On the Science of Changing Sex

A Voice of Their Own

Posted in Science Criticism, Transsexual Field Studies by Kay Brown on July 9, 2016

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


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

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Gender Allusions

Posted in Brain Sex, Science Criticism by Kay Brown on February 24, 2015

critical-thinkingIs “Gender Identity” biological?  For most people, the answer is intuitively obvious, “duh!”.  Of course, for these people, they usually also insist that the markers for such identity is some privileged and testable characteristic, like genitalia, which is easy to observe, or karyotype (sex chromosome configuration) which requires a microscope.  But for people with Disorders of Sexual Development (DSD), these markers may not be all that clear.  Further, what are we to make of the gender identities of transsexual and transgendered people, people whose experienced / stated gender identity is at odds with all currently known sex markers?  IS there a biological etiology?  And is that etiology the same as that that gives rise to the gender identity of non-trans people? A recent review article attempts to answer these very questions.  Sadly, I believe that it falls far short of a conclusive answer.  In fact, as I will show, it invokes conclusions from several papers as evidence that are quite questionable.  Further, the authors failed to note the very probable multiple etiologies for Gender Dysphoria and their associated gender identity resolutions suggested by the Freund/Blanchard two type taxonomy of MTF transsexuality. First, they reviewed evidence for a biological basis for the phenomenological existence of “gender identity” in non-transfolk which comes from those with certain DSDs,

A seminal study by Meyer-Bahlburg et al involving outcomes of XY individuals raised as females due to severe non-hormonal, anatomic abnormalities of sex development has provided the most convincing evidence that gender identity is fixed. These congenital abnormalities include penile agenesis, cloacal exstrophy, and penile ablation. For many years, female gender assignment along with surgical feminization was the dominant approach for these patients. In this study, it was observed that 78% of all female-assigned 46 XY patients were living as females. While the majority of these patients did not initiate a gender change to male, none of the 15 male raised 46 XY patients initiated a gender change to female. Thus, risk of questioning gender identity was higher in those patients raised as females than in those raised as males among 46 XY subjects with one of these conditions. A study by the same group that examined the degree of satisfaction with surgical intervention reported by patients with 46 XY genotype also found that those subjects raised as boys were considerably more comfortable with their gender identity. – Another seminal study relevant to this topic was by Reiner and Gearhart in their review of 16 XY genotype subjects with cloacal exstrophy who underwent female gender reassignment surgery. Out of the 14 individuals raised as girls, 4 announced they were male and 4 later chose to live as boys when they became aware of their genotype. The 2 individuals who were raised as males identified as males throughout life. The sexual behavior and attitudes of all 16 subjects ultimately reflected strong masculine characteristics regardless of gender assignment. Thus, children who were born genetically and hormonally male identified as males despite being raised as females and undergoing feminizing genitoplasty at birth. Although cohort size in these studies is small, these data provide the strongest evidence for biological underpinnings of gender identity.  …  In a study of affected subjects, gender role changes were reported in 56-63% of cases with 5 alpha-reductase-2 and 39-64% of cases with 17-beta-hydroxy-steroid dehydrogenase-3 who were raised as girls (6). These data support the concept that gender identity might be attributed to hormone milieu during intrauterine development on some occasions.

These studies are indeed very strong evidence.  Looking at the data, we see that of those raised as girls, 22% of of these subjects in the first study and 57% in the second study, while in the third study, those with hormonal abnormalities, 56-63%, chose to socially transition from female-to-male.  Compare that to the very, very small number of 46XX individuals in the general population who experience severe gender dysphoria and choose to transition.  As an aside, the fact that not all chose to transition should not be taken as proof that gender identity is all that malleable, but should probably be taken as a demonstration that social transition has very high social costs and is not undertaken lightly. Strangely, this paper did not explicitly mention that the majority of these individuals, whether they experienced gender dysphoria or not, were exclusively gynephilic, but they did allude to it.  Also puzzling was their failure to include the converse situation of individuals with 46XY and complete androgen insensitivity syndrome (CAIS), all raised as female, who are extremely unlikely to experience gender dysphoria or sex reassignment, and are universally exclusively androphilic.  Or the even more interesting case of 46XX progestin influenced females raised as male, 50% of whom transitioned from male to female and all are exclusively androphilic.

