On the Science of Changing Sex

Fraternizing with the…

Posted in Transsexual Field Studies by Kay Brown on June 18, 2017

critical-thinking… Allies  Or, The Fraternal Birth Order Effect: Early Onset Transwomen vs. Gay Men

In a very recently published meta-study conducted by Ray Blanchard further exploring the Fraternal Birth Order Effect (FBOE), in which he had earlier noted that androphilic males tend to have more older brothers than sisters, he deals with several concerns and new research questions.  First, there had been some concerns with how best to handle the potential effects of family size.  But what really interests me is that here, for the first time, he carefully considers the effect of transgender (feminine presentation / identity) vs. non-trans androphilic men (masculine presentation / identity i.e. conventional gay men).  The results are striking!

“The pooled Older Brothers Odds Ratio for the feminine groups was 1.85, and the value for the non-feminine groups was 1.27. The corresponding risk ratios were 1.52 and 1.19.  The differences between groups were highly significant.  To sum up the results so far in common language:  Feminine homosexual males have more older brothers than non-feminine homosexual males, and non-feminine homosexual males, in turn, have more older brothers than heterosexual males.”

These results weren’t just “statistically significant”, the effect was very great with the 95% Confidence Levels not even overlapping!

But we should introduce a note of caution here.  The feminine androphilic data was very heterogeneous as can be seen in this plot of the data.  This may be caused by the differences between cultures sampled from all over the world.  Some of this data is from Samoan Fa’afafine, some from Western gender dysphoria clinics in the US, UK, and Spain, some from non-Western cultures like Brazil and Korea.  Blanchard also noted this issue and suggested exploration of this might interest some future researcher as more data becomes available.  But in any case, we are shown some very intriguing data that strongly suggests that we may be seeing a difference in etiology between feminine and masculine androphilic males.

Blanchard discusses possible conclusions regarding this,

“A … possibility is that the neurodevelopmental pathway triggered by older brothers is inherently more feminizing than path ways triggered by other etiologic factors (e.g., ‘‘gay’’ genes or prenatal hormone exposure). Thus, a group of homosexual males selected for generalized femininity is likely to contain a higher proportion of individuals who acquired their sexual orientation via the older brother pathway. Other hypotheses, equally speculative, are also possible. … Blanchard and Bogaert (1996) proposed that the FBOE reflects the progressive immunization of some mothers to male-specific (i.e., Y-linked) antigens by each succeeding male fetus and the concomitantly increasing effects of anti-male antibodies on sexual differentiation of the brain in each succeeding male fetus. According to this maternal immune hypothesis, cells (or cell fragments) from male fetuses enter the maternal circulation during childbirth or perhaps earlier in pregnancy. These cells include substances that occur only on the surfaces of male cells, primarily male brain cells. The mother’s immune system recognizes these male-specific molecules as foreign and produces antibodies to them.  When the mother later becomes pregnant with another male fetus, her antibodies cross the placental barrier and enter the fetal brain. Once in the brain, these antibodies bind to male-specific molecules on the surface of neurons.  This prevents these neurons from ‘‘wiring-up’’ in the male-typical pattern, so that the individual will later be attracted to men rather than women.”

Something not discussed, indeed I’m not sure how it can even be explored – unless the curve in the data shown for the odds of an older brother per other sibling is evidence for the effect of first born males experiencing self-induced maternal immunity creating the same etiological pathway.  I would also expect that some first born males may have this etiology due to previous maternal miscarriages and abortions of male fetuses since they too would be expected to have Y-linked antigen challenges to the maternal immune system.

Still, and all, very exciting paper well worth reading.

