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Hugh Easton

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DES is a powerful sex change hormone in fish. It's possible to produce 100 percent female development in newly hatched fish, just by administering the appropriate dose of DES at the appropriate time.

DES isn't the only hormone that acts as a sex change hormone in fish, to have been used in human pregnancies either. According to this brief note I found on the FAO website,

DES or ethinylestradiol can be used to produce all female fish populations, while methyltestosterone (an anabolic steroid) or ethynyltestosterone (ethisterone) can be used to produce all male populations. I've found a couple of other pages saying much the same thing. Apparently the fish who've developed as the opposite sex to their genetic one are fertile, but may have reduced fertility. In order to cause complete sex conversion, the drug is administered soon after the fish fry have hatched, and at a point which would be partway through the first trimester in human development (intersexed fish are generally the result if the timing of the exposure is wrong).

I don't know about the others, but both DES and ethisterone have seen considerable use in human pregnancies as miscarriage preventatives. As you can see from some of the other stuff I've posted in this collection, both appear to act as sex change hormones in human beings just as they do in fish, except because the exposure nearly always only happens during part of the time sexual development is taking place, they're tending to produce gender blended people, or people whose physical sex appears normal but whose brain has developed as the wrong sex for their body.
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One interesting thing I've noticed is that antiandrogens (drugs which block the action of testosterone or the testosterone-derived hormone DHT) all carry strict warnings against use during pregnancy, due to the fact that they interfere with normal male development. On the other hand, synthetic female hormones (such as DES, ethinyl estradiol and progestins), drugs which prevent testosterone from being produced in the first place, not only don't carry these warnings, they were (or are) recommended treatments for preventing miscarriages and premature births, and have been given to large numbers of pregnant women in doses that would have profound feminizing effects on an adult man. It leaves me with the uncomfortable feeling that people within the medical industry must know that males prenatally exposed to these miscarriage treatments are being feminized, but they've carried on regardless because these treatments carry a very high profit margin. For instance, the progestin Makena (hydroxyprogesterone caproate) sells in the US for an average price of around $1000 per dose, when it probably costs less than a dollar per dose to make.

Here are some examples of the pregnancy warnings associated with antiandrogens.

"Spironolactone has been assigned to pregnancy category C by the FDA. Animal studies at the maximum human dose showed feminization of male fetuses during early pregnancy and indications of endocrine dysfunction in both male and female offspring during late pregnancy that persisted into adulthood. "

"PREGNANCY CATEGORY X [see CONTRAINDICATIONS]. Based on its mechanism of action, CASODEX (bicalutamide) may cause fetal harm when administered to a pregnant woman. CASODEX (bicalutamide) is contraindicated in women, including those who are or may become pregnant. If this drug is used during pregnancy, or if the patient becomes pregnant while taking this drug, the patient should be apprised of the potential hazard to a fetus.
While there are no human data on the use of CASODEX (bicalutamide) in pregnancy and CASODEX (bicalutamide) is not for use in women, it is important to know that maternal use of an androgen receptor inhibitor could affect development of the fetus.
In animal reproduction studies, male offspring of rats receiving doses of 10 mg/kg/day (approximately 2/3 of clinical exposure at the recommended dose) and above, were observed to have reduced anogenital distance and hypospadias. These pharmacological effects have been observed with other antiandrogens."

"Finasteride use is contraindicated in women when they are or may potentially be pregnant. Because of the ability of Type II 5α-reductase inhibitors to inhibit the conversion of testosterone to 5α-dihydrotestosterone (DHT), finasteride may cause abnormalities of the external genitalia of a male fetus of a pregnant woman who receives finasteride. If this drug is used during pregnancy, or if pregnancy occurs while taking this drug, the pregnant woman should be apprised of the potential hazard to the male fetus."

Androcur "Use in Pregnancy (Category D1)
The use of GenRx Cyproterone Acetate 50 mg is contraindicated during pregnancy (also see CONTRAINDICATIONS).. Administration of cyproterone acetate during the hormone - sensitive differentiation stage of the genital organs (after approx. day 45 of pregnancy) could lead to signs of feminisation in the male foetus."
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In trying to answer the question of whether members of the progestin class of hormones could interfere with normal male development, I came across the following paper:

It's a report on the use of a progestin, medroxyprogesterone acetate (MPA), to chemically castrate sex offenders. I'm not expecting people to read it; the key piece of information it contains is just that a weekly 400mg intramuscular injection of MPA will reliably lower an adult man's testosterone production down into the female range. In the Discussion section, it also mentions that a dose 100mg lower is equally effective at suppressing testosterone, and they use a higher dose because it has additional sedating effects that further reduce the likelihood of the patient reoffending. So it would appear that a dose of 300mg per week of MPA is enough to suppress men's testosterone down into the female range.