Thus, they failed to explicitly show the very high correlation of brain sex with gender identity, gendered behavior, and sexual orientation. Having shown that there is indeed very strong evidence that “gender identity might be attributed to hormone milieu during intrauterine development on some occasions”, which supports the notion that gender identity has a basis in biology (as opposed to being purely a social construct overlain on observable sex differences), it is tempting to say that transsexuality, all transsexuality and transgender identity, is also the result of mismatched hormonal milieu.  In fact, many transsexuals hold to just such a position.

But they would be dead wrong.

The logical leap that all transsexuals have such an etiology is not supported by the above evidence.  In fact, given the very probable differing etiologies for Gender Dysphoria and their associated gender identity resolutions suggested by the Freund/Blanchard two type taxonomy of MTF transsexuality, at least one of these types must NOT have been caused by such.  Blanchard went on to predict that this would be born out by studies of the sexually dimorphic structures in the brain, predicting that the exclusively androphilic MTF transsexual would show shifts toward the female morphology, while the other type would not. It is here that this recent paper has its biggest failings, in that not only did they not discuss this issue, but included very problematic studies by Swaab that purported to have shown female like shifts in non-exclusively androphilic transwomen.  These papers did show the shifts in the BSTc and INAH3, but incorrectly concluded that they had existed prior to exogenous HRT and incorrectly concluded that these features in the brain were organization effects of endogenous hormones in utero, when the data clearly demonstrated the opposite, that these shifts were purely activational effects from exogenous estrogenic and anti-androgenic HRT.  To be fair, they did mention that the BSTc was potentially questionable, but completely failed with regards to the INAH3, which demonstrably is not evidence for a biological basis of gender identity.

In reviewing the recent grey and white matter studies, they failed to note that it fits and supports Blanchard’s prediction, which had they done so, would have strengthened their argument for a biological basis for a conventional gender identity in exclusively androphilic MTF transsexuals.  That is to say, that they experience the same feminine “gender identity” as females because their brains are female like.  Conversely, they would also have evidence for a biological underpinning to autogynephiles sexuality, a non-sexually-dimporphic one, which lead to an epiphenomically generated “female gender identity” later in adulthood.  (See my essay on the different origins of cross-gender identity in transsexuals.)

The authors reviewed the literature on possible genetic factors that could lead to transsexuality, noting that they were inconclusive. Totally absent in this paper was any mention of the papers that document the fraternal birth order effect found in exclusively androphilic MTF transsexuals. All in all, I was disappointed in this paper.

I found it shallow, lacking in both depth and breadth, and literally out of step with much of the literature on the cutting edge of the science.

(Addendum 7/7/2015:  I got suspicious of this paper as it reads like a cherry-picked list of papers that support the brain sex hypothesis for all transsexuals, including “late onset” transwomen, so I checked into the background of the authors.  Sure enough, one of the authors is transgendered.  While that alone is NOT damning (after all, so am I), it does explain why this paper only referenced the studies it did, and did not include those studies that when considered as a whole, would show that while one subset of the larger transsexual population could possibly be explained by the brain sex hypothesis, most transwomen could not.  This paper then can and should be considered part of the ongoing effort by some in the transgender community to deny the evidence of the two type taxonomy.)


Aruna Saraswat, MD, Jamie D. Weinand, BA, BS; Joshua D. Safer, MD, “Evidence Supporting the Biological Basis of Gender Identity” (2015) DOI:10.4158/EP14351.RA

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Love’s Labour’s Lost

Posted in Transsexual Field Studies by Kay Brown on September 29, 2010

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.


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”

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”

Karen Pazol, Mark E. Wilson and Kim Wallen, “Medroxyprogesterone Acetate Antagonizes the Effects of Estrogen Treatment on Social and Sexual Behavior in Female Macaques”

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”

John M. W. Bradford and Anne Pawlak, “Double-blind placebo crossover study of cyproterone acetate in the treatment of the paraphilias”

Barry M. Maletzkya,Gary Field, “The biological treatment of dangerous sexual offenders: A review and preliminary report of the Oregon pilot depo-Provera program”

A case of mistaken identity…

Posted in Transsexual Theory by Kay Brown on December 28, 2009

… or at least of mistaken theory.

phrenologyCase 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:


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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