Reference:

Blanchard, R., “Fraternal Birth Order, Family Size, and Male Homosexuality: Meta-Analysis of Studies Spanning 25 Years”, Archives of Sexual Behavior, (2017),
https://link.springer.com/article/10.1007/s10508-017-1007-4

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Going to the Chapel… ♫♫

Posted in Book Reviews, Transsexual Field Studies by Kay Brown on March 13, 2013

♫♫… and We’re Going to Get Married…♫♫ Greens book

Dr. Richard Green in his 1974 book on transsexuals, “Gender Identity Conflict in Children and Adults” wrote,

“The men who fall in love with and perhaps marry women who are themselves former males, by and large, have known their partners only as women.  Their prior sexual experiences have been only with females.  They consider themselves heterosexual and their relationships heterosexual.  To varying degrees they are consciously and unconsciously aware of the biologic status of their partners, but it would be simplistic and would furthermore blur generally accepted definitions to call these men homosexual.  Rather they are men who respond to the considerable femininity of male-to-female transsexuals, ignoring the dissonant cues of masculinity.”

Those very words, read when I was 17 years old, gave me hope that my dearest wish, to find and marry a straight man, hopefully to also adopt children, just might be possible, in spite of my own mother’s words of encouragement that “No man will ever love you, you know.”  Fortunately, Dr. Green was right, and my mother quite wrong.  Although there are few references, and almost no serious studies, that specifically look at the men who marry transwomen, either “early onset” or “late onset”, I believe from my own observations that most MTF transkids who marry, do find husbands who are straight and narrow (but not narrow minded), because gay men just aren’t interested in transkids. As by negative proof, Green describes a married couple in his book, a pre-op transwoman and a putatively, self-described, straight man.  In quoting this man, he describes the day he met his ladylove,

“The first time I ever remember was she was walking across the street, and one of the fellows I work with said, “Hey, that looks like a guy wearing capris.”

Thus, this man knew she was a transwoman from the very start, as she was just barely beginning to transition.  From the description given both by Dr. Green and by this man, it is clear that this transwoman was a classic transkid.  This transwoman, in the same section, lamented that she very much wanted SRS, but was getting serious resistance from her husband,

“My marriage is not doing so good.  It’s not good because my husband more and more has turned to — now he’s turned to more and more to homosexuality.  It’s something I’ve found very difficult to live with.  I could understand his turning to another woman, because of my position, but not another man.  It really tears me up.”

Thus, we see that this transwoman has married a gay man who used her as a stepping stone in coming out.  It seemed clear reading the book that this marriage would soon end, because when asked if she thought her husband was possibly against her transitioning she replied,

“Yes, I do, because were were closer before I started dressing as a woman regularly.  The point was when I got my breast  operation.  It was one thing I didn’t understand.  It meant so much for me to get this operation, and when I did get it, he was very cold for about two months afterwards.  He was very nasty to me. and he told me that as time goes by I’m getting more womanly and more adjusted and this is bugging him.”

Thus, he showed that MTF transkids’ husbands are by and large heterosexual, because gay men lose interest as we transition. Green interviews a number of other men who are either married or engaged to MTF transkids, who were all clearly straight.  Green was mostly right… but in some respects he missed a few nuances.  Back in the early 70’s he failed to differentiate between transkids and autogynephilic transwomen, and the nature of the men who married AGP transwomen.  But we still find hints.  In his book he writes about a candidate for surgery who detransitions when he falls in love with a post-op transsexual.  This individual is in fact gynephilic, and as a man who detransitioned, would be described as heterosexual, but he is also autogynephilic and gynandromorphophilic. While it is obvious why MTF transkids, who are, after all, genuinely androphilic would wish to find and marry heterosexual men.  It has always puzzled me as to why obviously autogynephilic, and just as obviously, truly gynephilic, transwomen would chose instead to marry men.  Further, just what motivates such men to marry these autogynephilic transwomen?  Lawrence, in her 2013 book speculates,

“… some of them go to great lengths to maintain a facade of “heterosexual normality.”  One can observe this phenomenon on a few internet web sites belonging to MtF transsexuals who fit the autogynephilic demographic (formerly married to women, male-typical occupational history, etc.) and have found men willing to marry them.  On their web sites, these transsexuals clearly convey their pride in their status as married women; sometimes they even display their wedding photographs…”

I can almost see this… but it doesn’t explain the men involved, nor why these transwomen are able to maintain such relationships.  Perhaps we saw a hint of who these men are, and what dynamic maintains the relationship in Green’s book, mutual gynandromorphophilia and autogynephilia?  Consider that Green’s detransitioned transgendered individual likely still experiences autogynephilic arousal to cross-dressing?  Could it be that such men who AGP transsexuals marry are themselves autogynephilic and gynandromorphophilic?

