Transsexual Teens In UK Gender Dysphora Treatment
In a spate of recent UK media there was a wild accusation that a “thousand” youths were suing the National Health Service for wrongly pushing them into transsexual medical treatments. But there is a serious problem with this statement. That number, a thousand, is roughly the TOTAL number of transsexual teens that have been treated in the UK from 2008 through 2021. Are ALL of them suing the NHS? No, the story is disinformation generated by a transphobic propagandists under the rubric of the “Big Lie” theory, that the bigger the lie, the more believable it is. In truth, very few teens would be unhappy with receiving treatment and most would be very grateful. (Though they may grumble about aspects of the hoops they had to clear to get it.)
I’m a US citizen living in California, so I have zero direct experience with the UK NHS and their gender dysphoria treatment system. But as I understand it, to get treatment, one must jump through multiple hoops, first convincing a (potentially transphobic) skeptical General Practitioner (GP) to provide a referral to the Gender Identity Service (GIDS). The GIDS does a psych and history evaluation and may or may not provide a referral to the Endocrine Service which may or may not then provide puberty blockers (PB) or cross-sex Hormone Replacement Therapy (HRT).
If you were to believe the propaganda, you would be think that the NHS hands out HRT like candy on Halloween. They do not. Further, the real numbers from these clinics show that the number of teens treated is NOT indicative of an “epidemic” of gender dysphoria. Far from it.
We need to review some stats. The current population of the entire UK is a bit over 67 million people. The long time historical estimate of actual transsexuals, those who experience gender dysphoria, seek medical treatment, and live full time as the opposite sex is known to be less than one in ten thousand (<1:10,000). That includes those that seek treatment as adults. So, the maximum number of people we expect in the NHS system receiving HRT and later Sex Reassignment Surgery for gender dysphoria would be less than 7,000 people TOTAL. So, we expect, that the number of transsexual teens would be some lower number. And that is exactly what we see.
Consider the recent paper published in the British Medical Journals by Butler, et al. In it we learn that the NHS Gender Identity Services referred only 1,151 teens for evaluation between 2008 and 2021 inclusive. Of that only 1089 had known outcomes. Of those, 32 did NOT receive hormonal medical treatment, likely realizing that they weren’t actually gender dysphoric when confronted with the reality of what that really meant. (That is, they were likely falsely claiming to be “trans”, which has become a very popular fad among teens and young people such that there are likely over 500 people falsely claiming to be “trans” or “non-binary” for every actual transsexual.) Of the remaining 1,057 teens, 58 (5.5%) later elected to cease medical treatments leaving 999 that continued into adulthood.
Again, this is NOT indicative of a sudden epidemic of gender dysphoria among teens. In fact, it is perfectly in keeping with the number we expect from decades of clinical experience. Most especially, these numbers put the lie to the assertion that a thousand youths are planning to sue the NHS for medical malpractice. It also gives us an insight into the relative stability of gender dysphoria and of transsexual identities in teenagers, that so called “desistence” occurs before puberty onset.
Further Reading:
More Proof That Transsexual Teens Persist
How Many Transfolk Are There, Really?
Lost In The Crowd – The recent phenomena of young people falsely claiming to be “trans” or “non-binary”
Age Of Innocence – Clinical evidence that “desistence” occurs before puberty onset.
Reference:
Butler G, Adu-Gyamfi K, Clarkson K, et al., “Discharge outcome analysis of 1089 transgender young people referred to paediatric endocrine clinics in England 2008–2021” Archives of Disease in Childhood (2022) doi: 10.1136/archdischild-2022-324302
Biological Reality! Transsexual Women’s Breasts Are Female Breasts
Yesterday, a post about a transwoman breastfeeding a baby went viral. As one could imagine, transphobic commentators had many nasty, ugly comments to make. However, it also became clear that they were under the misapprehension that transwomen couldn’t breastfeed, “Your male body can’t produce milk!” “You don’t have female breasts.” “Where is the colostrum?” “Where are the lobules?” Why do they object to this knowledge and go into deep denial? Could it be because of their reliance on an ugly propaganda slogan of “biological reality” which they say transsexuals are in denial of… yet, here is something that they claim can’t be done, a true female biological function that can only be performed by women, by only natal female women, that is being done by transwomen. Learning that transwomen can and do perform this uniquely female, womanly function of sharing life giving milk with a baby upsets their world view and their propaganda.
So, sad as the need to explain such basics of mammalian biology to the world is, it must be done, as these ignorant and false assertions from these transphobes proves.
First, it important to understand that each and every gene that a woman has is also found in males. Females have two copies of the X chromosome while males have only one. But they still have that one. Further, many of the genes needed to express female phenotype aren’t even on the X chromosome, they are spread over the various autosomal chromosomes. To get a male, one need the genes on the Y chromosome, most particularly the SRY gene that first tells the proto-gonads to become a testes instead of the default ovary. But after that, nearly all the rest of sexual development is under the control of hormones produced by the testes.
If the body lacks the usual androgen (testosterone) receptor gene(s), even if that body has all the other typical genes and chromosomes for a male, that body develops in a rather typical female pattern. This condition is called 46XY CAIS, complete androgen insensitivity syndrome. They have typical testes in a seemingly typical female body phenotype, and most importantly for our discussion, women’s breasts at puberty.
Breast tissue does not care if there are XX vs. XY chromosomes. Breast tissue, like all secondary sexual characteristics that develop at puberty, are under the influence of sex hormones. Sex hormones can and should be viewed as specialized growth hormones. Various tissues express different sensitivities to the various sex hormones and will grow or not grow depending upon the presence and balance of these specialized growth hormones. In particular, breast tissue responds to estrogen and progesterone and are somewhat suppressed by androgens.
