zlacker

Full text: https://www.mdpi.com/2072-6643/15/17/3772

What is interesting here is that drinking 'diet soda' actually decreased the odds for girls (though not reaching statistical significance) - that strikes me as an extremely odd finding. Their discussion of 'why' was not very compelling. I have a hard time thinking there's anything causative with such a disparity in sex.

I also noticed that adjusting for some of the larger confounders for autism (maternal age, SES) didn't move the needle much. I would expect there to be a much larger difference between adjusted/not-adjusted OR. Maybe there's other confounders lurking or the adjustment was insufficient.

>>briHas+(OP)
Anything involving estrogens (such as plastics) will have sex-linked impacts.

>>foobie+t1
Common misconception: Most estrogens (particularly phytoestrogens, but also plastics) bind to receptors so weakly, they work more like antagonists in the presence of stronger estrogens (like red meat).

It'd be like trying to do anabolic steroids while your natural testosterone is very high.

>>asmor+D3
The endocrine system is complex and involves multiple pathways and feedback loops. A single compound's weak or strong binding affinity to a receptor doesn't provide a complete picture of its physiological impact.

>>briHas+(OP)
girls are already underdiagnosed for autism, and cultural norms allow their neurodivergence to blend in, so the data will always be bad if the parent doesn't have a daughter diagnosed with autism

>>awestr+56
This was not meant to be an exhaustive explainer, rather a single caveat to stop the "all you need is high absolute T and low absolute E" simplification in its tracks.

Receptor saturation (in this case, E1 vs E2; first pass metabolism turns E2 into E1) is something I had to learn out of neccessity because my endocrinologist didn't really do anything beyond loosely following ancient standards of practice (we don't have specialized gender clinics in Germany).