About twenty years ago, a young transwoman in her mid-20’s called me up because she wanted me to meet her new boyfriend.  This news very much surprised me because I had never gotten the impression that she was terribly interested in men.  She had, after all, been in the Navy, on board submarines, for months at a time, and never felt any desire toward her shipmates (me?  I would have gone nuts trying to keep my hands off of them!).   We discussed our conflicting schedules and finally agreed that the best time would also coincide with her support group meeting time.  So off I trudged to an AGP transgender support group meeting.  When I finally met my friend’s new boyfriend, all was made clear… her “boyfriend” was also her “girlfriend”… as he was a classic and typical cross-dresser, fully dressed in women’s clothes for this CD/TG/TS support group meeting. To the outside world, they were a heterosexual couple.  To TG ‘insiders’ it was known that they were a pre-op TS woman and a semi-closeted cross-dresser.

Some time ago, when I was still single, I was introduced to a man who sounded like a potential mate.  He took me to classical music concerts, romantic drives in the country in his sports car, cooked a fine meal… seemed ideal… yet I wasn’t attracted to him, though he was to me, strongly.  He broached the idea of marriage.  It couldn’t have been described as a proposal, likely because he “knew” I would turn him down,   because included in his reasons for why the match was perfect was the idea that we could share the same wardrobe, as we wore the same size 12 dresses.  Although this was personally repugnant, we know for a fact that many autogynephilic transwomen would find this to be ideal.

In the Daskalos paper purportedly about changes in sexual orientation after transition, we see two more examples of exactly such relationships.  In combination with autogynephilic pseudo-androphilia, this makes a potent brew of mutual sexual attraction.  Exactly how many AGP transwomen have found such a mutually agreeable relationship with a cross-dressing man is uncertain.  That such relationships exist is beyond doubt.  This would make for a very interesting research paper.

You may wish to read more from Green’s book here.

Further Reading:

Essay on men who are interested in pre-op transwomen

Essay on autogynephiles being sexually interested in pre-op transwomen

References:

Richard Green, M.D., 1974, “Sexual Identity Conflict in Children and Adults“, Basic Books

Anne Lawrence, 2013,Men Trapped in Men’s Bodies, Springer

Daskalos CT., “Changes in the sexual orientation of six heterosexual male-to-female transsexuals.” http://www.springerlink.com/content/pu44808u15q78k21/

Anne Lawrence, “Letter to the Editor” (in response to Daskalos) http://link.springer.com/article/10.1023/A%3A1018725518592

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Etiological Conjectures, Part 2

Posted in Science Criticism, Transsexual Theory by Kay Brown on December 25, 2012

androgynous faceAs I alluded in my previous post, scientists also like to speculate and generate conjectures regarding the etiology of transsexuals. In this post, I will explore and comment on some of them.

Many of the earlier conjectures were highly influenced by psychoanalysis, shoehorning observations into existing, yet completely untested, models of psycho-sexual development.  These were largely psychogenic theories, that is to say, that mental process create the condition, either transsexuality or homosexuality.  More specifically, they theorized that family constellations, usually an overly involved mother and a distant father create the conditions whereby a male child gets the erroneous idea that they must be female, as they can’t separate themselves as individuals from their mothers.  Or, the theory might be that fear of losing their precious penis causes them to overly-identify with their mother so that losing it doesn’t  seem such a bad alternative.  (Yes, I’m over simplifying, deliberately, sarcastically.)