Circling back to transwomen, we note that Hormone Replacement Therapy (HRT) uses the very same hormones that induce breast tissue development in women. Transwomen have all the genes and breast tissue stem cells needed to develop fully functional FEMALE breast tissue. When a transwoman begins HRT, her breasts respond and begin to develop. After sufficient time, her breasts are histologically identical to adult natal female breasts. That includes the potential for lactation.
A woman does NOT have to have given birth or even have been pregnant to lactate. It certainly helps, given that certain hormones automatically are produced in amounts that prepare the breasts to produce first colostrum then milk, but isn’t an absolute requirement. The key requirement is that of tactile stimulation that a baby’s suckling produces and that once a flow of colostrum is present, that it be drawn out, either by a baby suckling or by manual expression / pump.
If a woman is adopting or working with a gestational surrogate, she may elect to breastfeed her baby by following a regimen of stimulation, expression, and pumping. In some cases, medication may aid in this process.
Many transwomen have produced colostrum due to HRT which in some cases, primes the breasts in the same manner as being pregnant. (I myself have produced colostrum.) If a transwoman is adopting, working with a gestational surrogate, or has a female partner who is expecting a baby, she too may elect to breastfeed her baby in the same manner as would any other non-birthing woman.
The milk produced by a transwoman is identical to milk produced by a natal female. Transwomen have been quietly, successfully, and safely breastfeeding babies for decades. They will continue to do so.
Biological Reality.
Further Reading:
References:
de Blok, et al, “Frequency and outcomes of benign breast biopsies in trans women: A nationwide cohort study” The Breast: Official Journal of the European Society of Mastology, (2021) https://doi.org/10.1016/j.breast.2021.03.007
Wambolt, R. et al, “Lactation Induction In A Transgender Woman Wanting To Breastfeed: Case Report”, Journal of Clinical Endocrinology & Metabolism, (2021), https://doi.org/10.1210/clinem/dgaa976
Kulski, J., et al, “Composition of breast fluid of a man with galactorrhea and hyperprolactinaemia”, Journal of Clinical Endocrinology & Metabolism, (1981), https://doi.org/10.1210/jcem-52-3-581
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Testosterone Poisoning Real?
How T Makes Men Dysrational
Back in the early ’90s when I was staying home from work because of some bug, I recall watching daytime reruns of really dumb shows. I chanced upon a silly sitcom for ‘tweens where one of the plot elements was a math problem which was supposed to be challenging for the middle school students. It was a classic dual rate problem: How long it would take two boys washing cars if they did the next car together instead of separately. As I was bored, I set up and solved the simple (to me) algebra problem during the next commercial break. I looked forward to seeing that I was correct. As the show progressed, the kids were becoming more and more agitated that no one could solve it, not even the stereotypical “brain” of the class. Only the stereotypical airhead girl (obnoxious portrayals) seemed to be immune. At the climax of the show, no one has solved it, but the airhead… who states, “It can’t be solved.” “Right!” the math teacher concurs. WTF!?!?! I think. The “brain’s” head explodes.
I was dumbfounded. I checked my work. No, I could easily solve it. No, it didn’t take a genius. It was a very straight forward bit of algebra any first year high school algebra student could solve. How could the writers, producers, stage crew, and actors not know this? What the &^%$#@! were they doing telling their young audience; that it couldn’t be solved?
This episode (pun intended) stuck in my mind. I couldn’t understand it until I learned of the phenomena of Dysrationalia, researched by Keith Stanovich. It was a revelation. But I never thought this topic would find it’s way to my blog here, not being related to trans issues (save perhaps as one possible explanation for the irrational denial of the two type taxonomy). But, here it is…
High testosterone levels increase dysrationality. Seriously.
In a recent study, healthy men were randomly given T gel or placebo gel to apply to their skin. Hours later, their plasma T levels had doubled. They then took on a series of cognitive tests buried within them were three “trick questions” that measure “Cognitive Reflection”, a subset of the Stanovich’s original seven dysrationality questions. These three questions, mathematical in nature, are extremely easy, deceptively easy, in that unless one slows down and thinks, one will all too easily try to use irrational mental shortcuts that get the wrong answers. The key to being rational is that another part of the brain double checks one’s thinking to spot this and says to one’s self, “hey, hold on, that type of thinking is flawed.”
The results were dramatic. Those who had been given T got 20% more wrong answers than those given the placebo. The difference was quite robust ( Cohen’s d=0.41 ). High T levels seem to reduce the ability of the brain to spot irrational thinking processes.
This has implications for transmen as they begin and continue hormone replacement therapy (HRT) using testosterone, as transient high levels of T occur. Transmen should be counseled on this phenomena and given cognitive tools to compensate.
Researchers should also look at the effects of androgen suppression in transwomen. Does this effect go in reverse? Does low T make one less prone to cognitive reflection errors?
Further External Reading:
Rational and Irrational Thought: The Thinking That IQ Tests Miss
Reference:
Nave, Gideon and Nadler, Amos and Zava, David and Camerer, Colin (2017) Single dose testosterone administration impairs cognitive reflection in men. Psychological Science . ISSN 0956-7976 . http://resolver.caltech.edu/CaltechAUTHORS:20170428-091020875
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A Voice of Their Own
Or, What Do Transkids Think About Puberty Suppression?

Transkids after transition
In the media and especially in social media, we see lots of discussion regarding what is the appropriate standard of care for transkids. Many adults seem to be horrified by the idea that kids should be treated at all. Of course, anyone that thinks about it clearly will see that without puberty suppression, one is already making a decision to treat them with hormones, the ones that the body starts to make at puberty. Thus, the justification for puberty suppression, under the notion that delaying it isn’t really making a hard and fast decision.
But what of transkids themselves? What do they think about it all? How about asking them? Well, a recent paper does just that, as the paper describes them,
“They were between 13 and 18 years of age, with an average age of 16 years and 11 months, and a median age of 17 years and 4 months. All adolescents, except for one, were treated with puberty suppression. The mean age at which the adolescents started treatment with puberty suppression was 15 years and 10 months. The adolescent who was not treated with puberty suppression immediately started treatment with cross-sex hormones because she was above the age of 18 when treatment was indicated, which is in line with the Dutch protocol. Five adolescents were trans girls (natal boys with a female gender identity) and eight were trans boys (natal girls with a male gender identity).”