The reason this is so important is because testosterone is the substance responsible for a male fetus developing as male (both in terms of physical development and masculinization of the brain), and this research shows that doses of progestins of 300mg and upward per week, can reliably reduce a male's testosterone production down to female levels. That is right in the ballpark of historical and current progestin doses used in pregnancies where the mother is judged to be at risk of miscarriage or premature birth.

Note that this is the dose that can reliably suppress testosterone to female levels. It may be that doses considerably lower can cause testosterone suppression in many, but not all, males exposed to them. For instance, the artificial estrogen DES was, for many years, the standards treatment for prostate cancer. Initially the standard dose used was 5mg per day, but in due course doctors realised that patients given that dose were suffering very high death rates from thromboembolisms and heart attacks. It was then discovered that, in many patients, a dose of just 1mg per day was sufficient to suppress testosterone to castrate levels, and even in the more resistant patients, 3mg per day would suffice.

There's a member of the progestin class of hormones, called hydroxyprogesterone caproate, which was first introduced into the US market under the brand name Delalutin in 1956, and is now marketed there as Makena. In Europe, it's sold under the name Proluton Depot. The standard dose is a weekly intramuscular injection of 250mg. Treatment is typically commenced between 16 and 21 weeks after conception (after the critical period for genital development, and around the time the critical period for brain development starts), and is continued for the remainder of the pregnancy. I can't comment on how effective it is at preventing miscarriages, but what I have found out about it makes me think male babies exposed to it are at high risk of being born with incompletely masculinized brains, due to having their testosterone production suppressed by it. I haven't found any medical situations where hydroxyprogesterone caproate is administered on its own to adult men, but my bet is that if you were to give an adult man weekly 250mg injections of it, his testosterone would be suppressed to female levels, similar to what happens with MPA.

If I'm right, this would explain why more and more MTF transgender kids are continuing to be born, even though the first of these prenatally administered testosterone suppressing drugs, DES, was phased out 40 years ago.

I must emphasise that this is a treatment that's in current, widespread use in hospitals and maternity clinics throughout the developed world!
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This is an excerpt taken from the full version of one of the papers I've mentioned previously, featuring cases of baby girls masculinized by progestin exposure. The full version of the paper is paywalled, however I thought I'd talk about this little snippet from it, since "Case 17" would appear to be a confirmed case of FTM transsexuality caused by progestin exposure!

Case 17's body had been so altered by the hormone exposure that doctors didn't realise until his teens that he was actually a genetic female with ovaries and a uterus. Thus, he was spared having his penis amputated during infancy, and presumably was so well adjusted to living as a boy that, by the time the mistake was discovered, everyone involved with his care realised that it would be folly to try belatedly force him to live as a girl.

What this shows is that it wasn't just his physical appearance that had been masculinized, his brain and his gender identity had been as well. This confirms what commonsense says should happen: that these drugs don't just give baby girls masculinized genitals, they give them masculinized brains and, in some cases at least, a male gender identity. There are probably many other people who are FTM transgender as a result of progestin exposure, nearly all of whom will, unfortunately, have had their penis (or phalloclitoris, the term often used in intersex cases) amputated during infancy by doctors, needlessly leaving them with a lifelong inability to enjoy sex.

Doctors come out with all this crap about doing these surgeries for the patient's own good, but how many doctors would amputate their own penis because it didn't look right? The real reason they do it is to allay their own discomfort and the discomfort of the distressed parents. Worse than that, some of the stories I've heard have left me with a strong impression that many doctors secretly see us as freaks, have a very cavalier attitude to our healthcare in general, and often go out of their way to sterilize us to prevent us from reproducing! It's quite ironic because, if truth were known, they probably made most of us in the first place through their reckless use of hormones in pregnant women!

At the very least, that maxim from the Hippocratic oath, "First do no harm" generally seems to go straight out the window when dealing with intersex and transgender healthcare, and instead their main concerns are keeping us hidden from the public, gatekeeping our treatment, and protecting themselves from liability. That's why I'm such an advocate of bodily autonomy for us, both in terms of decisions on surgery, and also access to and administration of hormones. Many of us are dependent on lifelong hormone replacement, and doctors in general do a dreadful job of administering our HRT (or often refuse to administer hormones at all, even in situations where they're clearly needed, and instead try to push drugs that are more profitable to the pharmaceutical industry such as viagra and antidepressants).
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Another report of baby girls masculinized by progestin exposure, published in 1958. The culprit in most of the cases reported on in this paper was ethisterone, an early progestin that was superseded by drugs such as norethisterone, and is no longer used. As with norethisterone, although it's designed to mimic progesterone, ethisterone is actually a derivative of testosterone, and turned out to act as a potent androgen as far as fetal development is concerned.

