I think getting the word out about what happened with DES (and first generation progestins) would help.
Contrary to popular belief, the sex you develop as isn't determined by whether you have a Y chromosome or not, but by what hormones are present during the time your prenatal development is taking place. The medical and pharmaceutical establishment have done a great job of hiding the fact that, during the second half of the 20th century, they gave millions of pregnant women high doses of hormones which are now known to have gender bending properties, as part of treatment aimed at preventing miscarriages and premature births: DES and ethinyl estradiol, which can induce female development in a biologically male fetus, and anabolic steroids and androgenizing progestins, which can induce male development in a female fetus.
Genital development is largely complete by the end of the first trimester, whereas most of the exposure to these substances has tended to happen during the second and third trimester, when the main thing still ongoing is brain development. As a result (with DES, but I think the same applies to the others), the people exposed to these treatments have generally come out with relatively minor physical abnormalities (usually not enough to fall under the medical definition of intersex), but with brains that have undergone extensive cross-sex development. It looks like one of the ways this manifests itself later in life is through gender dysphoria. Considering how many people were exposed to these hormone treatments, the surprising thing is actually that more haven't come out as trans. Presumably there must be a lot of people who are stuck in a state of denial, or who've suicided without revealing to anyone that they were trans.
All the hormones with the most overt gender bending properties had largely been removed from use during pregnancy by about 1980, yet trans people have continued to be born in large numbers since then. I think the reason for this is that there must be hormones or other medicines still in use that can induce cross-sex brain development, without having much effect on genital development.
There's at least two subtypes of androgen receptor, one of which responds to both the main androgenic hormones (testosterone and DHT), the other of which only responds to DHT. We know from research on Rhesus monkeys, and from a rare intersex condition called 5-alpha reductase deficiency, that the androgen receptors in the genitals are mainly DHT-only ones, whereas those responsible for brain masculinization are (testosterone+DHT) ones. What this means is that the androgen receptors in the brain respond to a wider range of androgenic hormones than those in the genitals, and just because a possibly androgenic hormone doesn't masculinize the genitals, doesn't give it the all clear as far as masculinization of the brain is concerned.
Another thing I've discovered is that, for the first 20 weeks after conception, testicular testosterone production in a male fetus is mainly driven by the action of a hormone (HCG) produced in the placenta, whereas from about 20 weeks onwards, a hormone produced in the pituitary of the fetus itself (LH) takes over. Therefore, any drug or chemical that doesn't interfere with placental HCG production but does interfere with fetal LH production, wouldn't affect genital development in male fetuses, but could could nonetheless cause a big dip in testosterone production during the second half of the pregnancy, and brain development to predominantly occur as female instead of male. In the research on Rhesus monkeys, the important period when exposure (or lack of exposure) to testosterone determined whether the monkeys ended up with male or female brains, was the second half of the pregnancy.
Also, there are drugs besides hormones that can interfere with hormone metabolism, and thus have the potential to interfere with normal sexual development in the fetus. An example is phenobarbital, a drug that's used in epilepsy treatment and has been linked to both MTF and FTM ->-bleeped-<-.