Note that puberty suppression was their only option until age 18, a state of affairs that I have argued, and will continue to argue, it both unnecessary and cruel, but better than nothing. This protocol privileges desisters and indeed all non-gender-dysphoric teens in that an active or implicit decision to deliberately use endogenous hormones to masculinize or feminize (as the case may be) their bodies is socially sanctioned, actively encouraged even, but an active decision on the part of gender dysphoric teens is considered suspect and their ability to make such a decision is deemed problematic. {Can nobody else see the double-standard? Why, if this is all about not trusting teens to make this decision, are ALL teens not put on puberty blockers until they are adults?} All evidence points to the age of 14 being an appropriate age to end, not begin, puberty suppression, to be replaced with conventional Hormone Replacement Therapy. But concerns about transphobic public resistance prevents this evidence based medicine approach.
{On a personal note, I first learned about HRT at age 15, but my pediatrician recommended my mother send me to psychotherapy to “cure” me instead. I began actively requesting feminizing HRT from the Stanford Gender Dysphoria Clinic at age 17 in 1974. I was denied this. I had to wait until I was legally of age and began HRT very soon after my 18th birthday in the summer of ’75. In those days, puberty suppression was not available. I deeply regret what that delay did to my singing voice.}
So what did these modern teens have to say? Here’s a typical comment,
“I think it is hard to set an age requirement. On the one hand I think 12 years is a good age minimum, on the other hand I think that a transgender whose puberty started earlier should have the possibility to start treatment with puberty suppression before the age of 12.” (trans girl; age: 13)
You may wish to read the rest of what they had to say at the actual paper at the link below, as it is not behind a paywall, thankfully.
Further Reading:
Essay on evidence for best age to end puberty suppression based on age of desisting gender dysphoria
Essay by Alejandra Velasquez at the transkids.us website on treatment recommendations for MTF transkids. {Note: Ms. Velasquez was ~20 when she wrote the essay in 2004}
Essay on Advice to Parents of Transkids
References:
Vrouenraets, L. et al. “Perceptions of Sex, Gender, and Puberty Suppression: A Qualitative Analysis of Transgender Youth”
Archives of Sexual Behavior (2016). doi:10.1007/s10508-016-0764-9
Fun Reading:
Sincerity Espinoza didn’t go looking for trouble, it found her. All she wants out of life is the chance to go to the stars but she is caught in a web of misunderstandings, political & legal maneuvering, and the growing threat of terrorist plots by religious fanatics. She has a secret that if found out too soon could mean not only her own death but the ruin of the hope for humanity ever going to the stars. But even amidst momentous events, life is still about the small moments of love, laughter, and sadness. Available as an ebook at Amazon and Kindle Unlimited.
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Audio Sex Perception
I don’t suppose it would surprise anyone that straight men and women respond differently to men’s and women’s voices. In fact, I think we would be surprised if we didn’t. After all, straight men are attracted to women and their voices, and straight women are attracted to men and men’s voices. But that’s only the obvious part. They also tend to be different in their ability to perceive them, with both sexes responding stronger and faster to opposite sex voices. They also differ in the amount of cognitive resources used in the task, the amount of effort applied. Women use fewer resources than men… they are just better at it.
Now, before one says… OH, a sexually dimorphic difference in the brain! Whoa! Hold on! That may not be true at all. Other research into perception of other signals, ohh… such as emotional expressions have also shown sexually dimorphic difference in ability. But in that case, we also know that wealth and power differences also show up. Rich and/or powerful people are significantly and robustly less able to read emotions on other’s faces than poor and/or less socially privileged people. Further, practice at reading people’s emotional expressions significantly improves this skill. So, is that a built in, sexually dimorphic brain difference between men and women? Or does is simply reflect that women, as a class, have less wealth, power, and privilege than men? I’m betting on the latter.
And so it is with the amount of effort it takes to “read” one’s sex by listening to their voice. Is this built in? Or is it that women NEED to read voices better, just as they NEED to read faces better? I’m betting on the latter.
Now we come to transwomen (MTF transsexuals). In a study conducted in Germany, transsexuals seemed to be unique in some ways, like men in some, and like women in others. One thing that they did find is that during fMRI scanning of the brains of transwomen, they showed that they were using very little effort to determine which sex a given speaker was, similar to women. Interestingly, they analyzed both androphilic and gynephilic transwomen together and separately, though didn’t report them separately, instead they focused on testing pre-HRT and current HRT. They found little difference between the two populations, androphilic vs. gynephilic and pre-HRT and HRT. I’m not surprised by this. In fact, it supports my hypothesis that this is NOT an innate sexually dimorphic trait, nor mediated by hormones, but the result of the social differences in privilege and experience / learning. The two MTF populations have the same basic experiences regarding their own vocal history and needs, as the authors put it,
“Since we found no differences in accuracy between women and MtFs, decreased activation in MtFs might suggest that they need less effort to achieve levels of performance similar to women. This might be due to the fact that MtFs are more attuned to issues related to voice gender perception in everyday life. … In line with the behavioral results, MtFs showed differences (compared to men and women) in neuronal response patterns with respect to male vs. female voices. Presumably, a different strategy is used in MtFs’ voice gender identification due to early processing differences. They also might more intensively examine their own and aspired vocal characteristics during gender alignment, resulting in a certain expertise. In this sense, attentional differences due to automatized processing could lead to less brain activation in MtFs.”
