Vulnerable neurons linked to social dysfunction in autistic mice
www.riken.jp
RIKEN researchers have shown in a mouse model of autism that specific oxytocin-secreting neurons in the brain are disproportionately disrupted and that neurostimulation can restore social behaviors.

Initially I was all but I don’t want to be social. Then I was oh that’s what their talking about. I feel I am social enough though. And all science should be repeated for vapidity.

  • sp3ctr4l@lemmy.zipEnglish
    5·
    13 days ago

    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.