Before we completely laugh at the idea of psychogenic illness, we should remember that there are several very real psychiatric illnesses which have been identified and shown, using modern science, to be of such psychogenic origin.  The most heart breaking is Reactive Attachment Disorder, which is common among institutionalized children who as babies and toddlers were literally not cuddled.  The lack of physical / emotional contact with caregivers literally creates a condition whereby these children have severe emotional and behavioral problems as they grow up (but not autism).  Another illness that has a psychogenic origin is post-traumatic stress disorder.  Although traumatic events as adults act as the proximate trigger, horrific events in childhood have been identified as leaving these individuals without the emotional resilience to weather such events.  A history of physical abuse as a child is one of the more commonly identified preconditions for later post-traumatic stress syndrome, likely due to down-regulation of cortisol production.

But, during the early to mid-twentieth century, psychoanalysis claimed illnesses were psychogenic that we now have clearly established as neurological defects including schizophrenia and autism spectrum disorders.  Typically, the quality of mothering was blamed.  (Sound familiar?)  Mothers were blamed for nearly every sort of bad outcome in their children, without ANY corroborating statistics or evidence.  The ugliest of these was calling the mothers of autistic children, “refrigerator mothers” and the mothers of schizophrenic young adults, “schizogenic mothers”.

So, in a similar vein, I call the theories that invoke parenting styles, especially those that blame mothers, for MTF transkids, the “smother mother” hypothesis.  Without ANY corroborating statistics or evidence, many psychoanalysts and their medical colleagues, accepted many of these theories as “true”.  Although it is true that many parents become emotionally distant from a transkid, this is far more likely a result, not a cause, of the child’s gender atypical behavior.  These theories, although largely abandoned by scientists, still seem to have currency with a number of therapists that I’ve talked to.  In one odd conversation I had about two decades ago, an elderly therapist acknowledged that it didn’t seem to be true of her “early transitioners”, but she was convinced that her “late transitioners and transvestites” had come from such families with smothering mothers and distant fathers.  During the conversation, I began to suspect that she was guilty of confirmation bias and of  subtly “coaching” her clients in what she expected them to say, so that they could obtain their “letters”.

To a modern scientifically based intellect, the creation and wide scale acceptance of psychodynamic theories about the origins of both typical and atypical gender and sexual behavior seems incomprehensible.  How could they ever even entertain such odd notions?  But, if we understand that the ideas have at their core, the pre-Darwinian notion that humans are a special creation, unlike any other species on the planet, it starts to make some sense.  While to us, the thought that gendered and sexual behavior comes from a mental process that, if we translated to our rodent cousins, would make it sound, and be, ludicrous:  Baby rat sees Daddy rat’s penis and notices she doesn’t have one… and envies Daddy rat’s penis… so she starts acting like Mommy rat to get Daddy rat’s affectional attention, etc.   But, if humans are special creation, the theory doesn’t have to work for our rodent, or even, or maybe especially (?) our primate cousins.  These notions had their genesis in Late-Victorian Europe, which was then struggling with the implications of Darwin’s theory of natural selection and evolution and spread to North America which is still struggling (!) .

Another hypothesis is that an anomalous hormonal environment causes cross-sex neurological development.  This is bolstered by experimental research in various animal models, usually rodents, in which exogenous hormonal intervention at certain critical times in neurological development induces cross-sex behaviors.  When coupled with the discovery of cross-sex neurological features in the brain, this would seem to clinch the matter.  Yet… and yet… it doesn’t explain how or why these events occur in otherwise phenotypically normal individuals.  Further, phenotypical markers of prenatal hormone exposure, such as the 2D:4D finger ratio have failed to provide consistent, reproducible, results.

(Addendum 7/7/2017:  We may have found a consistent, reproducable marker of perinatal androgen exposure!  And lo… it correlates with gender atypical play styles in four years olds.)

Thus was born the “gay gene” hypothesis.  Studies of gay men and MTF transkids consistently show evidence of consanguinity, that male homosexuality and exclusive androphilic MTF transsexuality both run in families.  However, the idea of a “gay gene” caused problems with evolutionary theory, since how could such a genetic allele continue to exist against the obvious reproductive disadvantage that being gay (or transkid) naturally presented.  Researchers have spent the past two decades searching for an evolutionary advantage that the relatives of gay men and transkids might enjoy as a “carrier” of the putative “gay gene”.  But years of searching have failed to find such a gene(s).  Perhaps that’s because, there isn’t one?