Reference:
Junger, J., Habel, U., Bröhr, S., Neulen, J., Neuschaefer-Rube, C., Birkholz, P., … Pauly, K. (2014). More than Just Two Sexes: The Neural Correlates of Voice Gender Perception in Gender Dysphoria.(11), e111672. doi:10.1371/journal.pone.0111672
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A Novel Argument
A new argument was presented to me just yesterday involving the well documented fact that among those who transitioned as teenagers, far fewer report having experienced autogynephilia. What made the line of argument ironic was that the proponent had started out in absolute denial of any of the science and most especially of the the notion that autogynephilia existed in some transsexuals, “autogynephilia my ass!” However as the debate developed, she presented a novel take on the Nuttbrock data that I presented, to wit that in that study, 82% of self-reported exclusive gynephiles reported sexual arousal to cross-dressing, while only 14% of those who had begun HRT as adolescents (defined in the Nuttbrock study as before one’s 20th birthday) reported such arousal.
Here’s where it gets interesting: In an effort to win ANY point she could, she took the position that I was twisting the data to suit my position… yet in so doing she had to take the position, for her arguments’ logic to work, that autogynephilia is a UNIVERSAL phenomena among MTF transsexuals. I had to laugh privately, since this reversal of her position would obviate all of her previous positions and support some (but not all) of mine. Interestingly, this argument of universal autogynephilia mirrors the argument proposed by another contingent of autogynephilic transwomen, that autogynephilia is also normal and expected in natal women. I find it doubly ironic that there is such an extreme reaction to the two type taxonomy, but from two camps, those that deny any autogynephilia in transwomen, and those who insist that their autogynephilia is just part of being a woman, and thus, all transwomen must also be autogynephilic.
Her argument also starts with several assumptions that are not supported by the data, nor by community observation. She assumed first that HRT in these teens meant “puberty blockers” and that such blockers would preclude an individual from experiencing any sexual arousal. It wasn’t made explicit, but she may also have been making the false assumption that even traditional HRT precludes any sexual arousal. (I’ve heard several “late transitioning” transwomen make this statement, likely due to their own personal experience, while real for these individuals, is neither universal nor inevitable. From casual observation, it seems to occur more frequently in more senior transwomen than younger “late transitioning” transwomen. And from personal conversations with a fair number of transkids, not one had experienced this phenomena.)
So, she explains the significant difference between these adolescents (of whom only one had identified as gynephilic and 7% as bisexual, with the remaining 93% identifying as exclusively androphilic) and the gynephilic (all but one of whom had begun HRT as adults or had never had HRT, and yes, that one individual is in both groups… I couldn’t back her out of the data), as the adolescents not experiencing sexual arousal to cross-dressing due to them not experiencing sexual arousal in general.
So, having convinced herself that she had won her point… she began to crow that I was the one who was not willing to look at reality!!!
Ummm… Not so fast.
Hypothesis were meant to be tested.
I’ve already pointed out the canard that HRT stops sexual arousal in all transwomen. If it did, would we be having sex as often as we do post HRT and SRS, especially transkids? It simply isn’t true. Second, it is extremely unlikely that these youngsters were all on puberty blockers (e.g. Lupron) as it is still a fairly rare protocol. It is typically initiated by well meaning parents bringing their extremely gender dysphoric pre-adolescent children to specialists. While I would wish that all parents were so willing to medically intervene and save their transkid from the damaging effects of endogenous hormones, it is still a rare parent who does so. Most transkids have to fight to get medical help… and many never get parental support, either waiting until they are legally of age, running away early, or getting HRT “on the street” surreptitiously.
Although the Nuttbrock study did not give us the fine detail I would have liked regarding the exact ages which folks started HRT, we know that half of those who identified as androphilic and had started HRT did so before the age of 20. That also means that half did NOT. From other studies, we know that the age of 20 is the median and the mode, that most androphilic transwomen start HRT, not right at puberty, but nearer age 20, showing a Gaussian distribution centered on age 20, with the bulk having started HRT between the ages of 17 and 23 inclusive. This is enough after puberty to have allowed them to experience that first flush of sexual awakening that accompanies the onset of puberty and adolescence.
We know from countless personal narritives of autogynephilia that those early years of adolescence are typically when sexual arousal to autogynephilic imagery, most especially to cross-dressing, stereotypically in women’s lingerie, is the most obvious and intense. Thus, IF these youngsters who began HRT as teens were universally autogynephilic, they would have had ample time to experience it in all of its intensity, before begining HRT, even if, as was argued, HRT would preclude experiencing it!
Looking further at the Nuttbrock study, only 40% of the self identified exclusively androphilic population had started HRT before age 20. If this argument that HRT in adolescence explains the reduced number reporting autogynephilic arousal to cross-dressing, we would expect that those who did NOT start HRT as an adolescent to report at the same rate as the other sexual orientations. Of those who self-identified as androphilic, all of those, including adolescent onset HRT, adult onset HRT (40%), and not on HRT (20%), the combined population had 23% report autogynephilic arousal to cross-dressing. A little algebra and a calculator will show that those who were NOT adolescent onset HRT were reporting at the rate of 29%, far lower than the 82% of gynephilic transwomen, and even lower than the bisexually identified transwomen who reported at 67%, and the asexual at 66%.
Thus, even if HRT did what my erstwhile debating partner claimed… the data STILL would NOT show that self-reported exclusive androphiles report less than half the incidence of autogynephilic arousal to cross-dressing. We would instead expect the later onset HRT androphiles to report at rates that were at least similar to the bisexual population.
OH… and a note on why I keep using the term “self-reported”: There is, unfortunately for our research purposes, a well documented phenomena of “late transitioning” transwomen misreporting their sexual orientation. It is quite possible, even probable, that the 29% rate of adult onset HRT and no HRT, is from a number of such misreporting older transitioners.
Thus, I’ve outlined my theoretical and evidence based reasons why this novel hypothesis is not supported by the data. Instead, the data supports the two type taxonomy for MTF transsexuality, namely “exclusively androphilic vs. autogynephilic”.