This paper talks about the superficial similarities between progestin exposure and Congenital Adrenal Hyperplasia (CAH), which had been the main cause of female intersexed babies up to that point. This of course raises the possibility that some (or even most) of the progestin babies have been misdiagnosed as having CAH. This may explain why so few people are aware of progestin-induced virilization, even though large numbers of pregnant women were given these drugs, so the number of babies affected should be quite large. Progestins with androgenic properties were often co-prescribed alongside DES throughout the 1950s and 60's, and the total number of people who were exposed to DES is somewhere in the region of 10 million.
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An article published in 1962, reporting on cases where baby girls were virilized (experienced male genital development) after their mothers were given a synthetic hormone called norethisterone (aka norethindrone) as a treatment to prevent them from miscarrying. Norethisterone is a member of the progestin class of hormones. Although no longer used for miscarriage prevention, as the acetate ester, it's been extensively used in birth control pills, and is still a component of some contraceptive pills even now.

Although it's supposed to be mimicking a female hormone (progesterone), norethisterone is actually a derivative of the testosterone molecule. In adults, its main effects are to act as a progesterone mimic, and its androgenic effects are weak. However, it turned out to be a strong androgen in female fetuses, and this is one of several case reports I've tracked down, where baby girls exposed to norethisterone and similar drugs were born with masculinized genitals (in one case, so completely so, that it wasn't until their child started menstruating in his teens, that the parents discovered that their "son" was genetically female and had a uterus and ovaries!).

The case reports I've found all focus exclusively on genital appearance, and nearly all of the affected babies appear to have been operated on soon after birth to give them normal-appearing female genitals. However, if what happens in animals prenatally exposed to androgens also applies to human beings (and it almost certainly does), the affected people have a high likelihood of being infertile, developing polycystic ovarian syndrome, and having a masculinized personality and behaviour. It's highly likely some at least have ended up with a nonbinary or male gender identity too.

Unfortunately, as with other types of prenatal hormone exposure, it's usually impossible to confirm exposure. Medical records no longer exist, and parents have either died, forgotten, or were never told in the first place what drugs they were being given.

"During the course of evaluating the efficiacy of norethindrone in the management of abortion, a clinical trial among 385 consecutive obstetric patients revealed a high incidence of maternal and fetal virilization. More than 5 percent of treated women manifested masculinizing side effects, but of greater significance, more than 18 percent of the female infants born to mothers given this compound during pregnancy manifested some degree of masculinizaation of the external genitalia..."

But the pharmaceutical industry decided to promote it for use during pregnancy anyway. Good of them to not let a small side effect like intersexuality get in the way of making a profit!
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A report of four cases where female babies were born with partial masculinization of the genitals, whose mothers had been given synthetic estrogen (diethylstilbestrol) during the pregnancy. It was confirmed that no other hormones had been administered, and no other explanation could be found for why virilization (I.e. partial male genital development) had taken place, so it's presumed to be a result of the DES exposure.

Ordinarily, DES has feminizing effects (as many of us natal males who were prenatally exposed to it can attest!), so it is paradoxical that, in these four cases, it induced male development. The authors of this paper speculate that the affected children may have had some difference in their adrenal hormone production, that led their adrenal glands to overproduce androgens in the presence of DES, causing what was effectively a chemically induced form of congenital adrenal hyperplasia.

What these cases show is that the effects of prenatal exposure to synthetic hormones aren't always predictable. Identical treatment can induce intersexed development in some babies but not others, and even drugs that ordinarily induce female development in male babies, may also be capable of inducing male development in female babies in some cases.
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It's a form of intersex, so of course there are trans people whose gender identity doesn't neatly fall into a male or female category. Piers doesn't seem to get that.

Regarding his comments about race, would Piers argue that a mixed race person who identified as black, white, or didn't identify with blacks or whites, was delusional? In my mind, any of those identities would be entirely reasonable for a mixed race person to have.

There's no known circumstance in which a person can end up with an elephant's brain, so Piers's point about identifying as an elephant is ridiculous. I think he's right about the incidence of transgenderism being on the increase though, however it's not a fad, it's because so many people in Western countries have been prenatally exposed to hormones with gender bending properties.
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Here is a case report from 1959, of a male baby born with heavily feminized genitals following treatment with DES. Treatment in this case started with 50mg per day, and was quickly ramped up until a dose of 200mg per day was reached 8 weeks after conception, where it stayed for the remainder of the pregnancy. This means that the exposure during the first half of the pregnancy was quite a bit higher than was typical with DES miscarriage treatment.

