wildly incorrect, and at worst, totally bunk, I'd say this study is horseshit.

EDIT: When people make showerthoughts style questions like "what is going to be the 'oops we didn't know widespread cigarette or leaded gasoline usage was actually horrible for us' of our time?" ... the answer is mass use of manufactured psychoactive drugs.

The actual truth is that their efficacy in treating what they are prescribed to treat is far, far less than is commonly presented by most common people and professionals, that the proposed mechanisms to explain how and why they work are actually quite poorly understood and not backed up by real data (cough, almost all the studies are on psychiatric drugs are conducted or funded by the drug manufacturers themselves, cough), and that the deleterious side effects caused by them are far more common and severe than lay people and professionals believe.

Haven't you heard about the human autism detectors? Those people who say: "Oh, but you don't look autistic!"

/s

Observe it at mouse parties

Yeah, this is just another 'drenching a gestating mouse with valproic acid fucks up their oxytocin pathways' study for the pile.

My other comment links to... not quite a meta study, but a validity assesment of the valproic acid mouse autism model... done in 2015.

This isn't even news, people have known that in utero valproic acid fucks up oxytocin in mice for a decade.

The real question is:

Do autistic people actually have low levels of oxytocin, or something different going on with their oxytocin receptors?

The answer to this is:

Males have slightly lower than normal oxytocin levels as kids, but this disappears in adolescence and adulthood, and is not present for females.

https://pmc.ncbi.nlm.nih.gov/articles/PMC8615844/

We found that endogenous OT levels are lower in children with ASD as compared to NT controls (n = 1123; g = −0.60; p = 0.006), but this effect seems to disappear in adolescent (n = 152; g = −0.20; p = 0.53) and adult populations (n = 147; g = 0.27; p = 0.45).

Secondly, while no significant subgroup differences were found in regard to sex, the group difference in OT levels of individuals with versus without ASD seems to be only present in the studies with male participants (n = 814; g = −0.44; p = 0.08) and not female participants (n = 192; g = 0.11; p = 0.47).

Also, our methods of measuring actual oxytocin levels in humans don't seem to be very accurate:

An active controversy regarding the measurement of OT in biological fluids concerns whether these peripheral measures are actually reliable and valid approximations for levels of OT in the central nervous system [47].

In this regard, a recent meta-analysis revealed a positive correlation between peripheral OT levels and OT levels in the central nervous system, in particular after experimental stress induction.

As no correlation was observed under baseline conditions, it remains questionable to what extent peripheral OT levels may approximate central OT levels [25].

... Whats happening here is two things.

1: Drug manufacturers have decided that autism is a condition that can and should be cured and/or prevented.

2: Drug manufacturers are increasingly chemically lobotomizing gestating mice, to induce lower oxytocin levels, to then legitimize some future drug they'll design that will raise oxytocin levels in humans, and then promote and sell this as a cure for autism, even though there is no consensus whatsoever that that would actually 'cure' autism, as no one currently has any solid and verified concept of what autism even is, at biomechanical level.