To those who understand the limitations and implications of sociological and psychological studies, I’m sure that the above explication of the data is sufficient. I’m equally certain that to those who are in denial of this research and of the Fruend/Blanchard transsexual taxonomy, what I’ve outlined above will only back them further into their denial.
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Rolling the Dice…
Alice Dreger, who I deeply admire, has just published a paper regarding the disturbing off label use of powerful steroids… all in the hope of keeping female children from being tomboys, lesbians, and FtM transmen.
Reference:
Alice Dreger & Ellen K. Feder & Anne Tamar-Mattis, “Prenatal Dexamethasone for Congenital Adrenal Hyperplasia: An Ethics Canary in the Modern Medical Mine”
http://dx.doi.org/10.1007/s11673-012-9384-9
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The Age of Innocence
At what age should transkids start HRT?
WISHES
OH, if you were a little boy,
. And I was a little girl –
Why you would have some whiskers grow,
. And then my hair would curl.
Ah! if I could have whiskers grow,
. I’d let you have my curls;
But what’s the use of wishing it –
. Boys never can be girls.
–Kate Greenaway, Marrigold Garden, (1885)
For physicians and other health care providers, an over-riding concern is to “do no harm”. One of the fears for such care providers is that of starting a course of treatment intended to treat a condition, only to discover that they misdiagnosed the patient and gave a treatment that not only was unneeded, but potentially harmful.
In the case of trankids, both MTF and FtM, the sooner one can begin hormonal & surgical treatment and social support interventions to allow them to successfully transition into the appropriate gender/sex role so as to take advantage of the normal adolescent physical and social maturation process along side their peers, the better the long term outcome.
But, as the very recent Steensma study, as well as many before it, shows, not all gender atypical children will be gender dysphoric, and not all gender dysphoric children will persist as such into their teen years. Thus, the study was conducted in the hope of finding differences between persistors and desistors, so that clinical treatment decisions can be made as early as possible. The earlier one can separate the two, the earlier one can begin to treat the transkids, while letting non-transsexual teens grow up naturally, without potentially harmful iatrogenic trauma.
Because healthcare providers have not been able to accurately predict which gender atypical / dysphoric children will persist, a number of practitioners have begun recommending and using a puberty blocking protocol, under a harm reduction model in which the persistors are protected from the harmful effects of their endogenous hormones, while refraining from iatrogenic injury from exogenous cross-sex hormones in those who will desist from their earlier gender dysphoria. The current recommendation is that such puberty blockers be used until the individual is 16 or even 18 years old, at which time, if he/she is still a persistor, they may be switched to cross-sex hormones, while the desistors may terminate the puberty blocking protocol at any time. (There is a built in bias for desistors and against persistors in that desistors can begin a prefered hormonal protocol, simply by stopping the puberty blockers, but persistors must wait and “prove” to healthcare workers that they are ready.)
The problem with this protocol is two fold. First, it is not without its own potential for iatrogenic harm in that delaying puberty reduces the eventual strength of the bones in adulthood. This may not be immediately harmful, but those children will someday be older adults, whose bones will be more prone to breaks. Second, for MTF transkids, delaying puberty means that they will continue to grow taller, potentially reducing their ability to pass successfully as female. This effect may however be welcomed by the FtM transkids, but their desisting female peers may not feel the same.
Another problem with this protocol is that it is very expensive, far more expensive than cross-sex Hormone Replacement Therapy (HRT). For those who live in countries who do not have a generous state provided health plan, this may be a deal breaker.
So, for health care providers and parents alike, it may be better if they can accurately predict who will desist and who will persist. Getting this data is the object the Steensma study. The Steensma study is short on statistics, but what they do have is remarkable:
. Total group Persisters Desisters
. (N = 53) (N = 29) (N = 24)
Natal sex
% (N) Boys 56.6 (30) 58.6 (17) 54.2 (13)
% (N) Girls 43.4 (23) 41.4 (12) 45.8 (11)
Age at childhood
assessment
M (SD) 9.41 (1.46)* 9.92 (1.26) 8.81 (1.47)
Age at follow-up
M (SD) 16.11 (1.70) 16.14 (1.84) 16.07 (1.54)
Full-scale IQ
M (SD) 100.26 (12.82) 98.83 (12.28) 102 (13.50)
* Significant difference observed between persisters and desisters in age at childhood assessment (t(51) = 2.968, p < .05), Cohens d = 0.81 .
For starters, the IQ of the persistors is 98.83, essentially average. Although this is combining FtM and MTF, the number agrees with my earlier estimate of 98.6 for the MTF HSTS population.
But, the more important data is that there is a difference between the ages of childhood assessment, the age at which their parents brought them to a clinic for evaluation. (The difference being on average a little over a year, or over 10% of their age, and a very large effect size of d = 0.81 ) But, the study makes it very clear that there was very little difference between the two groups in their early childhood gender atypicality at presentation. So why is there this difference? Why would the parents of persistors wait longer than those of desistors?
Because they don’t! It wasn’t that parents of persistors waited longer, it was that many desistors, desisted at an earlier age, such that their parents never brought their children in for assessement. As they get older, fewer and fewer parents of desistors would bring in their children. But, the persistors would continue to be brought in at later and later ages. Indeed, the authors specifically stated that from the interviews, the desistors clearly articulated that from age 10 to 13 were critical for their change in gender dysphoric feelings. While, for persistors, that same age only confirmed and strengthened their feelings. Thus, both interview report and the statistics agree that something special seems to be happening starting at around the age of ten or even a little younger.
Starting around the age of 10, and for the subsequent years, the persisters indicated that their crossgender preferences and behaviour and their gender identity remained stable, but that their dysphoric feelings intensified. The intensification of gender dysphoria was attributed to three factors; (1) Certain changes in their social environment, (2) The anticipation of and/or actual physical changes during puberty, (3) The first experiences of falling in love and discovering their sexual orientation.