Finally, we have our new variant on the “gay gene”, the “gay epigene”.  An epigenetic model is based on the recognition that genes are controlled and regulated by other genes using chemical tags, dangling links, attached to the DNA in each and every cell in the body.  These marks are like the conditional branch points, the “flags” or variables, of a computer program.  The interesting thing about such epi-marks is that though it is believed that they should all be erased between generations, many of them are not always fully erased.  This might be a mistake… or it might even be an evolved ability for a crude form of transgenerational gene regulation “memory”.  For example, if an organism needs to adjust it’s metabolism to lean times, like not enough food, by becoming careful about not burning off fat too quickly, it might be advantageous to their progeny to have that adjustment already turned on.  Just such a behavior has been seen in humans, where grandchildren of individuals who knew starvation have slower metabolisms than individuals whose grandparents and parents never knew such lean times.

One of the earliest models to include an epigenetic explanation was from Richard Green M.D., ( a stalwart friend of the transsexual community) and E.B. Keverne, a noted geneticist.  This model suggests that the failure to erase/modify epigenetic markers on the X chromosome that are supposed to be passed down to only one generation, but when passed down past that generation, are theorized to cause severe harm:

A significant skewing in the sex ratio in favour of females has been reported for the families of homosexual men such that there are fewer maternal uncles than aunts. This finding is repeated for a large series of transsexual families in this study. Four hundred and seventeen male-to-female transsexuals and 96 female-to-male transsexuals were assessed. Male-to-female transsexuals have a significant excess of maternal aunts vs. uncles. No differences from the expected parity were found for female-to-male transsexuals or on the paternal side. A posited explanation for these findings invokes X inactivation and genes on the X chromosome that escape inactivation but may be imprinted. Our hypothesis incorporates the known familial traits in the families of homosexuals and transsexuals by way of retention of the grand parental epigenotype on the X chromosome. Generation one would be characterized by a failure to erase the paternal imprints on the paternal X chromosome. Daughters of this second generation would produce sons that are XpY and XmY. Since XpY expresses Xist, the X chromosome is silenced and half of the sons are lost at the earliest stages of pregnancy because of the normal requirement for paternal X expression in extra-embryonic tissues. Females survive by virtue of inheriting two X chromosomes, and therefore the possibility of X chromosome counting and choice during embryonic development. In generation three, sons inheriting the paternal X after its second passage through the female germline survive, but half would inherit the feminizing Xp imprinted genes. These genes could pre-dispose the sons to feminization and subsequent development of either homosexuality or transsexualism.

The latest attempt to explain the presence of homosexuality goes into greater detail of how epigenetic markers canalize (channel) the sex hormone influenced masculinization in males or protect against such masculization in females.  This model assumes that all of the epimarkers should have been erased between generations, but the ones from the cross-sex parent were not fully erased:

It is well established that fetal androgen signaling strongly influences sexual development. We show that an unappreciated feature of this process is reduced androgen sensitivity in XX fetuses and enhanced sensitivity in XY fetuses, and that this difference is most feasibly caused by numerous sex-specific epigenetic modifications (“epi-marks”) originating in embryonic stem cells. These epi-marks buffer XX fetuses from masculinization due to excess fetal androgen exposure and similarly buffer XY fetuses from androgen underexposure. Extant data indicates that individual epi-marks influence some but not other sexually dimorphic traits, vary in strength across individuals, and are produced during ontogeny and erased between generations. Those that escape erasure will steer development of the sexual phenotypes they influence in a gonad-discordant direction in opposite sex offspring, mosaically feminizing XY offspring and masculinizing XX offspring. Such sex-specific epi-marks are sexually antagonistic (SA-epi-marks) because they canalize sexual development in the parent that produced them, but contribute to gonad-trait discordances in opposite-sex offspring when unerased. In this model, homosexuality occurs when stronger-than-average SA-epi-marks (influencing sexual preference) from an opposite-sex parent escape erasure and are then paired with a weaker-than-average de novo sex-specific epi-marks produced in opposite-sex offspring. Our model predicts that homosexuality is part of a wider phenomenon in which recently evolved androgen-influenced traits commonly display gonad-trait discordances at substantial frequency, and that the molecular feature underlying most homosexuality is not DNA polymorphism(s), but epi-marks that evolved to canalize sexual dimorphic development that sometimes carryover across generations and contribute to gonad-trait discordances in opposite-sex descendants.