Under the "Smith and Smith" regimen (the recommended dosing schedule published annually in the Physician's Desk Reference, which is the official guide doctors in the US use for prescribing drugs), the starting dose was 5mg per day, started 7 weeks after conception, and progressively increased as the pregnancy continued, until a dose of 125mg per day was reached near the due date. Under "Smith and Smith", doses of 50mg and above weren't reached until the second half of the pregnancy.

The critical period during which genital development takes place is weeks 7 to week 12 after conception, so people given the standard dosing schedule had a relatively light exposure to DES during the critical period when their genitals were developing. The patient in this case report had a much heavier exposure during the critical period when their genitals were developing, which would explain why their genitals came out looking more female than male. However, people on the standard dosing schedule were receiving comparable doses during the second half of the pregnancy, which is when most of the important sex-specific differences between male and female brains are thought to arise. This probably explains why most DES sons have been classified as male based on genital appearance, yet many of us have psychological effects suggesting that our brains have predominantly developed as female instead of male.
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One of the very few places in which the link between prenatal DES exposure and transsexuality has been publically talked about, is in Deborah Rudacille's book, "The Riddle of Gender".

It has a chapter in it "Fear of a Pink Planet", which talks about the link between prenatal exposure to xenoestrogens, and MTF transsexuality. The chapter is prefaced by an interview with Dr Dana Beyer, who was prenatally exposed to DES herself, and coauthored the 2005 study in which 150 out of 500 DES "sons" identified as women rather than men. The chapter also prominently features Christine Johnson, who is also a DES-exposed transwoman, and who works as an environmental scientist. A partial preview of the chapter (with some pages missing) is available at the following Google Books link:

The book raises some important points. For instance:

"I told Johnson that I had been asking the transgendered and transsexual people whom I was interviewing whether or not there were more gender-variant people in the world today, or whether they were simply becoming more visible as society becomes more tolerant and accepting. She answered bluntly, "I don't think that asking transgendered people is the proper way to ask this question. This is equivalent to asking cancer patients if the rate of cancer is increasing. How can one know this? What is required is epidemiological studies, period. The fact that there is not a registry is suspicious in my view. Keeping track of the number of sexual developmental anomalies is important in gaining an understanding of the impact."

Johnson also rejected the notion that the growing visibility of transgender and transsexual people was due to greater social tolerance of gender diversity. "Ts find increased acceptance inside the T community, and to a lesser extent within the larger GLBT community, but to extend that acceptance to the general population is a bit disingenuous. Where is the evidence that society is more accepting of Ts? It seems to be that most people claim increased social benevolence, but in general are unable to identify in which ways this benevolence is manifested. We have not achieved many basic civil rights, and if you ask the average (non-TG) person to name a single TG, they would be hard pressed to name anyone, because we are, in essence, the invisible ones... So while I see relatively large increases in the number of teen Ts, I see no significant increase in benevolence, at least in the US, towards transpeople."

This is something I concur with wholeheartedly. There are very few accounts of transgender people in history from past centuries. If they'd been anything like as many trans people per head of population as there are now, there would surely be more mention of it, and the battles we're now fighting for recognition and acceptance would have been fought long ago.

"In 2002, Johnson submitted the results of her research on endocrine disrupting chemicals and transsexualism to the peer-reviewed International Journal of Transgenderism, published online. The journal rejected it in a somewhat cavalier fashion, Johnson says. She believes that the psychiatric profession in general and the HBIGDA "establishment" in particular don't want to promote discussion of the endocrine disruption hypothesis because it poses a direct challenge to their power and authority as gatekeepers of services for trans people. "They are arguing from their paradigm against our paradigm, but the paradigm is what is in question" she says... "Their attitude is "we're not going to talk about this. That is in violation of the scientific tradition." In her view, the scientific community and the trans community are so blinded by traditional ways of viewing gender variance that they are failing to see the obvious. "If you look at the evidence Benjamin presented, he acknowledged that 45 percent of his patients had hypogonadism. That's another thing they don't explain."

In my view, Christine is putting it kindly in that excerpt. Psychiatrists have a nice little billion dollar earner from their role as gatekeepers to transgender health care, a role that would be threatened if the public knew that being trans isn't a mental illness, but a form of intersex in which the brain is the main thing affected rather than the genitals (and that most cases of it have unwittingly been caused by the medical profession). Likewise, the pharmaceutical industry and regulatory authorities such as the FDA would have a great deal to lose if it became public knowledge that they've inadvertently created millions of people who aren't really one sex any more, because part of their prenatal development occurred as male and part as female. The good name of medicine itself would fall into disrepute.

In other words, all the people who would normally investigate the link between prenatal hormone exposure and transgenderism, have a big vested interest in ensuring that link never comes to light!
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