The authors, in focusing on what the teenagers said were influential, may have missed a critical factor. What’s so special about the age of ten? This is well before puberty. The authors focused on changing social factors, but could it be that biology is the important factor? McClintock and Herdt point out that sexual attraction is first noted well before our classic definition of puberty, that of the maturation of the gonads and subsequent increase in testosterone, estrogen and progesterone. Instead, other hormones start earlier, typically around ten years old with Adrenarche. And this is the age at which one’s sexuality begins to be recognizable.
So what’s so special about adrenarche? As the Wikipeadia page (linked above) explains it, “Unlike the physical changes that occur during puberty, adrenarche is primarily an emotional and psychological stage of development.”
And so, as their sexuality becomes visible,
With regard to sexual attraction, all persisters reported feeling exclusively attracted to persons of the same natal sex, which confirmed their gender identity as they viewed this attraction as a heterosexual attraction. They did not consider themselves homosexual or lesbian.
For the desisting boys, some came to recognize that they were gay or bisexual, essentially confirming the results of many other studies which have shown that gender atypicality in boys is highly correlated with homosexuality. However, a number of the boys self-identified as heterosexual, even though they also recognized some same sex attraction.
For the girls, all of the desistors had become aware of the fact that they were heterosexually attracted to boys and wanted to be sexually attractive to boys. Thus, they were the classic tomboys who grow up to be straight women. But the persisting girls were all attracted to girls.
Thus, this study showed that the key difference between persistors and desistors among female bodied gender atypical / dysphoric individuals was sexual orientation, but among male bodied, it was not as clear cut, desisting boys included both gynephilic and androphilic sexual orientations. However, what is clear is that persisting boys are all clearly unambiguously androphilic (HSTS). Persistors will demonstrate same sex attraction, while desistors may or may not. Thus opposite sex attraction is a key exclusionary sign for persistors. Although we still would have some desistors who don’t show this sign, we have at least conclusively identified some.
Further, none of the study group was autogynephilic.
This last point is important. Although many autogynephilic adults report having been gender dysphoric as children, it is rare, though clearly not unheard of, for them to have been noticed as such as children. They are the “non-aparent” population as children. However, for the HSTS population, of both sexes, MTF and FtM, their gender dysphoria was accompanied by obvious gender atypicality. Since obvious gender atypicality is not found in autogynephilic boys, who are universally gynephilic, we can safely say that anyone who is obviously gender atypical and sexually attracted to the opposite sex is not going to be a persistor.
Another point can be clearly found in the Steensma study is that the developmental process, what ever it is, for desistors, is finished by age 14. If a gender atypical 14 year old is still gender dysphoric and wishes to begin hormones and transition, we can be reasonably certain that he or she will not change his/her mind later. Thus, based on the evidence, we can safely begin such interventions. The sooner the better.
Conclusion
From the evidence, we draw the conclusion that for obviously gender atypical / dysphoric children, waiting until one is 16 or 18 years old to end puberty blocking protocols and beginning HRT is unwarranted and ill-advised. Instead the evidence points to the age of 14 as the latest that HRT may safely be begun with little risk of iatrogenic injury to desistors. Indeed, the evidence suggests that carefully evaluated, many of the desistors may be excluded by age ten to twelve. Another point to come of these studies is that anatomic dysphoria (discomfort with genitalia, etc.) is correlated with persistence. Thus, if delaying puberty is chosen, it should not be continued past the 14th birthday, and given proper screening, may be ended earlier, to switch to HRT. For both cost and health reasons, it may be best to start on HRT for those who clearly fit the profile of a transkid, who request and understand the consequences of HRT, as soon as would be indicated for their gender of choice. That is to say, that for MTF’s, HRT should begin at age 12, and for FtM, at around age 14, mimicking the natural maturational process for each target sex.
Addendum 2/23/2012:
If you are a young teen, finding this post: Welcome! To answer some questions. Yes, you can start blockers, maybe with low dose HRT, as young as 10 years old, but should start with very low doses, gradually increasing to the recommended level for teenagers as you reach 12-14 years old. Of course, you would need either your parents permission, or find a youth clinic that understands transkids’ issues, who would prescribe blockers & HRT on a “harm reduction model” . (Seriously, that’s the magic words, “harm reduction”… as in… “I’m going to get hormones on the street if I don’t get them here.”) Good luck!
Addendum 6/1/2012:
Please read my Advice to Parents of Transgender Children
Addendum 12/29/2012:
Please read my Advice to Transgendered Teens
Addendum 4/1/2021:
A newly published study, by Singh, but with individuals who had gone to a Toronto clinic years earlier (and thus evaluated with older criteria that we know are a bit loser than today’s) has data on persisting and desisting male youth. As before, we see that most of them turned out to be primarily androphilic with the persisters being universally so. And again, we see a difference in the age of evaluation with persisters being older at 8.85 years and the androphilic desisters being 6.96 years old (Cohen’s d = 0.84 a ‘large’ difference). Interestingly, there were a number of gynephilic desisters in the study who were also younger in age at evaluation at 7.49 which is very similar to the desisting androphiles (d = 0.2 a ‘small’ difference). Note that the difference, of d = 0.84 is essentially the same as the d = 0.81 found in the Steensma study. Thus, the characteristic difference has been replicated and may be trusted.
Another difference was found in IQ. Desisters were more intelligent than average at 110 while the persisters had the expected population average of 99 (100 is the population average, so this showed no significant difference). Thus, there seems to be a selection effect that smarter kids are being brought in by their families at a younger age by families with higher socio-economic status (which correlates with higher IQ that runs in families). Perhaps this is because they over-react to mild gender atypicality? The authors of the study suggested that it was the fault of the poorer parents, “delaying” instead. I stand by my assertion that it’s based simply on the fact that desisters desist and are no longer brought in for evaluation.
As seen in other studies, the persisters were more gender atypical and gender dysphoric at evaluation than desisters.