This model has much to recommend it.  For instance, it would fit with the conjecture I made in my last post regarding the possibility of multiple semi-independent genes controlling sexually dimorphic behavior being involved. Yet,the odd thing about this recently published paper is that the authors seem to have no understanding of the nature of homosexuality and the close relationship it has with transkids, childhood gender atypicality, childhood gender dysphoria in desisting pre-homosexuals, and persisting transkids.  Incredibly, they actually predict that such epigenetic marking will have no correspondence with “gender identity”:

We describe our hypothesis for an epigenetic cause of homosexuality as a series of statements (see Figure 3 for a graphical summary):

a) Empirical studies demonstrate that XX fetuses are canalized to blunt androgen signaling (lower sensitivity to T) and XY fetuses are canalized to boost androgen signaling (higher sensitivity to T).

b) Empirical studies demonstrate the production of XX- and XY-induced epi-marks in embryonic stem cells and extensive sex-specific differences in gene expression at this time. Epi-marks laid down during the embryonic stem cell stage are also established to influence gene expression later in development. This stem cell period is the most plausible candidate time point for the production of epi-marks influencing sensitivity to androgens later in development (canalization of fetal androgen signaling).

c) Epi-marks produced in embryonic stem cells are mitotically transmitted to cell lineages leading to both the soma and the germline, and hence can contribute to pseudo-heritability when they escape erasure across generations (nonerasure in the primordial germ cells and in the zygote and first few cell divisions of the next generation). Animal models as well as human data unambiguously demonstrate that such a multistep escape from erasure does occur at nontrivial frequency.

d) Epi-marks blunting (in XX fetuses) or boosting (in XY fetuses) androgen signaling will be sexually antagonistic (SA-epi-marks) when they have a nonzero probability of carryover across generations and are expressed in oppose sex descendants. Such carryover will contribute to discordance between the gonad and one or more sexually dimorphic traits.

e) Our modeling work shows that SA-epi-marks are favored by natural selection over a broad span of parameter space because there is a net benefit to the carrier (due to canalization of sexually dimorphic development) that is not offset sufficiently by transmission (and fitness reduction) to opposite sex descendants.

f) Genetic mutations causing SA-epi-marks are expected to fix in populations and are therefore not expected to be polymorphic except transiently during their initial spread within a population. Therefore, no association between genotype and homosexuality is predicted.

g) Because the androgen signaling pathways differ among organs and tissues (e.g., use of different AR cofactors), the same inherited SA-epi-mark can affect only a subset of sexually dimorphic traits, e.g., no effect on the genitalia, but a large effect on a sexually dimorphic region of the brain.

h) Shared, gonad-discordant SA-epi-marks that carryover across generations would contribute to the observed realized heritability of homosexuality, e.g., monozygotic twins share the same SA-epi-marks coinherited from a parent.

i) Unshared, gonad-concordant SA-epi-marks, produced during fetal development, would contribute to the low proband concordance of homosexuality observed between monozygotic twins, i.e., they need not share SA-epi-marks generated during development that occurs after the twins have separated.

j) Homosexuality occurs when an individual inherits one or more gonad-discordant SA-epi-marks that are not masked nor erased by the production of de novo gonad-concordant SA-epi-marks that accrue during ontogeny. The SA-epi-mark(s) influence androgen signaling in the part of the brain controlling sexual orientation, but not the genitalia nor the brain region(s) controlling gender identity.

Perhaps they are referring not to the existence of transkids “gender identity” but of the “gender identity” of autogynephilic transsexuals? If so, I would TOTALLY agree with them. But, somehow, I believe that they are simply basing this odd assertion on the mistaken acceptance of our late 20th Century adoption of the separation of sexual orientation and gender identity as being unrelated phenomena, without having read the scientific literature dispelling it.

