We have a much larger and more complex brain than most animals, and our brain continues to undergo development a lot longer than is the case for most animal brains. Our brain development continues throughout the 9 months of our gestation, whereas things associated with our physical attributes (like major organ development, limb development and so forth), have all largely finished by the end of the first trimester. Because it has such a long window of vulnerability, our brain tends to be disproportionately affected by any kind of toxic exposure taking place during our prenatal development, so it should hardly come as a surprise that it tends to be the main thing affected when you expose an unborn baby to feminising hormones such as DES.
Furthermore, the way miscarriage preventatives such as DES (and the drug that has since replaced it, hydroxyprogesterone caproate) tend to be prescribed means that the exposure during the first trimester is small, with much heavier exposure during the second and third trimesters. Since most or all of the exposure doesn't occur until after the physical things associated with your sex have already completed their development, that makes it even less likely that there will be obvious physical effects, and more likely that the main place the effects will show up is in the brain. A website called Hormones Matter recently published an article I wrote explaining how this works:
https://www.hormonesmatter.com/maternal-des-exposure-intersex-development-males/Once you understand that it's hormones produced in the testicles that drive male development, that DES works very well as a chemical castration agent, and that it was typically given in progressively increasing doses that went higher and higher as the pregnancy continued, it's easy to see how it could have produced male appearing people with female brains. The exposure was still small enough during the first trimester so that a male baby's testicles could still produce testosterone. However, the dosage was progressively ramped up, and from the second trimester onwards, enough DES was crossing the placenta to chemically castrate a male fetus, causing that future person's testicular hormone production to drop to zero throughout the second and third trimesters. Since testicular hormones are what drive male development, and in the absence of those hormones, whether XX or XY, a fetus will develop as female by default, it's produced people who developed as male during the first trimester, but as female during the second and third trimesters. Because of the way development takes place in an unborn child, this results in people who physically appear to be male, but have female brains.
I think it's highly likely that hydroxyprogesterone caproate is doing the same thing, since it has similar pharmacological properties to a drug often used to chemically castrate sex offenders (medroxyprogesterone acetate), and is being given to pregnant women in what look like very high doses. The difference between DES and hydroxyprogesterone caproate is that the guidelines say to not initiate treatment until at least week 16 after conception, whereas, under the standard dosing schedule, DES was already being given in quite high doses earlier than that. So you'd expect the physical effects from hydroxyprogesterone caproate to be a lot less than from DES, even though it could still be causing female brain development to occur.
On another note, I recently found something that reinforces my opinion that the medical authorities have known for a long time that the male assigned children from DES pregnancies are often heavily physically and psychologically feminized, and they've opted for a cover up:
https://twitter.com/HughEaston/status/1032050001428525056
