Here is a link to the first part of chapter 23 from Williams Endocrinology, "Development of Reproductive Systems". It explains in an amazing level of detail how the process of sexual development in the unborn child takes place, and how the whole thing is driven by hormones.
https://www.inkling.com/read/williams-textbook-of-endocrinology-melmed-polonsky-larsen-kronenberg-12th/chapter-23/development-of-reproductiveI think the information given there makes a very strong case that administering estrogens or progestins to a pregnant woman during the second half of the pregnancy, can produce people who appear to be male but have female brains.
First of all, there's a diagram covering the key events as far as physical male development are concerned:
Fig 23-1 "Events temporally related to sex differentiation in the male fetus"
This shows that differentiation of the male genitalia is complete by 13 weeks after conception, and the only things going on for the remainder of the pregnancy as far as physical sexual development is concerned are: Testis descent, and "External genital growth". My interpretation of this, is that if you have normal testosterone for the first 13 weeks, but then something goes drastically wrong with your testosterone production later on in the pregnancy, there won't be much physical indication that anything untoward has occurred. The only signs that anything has gone wrong are that your penis could end up shorter than it would otherwise have done, and that you might have abnormalities associated with maldescent of the testicles.
Reading through the next few sections makes it clear that any fetus has the potential to develop as either male or female irrespective of genotype; that the Y chromosome contains very few genes, and that its main function is to cause the gonads to develop as testicles rather than ovaries; and that the sex you develop as (your phenotypic sex) is entirely determined by what hormones are present during your prenatal development.
"The developing gonad produces several steroid and peptide hormones that mediate sexual differentiation and result in the phenotypic sex seen at birth. Alfred Jost first showed the importance of fetal testicular androgens in this process in 1947.12 In his classic experiments, Jost demonstrated that surgical removal of the gonads during embryonic development of the rabbit resulted in development of female reproductive characteristics, regardless of chromosomal sex of the embryo."
Now we get to a really key bit of information.
Fetal Leydig Cells and Steroidogenesis
Fetal Leydig cells develop within the interstitium of the developing testis and secrete androgens by 8 to 9 weeks' postconception (see Fig. 23-1 ).164 Luteinizing hormone/human chorionic gonadotropin (LH/hCG) receptors are present on the Leydig cells only from 10 to 12 weeks' post-conception, suggesting that the initial secretion of testosterone is independent of hCG and fetal LH. A massive expansion in fetal Leydig cells occurs between 14 and 18 weeks' gestation, resulting in marked increase in testosterone secretion at about 16 weeks.165,166 Fetal Leydig cell steroidogenesis is stimulated by placental hCG during the first two trimesters of pregnancy, but the developing hypothalamic-gonadotroph system produces significant amounts of LH from about 20 weeks' gestation.167
In other words, around 20 weeks after conception, there's a transition from processes independent of the fetal pituitary gland and its secretion of LH, to pituitary LH as the driver of testosterone production. This means that exposing a male fetus to a drug that specifically interferes with pituitary LH synthesis will have little effect on testosterone production for the first 20 weeks after conception, but from about 20 weeks onward, will start to impact testosterone production more and more. It's difficult to overstate the importance of this fact in relation to synthetic female hormones (estrogens and progestins) as a cause of MTF transsexuality.
Although Williams doesn't have much to say about when the brain development responsible for gender identity later in life takes place, there's a paper I linked to earlier discussing the effects of testosterone on brain masculinization in Rhesus monkeys:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3146061/In the Rhesus monkey, testosterone exposure during the first half of the pregnancy mainly affects genital development, whereas in the second half of the pregnancy, the main effects are to drive male brain development. Similar results are seen in sheep. If the same applies to human beings (and why wouldn't it?), then any drug that interferes with LH production will, if it's given during the second half of the pregnancy to a woman whose unborn baby happens to be male, be likely to result in a person who appears to be male, but whose brain has developed as female.
Both estrogens and progestins are known to interfere with LH synthesis, and have been (and in some cases still are being) given to pregnant women during the second half of the pregnancy.
http://en.wikipedia.org/wiki/Progestogen#As_antigonadotropinsTo me it looks like a massive mistake has been made, one that has been ongoing for decades. Considering how widely used these substances are, there must be a very large number of people alive today who've already been exposed - people who look male, but had some or all of their sexually dimorphic brain development occur as female. This is most likely something that's continuing to happen even now. No wonder transsexuality and gender variance have become so much more common in recent years.
What do people here think? Does what I'm saying make sense? If so, what to do about it?