Thus, we see that cultural biases have and continue to distort scientific discourse into the etiology of homosexual transsexuality.

References:

David E. Simpson, J.J. Hanley, Gordon Quinn, Documentary film: “Refrigerator Mothers”
http://www.pbs.org/pov/refrigeratormothers/#.UNntP6xLnkY

Pasterski, V., “Fetal Androgens and Human Sexual Orientation: Searching for the Elusive Link”, (2017) Archives of Sexual Behavior
https://link.springer.com/article/10.1007/s10508-017-1021-6

Pasterski, V., et al., “Postnatal penile growth concurrent with mini-puberty predicts later sex-typed play behavior: Evidence for neurobehavioral effects of the postnatal androgen surge in typically developing boys”, (2015) Hormones and Behavior
http://www.sciencedirect.com/science/article/pii/S0018506X15000033#f0005

Green, R., Keverne, EB., The disparate maternal aunt-uncle ratio in male transsexuals: an explanation invoking genomic imprinting.
http://www.ncbi.nlm.nih.gov/pubmed/10623499

Rice, et al.  “Homosexuality as a Consequence of Epigenetically Canalized Sexual Development”
http://www.jstor.org/stable/10.1086/668167

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Etiological Conjectures, Part 1

Posted in Transsexual Theory by Kay Brown on December 22, 2012

androgynous faceWe all love to speculate on what made us the way we are.  We all love to generate models for how the transgendered world came to be.  I’m certainly not immune to those speculations, and neither are many of the scientists who conduct research on the trans-phenomena.  About two decades ago, I formulated a model of how MTF transkids (HSTS) and conventional gay men were similar and dissimilar.  At the time, it was purely based on personal observation and conjecture.  Imagine my surprise and delight when I read a recent paper based on genetic manipulation (gene “knock-out”) on sexual dimorphic behaviors in mice that would support part of my conjecture.

Many animals who are bisexual (i.e. that come in two and only two sexes) also often have sexually dimorphic behaviors.  Typically, they involve reproductive behavior, sexual uniting of gametes, mating, and rearing or protection of their young.  The range of such behaviors found in the animal world are so diverse, that I would fill up an entire multi-volume set of books just to list them all.  However, for mammals, many of these behaviors are similar enough that we can use some animals as stand-ins for researching what is likely to be also true for humans, especially in the evolutionarily close relatives in primates and rodents.  The most useful, due to their short lifespans, small size, and ease of maintaining, are mice and rats.

My personal model has been that many sexually dimorphic behaviors are independently evolved and genetically encoded.  They are developmentally controlled by similar mechanisms such as sex hormone receptors on neurons.  This implied that masculinity and femininity (to be defined below) are not a “one shot deal” nor a simple one dimensional, nor even a two dimensional behavioral space.  That is to say, that many of the sexually dimorphic behaviors may be “switched on or off” independently.  In fact, when describing this model to others, I often asked my listener to imagine a long row of switches, which may be up or down.  Some of these switches control masculine behaviors and some feminine.  In theory, they could be in any combination, but during development, processes come into play such that the vast majority of people have all of one type, masculine or feminine in the on, while the opposite type are in the off positions.  However, in a small number of individuals some of the switches are flipped to the “wrong” state.  In an even smaller number of individuals, quite a few of the switches are flipped to the wrong state.  Some of those switches have only small effects.  But some of the switches have rather dramatic effects.

To say that a given behavior is masculine or feminine is to say that that behavior is more likely to be produced by one sex than the other.  For example, in common rabbits, a female is far more likely to pull hair from its belly to line an underground nest in preparation for caring for kits (newborn rabbits).  Thus, in rabbits, nest lining would be a “feminine” behavior.  In rodents, females are far more likely than males to exhibit lordosis, arching of the spine to tilt and raise the pelvis, than males, usually in the presence of adult male.  So we can describe lordosis as also being “feminine” behavior.  Conversely, mounting behavior is usually only seen in males, and thus may be described as a “masculine” trait.

