OK. Several possible estrogen-related connections have emerged in the last few days.
First, if estrogen is a trigger in teenaged girls for entering puberty, thus beginning the testosterone surges that freeze brain growth, and it is also true for males (a stretch) that estrogen levels trigger pubertal timing, might this also apply to male and female infant/toddler testosterone-surge synapse pruning that results in asymmetric cerebral lateralization? If so, might infant/toddler estrogen levels be instrumental in causing autism, low estrogen resulting in delayed growth?
Second, noting the seeming connection between estrogen’s focus on the young and the exhibition of maternal behavior along with estrogen’s focus on very specific features in a mate (thus driving the emergence of unique male species traits), is it true that species that engage in female sexual selection are also species where the mother exhibits maternal behavior? An implication is that K vs. r strategies might compel female choice and changes in the exhibition of male behaviors.
Third, might it be the case that estrogen, predating testosterone, is somehow responsible for early proliferation of life on earth insofar as estrogen is associated with creation, discrimination and focus on the young?
In the old religions, there is a view of life characterized by the triple symbol of virgin, mother and crone. There are goddesses that are both creator and destroyer. If we approach estrogen as contributing to the three hypothetical frames noted above, the female acquires a depth and power that is mythical in scope.
Estrogen nurtures the young. Estrogen focuses on particular features in mates and then encourages the proliferation of those features over generations. Whereas it seems like testosterone is deeply involved in the creative process, perhaps testosterone’s lack of discrimination places in the hands of the female the direction that evolution travels.
Whereas testosterone assigns the power, energy or speed with which evolution unfolds, estrogen governs creativity and direction.
The first two of the three premises noted above are testable hypotheses. If it is discovered that species that engage in female choice also display maternal behavior, I’m not sure how useful that information is, except that it supports the dynamic I’m proposing regarding human social evolution. It doesn’t prove anything. If, indeed, estrogen is a trigger for pubertal timing in males and females, then estrogen may be the trigger for early childhood testosterone surges, which are integral to the timing of maturation changes.
If males that are naturally maturational delayed experience a further delay in the timing of testosterone surges, then Asperger’s or autism might result.
It just struck me that whereas low estrogen in girls approaching puberty delays pubertal onset, in males it might be reversed. High estrogen in males might delay pubertal onset.
And there is the fact that I am an amateur. I’m associating fat levels with estrogen levels. The two may not be as closely related as I am assuming.
There are a lot of situations where male or female estrogen or testosterone levels go in opposite directions with the same environmental effects. What if baby males need low estrogen to time testosterone surges and baby females need high estrogen to time those surges?
High-fat diets would result in males with increased likelihood of autism.



Fat levels in males are tied to estrogen levels, e.g, the more body fat the higher the estrogen. Interesting post!
[...] autism. I’m not absolutely that is the case here, but there is that potential. But, as noted here and here, I’m playing with that [...]