Addendum 6/15/2022: Amazing News! WPATH has finally accepted the science and has now lowered the recommended age for HRT to 14, as I’ve been arguing for over a decade: https://apnews.com/article/gender-transition-treatment-guidelines-9dbe54f670a3a0f5f2831c2bf14f9bbb–
Further External Reading:
References:
Thomas D. Steensma, Roeline Biemond, Fijgie de Boer and Peggy T. Cohen-Kettenis, “Desisting and persisting gender dysphoria after childhood: A qualitative follow-up study”
http://ccp.sagepub.com/content/early/2011/01/06/1359104510378303
Vicente Gilsanz, James Chalfant, Heidi Kalkwarf,Babette Zemel, Joan Lappe, Sharon Oberfield, John Shepherd, Tishya Wren, Karen Winer, “Age at Onset of Puberty Predicts Bone Mass in Young Adulthood”
http://www.jpeds.com/article/S0022-3476%2810%2900566-4/abstract
Martha K. McClintock and Gibert Herdt, “Rethinking Puberty: The Development of Sexual Attraction”
http://homepage.univie.ac.at/Michael.Berger/lit/McClintock.pdf
Madeleine S.C. Wallien, Peggy T. Cohen-Kettenis,”Psychosexual Outcome of Gender-Dysphoric Children” Journal of the Academy of Child and Adolescent Psychiatry (2008)
https://doi.org/10.1097/CHI.0b013e31818956b9
Annelou L.C. de Vries, Jenifer K. McGuire, Thomas D. Steensma, Eva C.F. Wagenaar, Theo A.H. Doreleijers, Peggy T. Cohen-Kettenis, “YOUNG ADULT PSYCHOLOGICAL OUTCOME AFTER PUBERTY SUPPRESSION AND GENDER REASSIGNMENT” Pediatrics (2014)
http://pediatrics.aappublications.org/content/early/2014/09/02/peds.2013-2958
Kelly Winters, “Methodological Questions In Childhood Gender Identity Desistence Research” Blog Link
Brik, T., Vrouenraets, L.J.J.J., de Vries, M.C. et al. Trajectories of Adolescents Treated with Gonadotropin-Releasing Hormone Analogues for Gender Dysphoria. Arch Sex Behav(2020). https://doi.org/10.1007/s10508-020-01660-8
Singh D. et al., “A Follow-Up Study of Boys with Gender Identity Disorder”, Frontiers in Psychiatry, https://doi.org/10.3389/fpsyt.2021.632784
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Love’s Labour’s Lost
About fifteen years ago, in my mid-30s, my physician switched me from Premarin to the so called, “bio-identical hormones” estradiol and micronized progesterone. She told me that she had seen better results with other clients, and thought I would as well. I can personally attest, she wasn’t kidding! Even after twenty years of taking Premarin (conjugated estrogens from pregnant mare’s urine) and/or Estinyl (17α-ethynylestradiol) with intramuscular injections of medroxyprogesterone, I was still fairly flat-chested. The new ‘meds’ fixed that! While welcome, the real surprise is how much the new protocol improved my libido. As I had begun HRT in my teens, I hadn’t noticed any drop off for the first years, perhaps because I couldn’t afford surgery until I was 23? But even then, the drop off in libido had been slow, only showing a severe drop during and subsequent to a life threatening illness I suffered around my late 20’s. It had taken years to recover my health.
After I shared my observations regarding the new meds and its effect on my romantic life, my doc then told me that she had noticed a bimodal response to the new protocol. While all of her clients showed better breast development and feminizing fat redistribution, her “young transitioners” had nearly universally experienced noticeably increased libido compared to her previous protocol of using Premarin or Prempro for post-ops. However, the effect was not as strong with her “late transitioners”. She hadn’t told me to expect the possible increase in libido because she didn’t want to induce a possible placebo effect. As a primary care physician, she was more concerned with providing the best care for her clients, then for publishing, so I don’t know of any papers where this bimodal response has been noted in the literature.
There is however, a very good paper on the effect of MedroxyProgesterone Acetate in experiments with female macaques. Medroxyprogesterone Acetate (MPA) is the synthetic progestin that is in Prempro, Provera, and Depo-Provera. It’s also in a number of contraceptive pills. Female macaques, like human females, are physically capable of having sex at any time in the estrus cycle, making them ideal candidates for experiments on the effect of hormones on libido. The macaques had had their ovaries removed. This caused them to lose interest in sex. When given estradiol their libido returned. Given a combination of estradiol and MPA their libido was killed. As a side effect, the MPA also makes them more aggressive and irritable. Thus, MPA nullifies the libidinous effect of estradiol in female primates. However, given estradiol and progesterone (the “bio-identical” kind) and although there was a slight decrease in the libidinous effect of estradiol, it had no side effect of increased aggression and irritability. So, we have in the female macaque, confirmation of the improvement in libido while using the estradiol and progesterone combination over estrogen plus MPA.
Another problem with synthetic progestins like MPA is that they lack the neuroprotective effects of progesterone. Progesterone reduces neuron death from cytotoxic chemicals that naturally occur in the brain. It also encourages the healing of damaged myelin that surrounds the axons of nerves. MPA not only fails to be neuroprotective, but actively suppresses the ability of the brain to biosynthesize its own progesterone that would have served as a locally neuroprotective agent. So, taking MPA is worse than using no progestin.
So why is MPA prescribed for women? Largely because of the pharmacokinetics; Progesterone has a half-life in the body of only a few hours, requiring the patient to take it twice daily, while MPA’s half-life is on the order of two to three days, making dosing easier. Why is it prescribed for MTF transsexuals? Perhaps it is a combination of ignorance of the benefits of micronized progesterone on somatic feminization and on the general lack of differentiation by primary care physicians between AGP and HSTS transsexuals? Another possibility is that primary care physicians are focusing on reduction of free testosterone in their pre-op patients and MPA has strong anti-androgen effects.
