MarkTwainiac

It occurs in prenatal development when the nervous system starts to develop - it can be affected by raised hormones in the mother's blood (testosteron for XX ferus and estrogene for XY fetus) and the brain will start developing as it should for opposite sex. (also the neuronal connection for your "gender" will be performed - idk how to describe it better in english im not native english speaker sorry).

This is hogwash. The med student who wrote the passages you quoted seems to think that during gestation in utero pregnant women pump out sex hormones willy-nilly that then pass directly to the embryo/fetus unmediated. This isn't the case.

The extent to which the mix and levels of hormones made by pregnant women's gonads and glands get into a developing embryo or fetus and match up to the hormones inside an embryo/fetus is unclear. For obvious reasons, getting samples of human embryonic or fetal blood is so risky that it's unethical and just not done, so there is much that science and medicine don't know about the relationship of maternal and fetal hormones in humans.

But the sex hormones that most heavily influence the development of human fetuses appear to be those made by each fetus's own internal organs - mainly the fetal gonads, which are either testes or ovaries, and develop at 7-8 weeks post-fertilization, and the fetal adrenal glands. If anything, it appears that the hormones a fetus makes from its own gonads and adrenals have at least as much - or even more influence - on the mother's hormones than the hormones made by the mother's own ovaries and glands have on the fetus.

Yes, of course a human fetus is exposed to circulating maternal hormones to some extent. But it's not like whatever hormones the mother's ovaries, adrenals and fat cells pump go directly into a developing fetus. This is because of the role of the placenta, the special endocrine organ grown during pregnancy that connects the circulatory systems of the mother and the embryo/fetus and serves as a protective interface between the two.

The placenta does many different things to insure that an embryo/fetus won't be harmed by things the mother ingests or is exposed to that get into her blood.

One role of the placenta is to prevent the mother's immune system from responding to the offspring she is gestating as though it didn't belong the way transplant recipients customarily mount rejection responses to transplanted organs. BTW, a sex hormone seems to play the most important role in suppressing the maternal immunologic response to fetal antigens - but that sex hormone is neither testosterone or estrogen; rather, it's progesterone.

Another role of the placenta is to protect female fetuses from exposure to maternal testosterone. A fact few genderists seem aware of is that pregnant women don't just have naturally elevated levels of estrogen, they have have naturally elevated testosterone. The normal range for women age 18 and up is 0.02-1.68 nmol/L. Pregnancy range is 1.7-4.2 nmol/L. When a woman is pregnant with female offspring, the placenta converts the high levels of the natural T in the mother's blood into estrogen through the process of aromatization.

During fetal development, aromatase converts androgens to estrogens in the placenta, which is the link between the mother's blood supply and the fetus. This conversion in the placenta prevents androgens from directing sexual development in female fetuses. After birth, the conversion of androgens to estrogens takes place in multiple tissues.

https://medlineplus.gov/genetics/gene/cyp19a1/

In the extremely rare event that there is an aromatase deficiency in the placenta, a female fetus will become androgenized. Aromatase deficiency used to be considered a disorder incompatible with life, but a few cases of the deficiency have been reported in children and adolescents. However, aromatase deficiency in females leads to a disorder of sex development in which the sex organs are visibly affected. The med student who wrote the passages you quoted seems to think that the excess testosterone could and would affect a female fetus's developing brain and nervous system without affecting the development of the genitals. But this isn't the case.

The role of the placenta in regulating the hormones a male fetus will get from the mother is less clear. However, studies of women babies in parts of the world with very high pollution and environmental toxins suggests the human placenta is capable of protecting male fetuses from exposure to harmful environmental chemicals and hormone disruptors that mimic estrogens and could interfere with normal male development, such as Bisphenol A.

The med school student who wrote the passages also makes the error of thinking that the development and functioning of brains in males in utero and later on in life are entirely dependent on testosterone. But that's not the case.

Male behaviors require both testosterone and estrogen. Circulating testosterone activates the androgen receptor (AR) and is also converted into estrogen in the brain via aromatase. This conversion is the primary source of estrogen to the male brain. It is unclear whether testosterone and estrogen signaling interact to masculinize neural circuits. Using a genetic approach, we show extensive sexual dimorphism in the number and projections of aromatase expressing neurons. The masculinization of these cells is independent of AR but can be induced by either testosterone or estrogen, indicating a role for aromatase in sexual differentiation of these neurons.

Testosterone is required for male behaviors in most vertebrates, including mice and humans. Testosterone mediates its effects by activating AR and male mice mutant for this receptor do not display sexual behavior or aggression (Ohno et al., 1974). Testosterone is essential in newborn and adult male mice for the display of sex specific behaviors such as aggression (Finney and Erpino, 1976; Peters et al., 1972; Wallis and Luttge, 1975). This testicular hormone is thought to masculinize neural circuits in neonatal rodents, and to act upon these pathways in adult males to permit the display of dimorphic behaviors (Phoenix et al., 1959).

Estrogen is also essential for male behaviors. The requirement for estrogen to masculinize behavior seems counter-intuitive as this ovarian hormone is essentially undetectable in the male circulation. All estrogenic steroids are synthesized in vivo from testosterone or related androgens in a reaction catalyzed by aromatase. Aromatase expressing cells in the brain convert circulating testosterone into estrogen, and it is this local estrogen that is thought to control dimorphic behaviors in males (Figure 1A) (MacLusky and Naftolin, 1981; Naftolin and Ryan, 1975). Consistent with a requirement for estrogen in male behaviors, aromatase activity is essential for male behaviors. Mice mutant for aromatase exhibit a profound reduction in male sexual behavior and aggression (Honda et al., 1998; Toda et al., 2001). Similar to testosterone, estrogen is essential in neonates and adults for the display of dimorphic behaviors in males (Finney and Erpino, 1976; McCarthy, 2008; Scordalakes and Rissman, 2004; Toda et al., 2001; Wallis and Luttge, 1975). Estrogen mediates many of its effects by signaling through the estrogen receptors ERα and ERβ, which exhibit overlapping expression patterns, and regulate masculinization of the brain and behavior in a complex, redundant manner (Bodo et al., 2006; Ogawa et al., 1999; Ogawa et al., 2000; Ogawa et al., 2004; Perez et al., 2003; Rissman et al., 1997). The role of a third estrogen receptor, GPR30, in male behaviors is presently unknown (Revankar et al., 2005

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2851224/

Another problem with the med student's theory is that puberty of adolescence is not the first time in a male child's life after his birth that he produces very high levels of testosterone that will reach and presumably impact his brain.

In the first year after birth, male humans also go through male mini puberty of infancy in which for several months their testes produce testosterone in adult amounts. So even if it were true that gender dysphoria results when a male child's brain somehow gets too much maternal estrogen during development in utero, then surely the baby's emergent "girl brain" and nascent opposite-sex gender identity would be counteracted by his brain, neurons and nervous system being flooded by the massive amount of testosterone his testes pump out for months during male mini puberty of infancy. Years before a male child would start developing secondary sex characteristics that the med student's theory says he'd sense as "errors" and would trigger gender dysphoria and a sense of being "in the wrong body," his testicles should already have generated more than enough testosterone for several months in babyhood to completely drown out and stamp out any incipient "feminized neurons" in his brain and any "girl/lady feelz" in his mind once and for all.