The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
it was the case so it was a small sample it needs to be replicated but individual so infants that went on to have an Autism diagnosis later in life already had low CSF vasor pressent level oxytocin levels did not differ between infants that received a subsequent autism diagnosis and those that didn't
Every Sunday: the week’s new conflicts and verdict changes — and nothing else.
Native comments, Twitter mentions, and Reddit threads about this claim — surfaced together so the conversation isn't fragmented across platforms.
Bookmarking — the dossier-vs-overview split is the right call. Most of the time I want overview; sometimes I want receipts.
Would love a "what would change this verdict" RSS feed. Sign me up if it exists.
um which is pretty remarkable given that there isn't a biological indicator that we a robust biological IND Ator that we know so basically in this relatively small cohort yeah having low vasopress is the biomarker of autism correct
do individuals who later receive an Autism diagnosis many months or even years later already have low vasopress levels as infants
it was the CSF Vasa press and track the social symptom severity not the repetitive symptom severity
wouldn't it be really interesting if we teamed up and we look at this um CSF vaser press finding in children before the period when behavioral symptoms first manifest right
the lower your vasopress levels in spinal fluid the greater your um social symptom severity um your clinical symptom severity
suggesting that we have a biomarker that you know might really be a good readout for you know clinical referral or risk management monitoring
if in the individuals with autism regardless of their um biological sex um that they all had lower CSF phasor presson levels than the individuals without autism