MPA and cyproterone acetate are used in “chemical castration” protocols for certain types of paraphilic sex offenders, those with courtship disorders and pedophilia. Although ethically and legally controversial, for those paraphilic sex offenders for whom reduction of libido allows rational impulse control, the reduction of recidivism is dramatic.
In pre-op transsexuals MPA alone, or in combination with cyproterone acetate (Androcur), can significantly reduce the levels of free testosterone, reducing the masculinizing effects such as body hair, head hair loss, etc. But along with the reduction of testosterone is the expected reduction of libido. For AGP transsexuals, this reduction has often been noted by clinicians to be a welcome side effect. This is likely because it reduces the intrusiveness of uncomfortable autogynephilic ideation. It is part of the now standard “transsexual myth”, promulgated by the AGP transsexual community that concerns for “gender identity” are their motivation and that sexuality, sexual motivation, plays no part in the decision making of transsexuals to transition. For transkids, this side-effect is most unwelcome, and would only be tolerated as part of the cost of reasonable somatic feminization.
Thus, for pre-op AGP transsexuals, the best course may be to continue to use MPA, as it will help reduce unwanted testosterone and reduce unwanted autogynephilic ideation.
But for pre-op transkids, prescribing estrodiol plus micronized progesterone, possibly in conjunction with cyproterone acetate, appears to be a better choice.
It would appear that for post-op transsexuals of both types, estradiol plus progesterone appears to be the best protocol. It affords maximal somatic feminization for both types, while increasing libido for the transkids and leaving the libido low for AGP transsexual, both welcome effects for each. It would be very helpful, if researchers would report results of hormonal treatments for each of the transsexual types separately to confirm or refute this early clinically observed result.
Addendum 1/12/2019:
A recent paper looking at the risk of venous thromboembolism (blood clots) and various HRT protocols has now shown that the safest is estradiol dermal patches with no increased risk over no HRT… which the worst was Premarin and MPA combination, increasing the risk by 50%. More reason to avoid this protocol.
References:
Marie Kwan, Judy Van Maasdam and Julian M. Davidson, “Effects of estrogen treatment on sexual behavior in male-to-female transsexuals: Experimental and clinical observations”
http://www.springerlink.com/content/x6157u550gjk5730/
Johannes F. L. M. van Kemenade, Peggy T. Cohen-Kettenis, Leo Cohen and Louis J. G. Gooren, “Effects of the pure antiandrogen RU 23.903 (anandron) on sexuality, aggression, and mood in male-to-female transsexuals”
http://www.springerlink.com/content/k166622818517235/
Karen Pazol, Mark E. Wilson and Kim Wallen, “Medroxyprogesterone Acetate Antagonizes the Effects of Estrogen Treatment on Social and Sexual Behavior in Female Macaques” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1440328/
Michael Schumacher, Rachida Guennoun, Abdel Ghoumari, Charbel Massaad, Françoise Robert, Martine El-Etr, Yvette Akwa, Krzysztof Rajkowski and Etienne-Emile Baulieu, “Novel Perspectives for Progesterone in Hormone Replacement Therapy, with Special Reference to the Nervous System”
http://edrv.endojournals.org/cgi/content/full/28/4/387
John M. W. Bradford and Anne Pawlak, “Double-blind placebo crossover study of cyproterone acetate in the treatment of the paraphilias”
http://www.springerlink.com/content/g078314p081rn20l/
Barry M. Maletzkya,Gary Field, “The biological treatment of dangerous sexual offenders: A review and preliminary report of the Oregon pilot depo-Provera program”
http://www.sciencedirect.com
Vinogradova, et al., “Use of hormone replacement therapy and risk of venous thromboembolism: nested case-control studies using the QResearch and CPRD databases”, https://doi.org/10.1136/bmj.k4810
A case of mistaken identity…
… or at least of mistaken theory.
Case histories are often used in the medical, psychological, and therapeutic literature to explore and illustrate more general concepts. Reading such case histories sometimes allows us to reinterpret the case, come to different conclusions. Consider the case histories posted by Anne Vitale, a therapist specializing in gender issues:
http://www.avitale.com/TNote15Testosterone.htm
In this first case history, her client, “S”, had been living as a woman for approximately twenty years, but recently entered a relationship with a straight woman. To please the new girlfriend, this AGP transsexual ‘de-transitioned’ to living as a man and began taking male hormone, testosterone. The use of testosterone is known to increase libido, which was the desired effect. However, with the use of testosterone came the desire to cross-dress, largely defeating the purpose for taking the testosterone, that of increasing his partner’s approval of him.
In case #2, an internet correspondent reported essentially the same effect:
“That’s the third time I’ve taken testosterone and every time I’ve had overwhelming desires to present myself as a female.”
In both cases, testosterone increased the libido, which in turn increased autogynephilic desire. These cases are very easy to interpret and understand if one understands the nature of autogynephilic desire and arousal as an essential part of their sexuality. Increasing libido simply increases the expression of their sexuality which is autogynephilic.
However, quite inexplicably, Dr. Vitale, who clearly knows about the autogynephilic model from her reading of the literature, proposes a new model of “testosterone toxicity” to explain the effects. All jokes about “testosterone poisoning” aside, this model fails Occam’s razor; Autogynephilia easily explains these two cases.
This brings us to the topic of gender therapists in general. Given the natural predisposition of the type of people who enter this field to want to help relieve the suffering in their clients, there is a danger that they may begin to accept, uncritically, the narratives that their clients present. It is doubtful that the therapists are completely fooled, but over time, failure to directly question AGP individuals on the nature and consequences of their sexuality has led to unquestioned acceptance of the “hidden feminine gender identity” model, and even of the more unlikely model of female brain sex etiology for clearly masculine, heterosexual male’s desire for somatic feminization. This unquestioning acceptance does not serve their clients’ best interests.
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