Now, at least in mice, we have confirmation that it is possible to switch “off” individual genes that are associated with such behaviors, both masculine and feminine.  This study did not demonstrate turning “on” a cross-sex behavior, but that has been demonstrated repeatedly, if crudely, by administering cross-sex hormones to neonatal rats.   Further, in sheep, we have seen that a mix of masculine and feminine traits can coexist in that one finds male sheep who preferentially mount (masculine) other male sheep for sex (feminine).  (I needn’t provide references, given that these are well known in the literature.)

In humans, there are a range of behaviors that show varying levels of sexual dimorphism.  Simple observation would suggest that the single most sexually dimorphic trait in humans is the propensity for sexual attraction to men.  In women, approximately 98% exhibit sexual attraction to men, while in men perhaps only 5-10% are attracted to other men, and only 3% are exclusively so.  Thus, sexual attraction to men would, by our definition, be a “feminine” trait.  Interestingly, there appears to be analogs to “mounting behavior” and “lordosis” in humans.   Men who are sexually attracted to other men, also exhibit a preference for mounting (active or “top”) or lordosis (passive or “bottom”).  It is my thesis here that in gay men, independent sexually dimorphic behaviors have been feminized while others have not, and that this independent switching has occurred in varying combinations in individual men.  That is to say, that a gay man could be quite feminized in at least one behavior (androphilia) but show a range of other behaviors that may or may not also be feminine.

Which brings us to MTF transkids.

Transkids are universally attracted to men.  They are also universally obligate “bottoms”.  In fact, they are also universally “avoidant” as well.  That is to say, that they refuse to allow a partner to take notice of, or touch, their pre-op genitalia.  Transkids are also, by definition, persistors, while most gay men were at least somewhat gender atypical as young children and may or may not have also been gender dysphoric, yet they desisted being so by the time they were eleven or twelve.  Transkids remain behaviorally feminine in voice production, motor movements, etc.  I’ve often noted that many transkids are especially interested in small children and babies.  As a speculative conjecture, might the difference between conventional gay men and transkids be the number, or a key subset, of the sexually dimorphic behaviors that are possible?  That it is not so much that they are “more feminine” than most gay men, but that they are “feminine in more ways”?  So much so, that they find it far more comfortable and advantageous to transition?

Etiological Conjectures, Part 2

Etiological Conjectures, Part 3

References:

X. Xu et al. “Modular Genetic Control of Sexually Dimorphic Behaviors”
http://dx.doi.org/10.1016/j.cell.2011.12.018

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The Sound of Your Voice…

Posted in Transsexual Field Studies by Kay Brown on December 1, 2012

female_scientist…Oh, how I miss waking up to the sound of your voice…
-Bare Naked Ladies

Each time we utter a word, we communicate far more than just the lexical unit of speech; we also announce to the listener our native language, our hometown, our age, our gender, and possibly our sexual orientation.  In the transgender field guide videos, I asked the viewer to pay attention to the vocal inflections of each of the transwomen.  If you listened carefully, you probably noted that the HSTS transkids each were distinctly different than the AGPs.  This vocal difference that transkids have, compared to non-gender-atypical boys, is present since childhood.  It is not a recent development, not a conscious attempt to sound like women.  That voice is largely untrained.

Many gay men have a discernibly “gay voice”, but not all.  Interestingly, this voice quality corresponds to the level of gender atypicality that they exhibited as children.  That is to say, that straight sounding gay men report having been typically masculine as boys, but “gay” sounding men report having been gender atypical as boys.  Research also shows that this “gay voice”, far from being a speech defect, the stereotyped “lisp”, it is actually clearer sounding speech.  This speech is also more like how heterosexual women speak, than how straight men speak.  Given this, it shouldn’t surprise anyone that gender atypical boys should sound more like girls than gender typical boys.

A large percentage of boys who were gender atypical grow up to be gay, though some do grow up to be straight identified.  (Given that being gay is still socially stigmatized and discriminated against, I personally suspect that many of these so-called “straight” men are in fact closet homosexuals.)  A number of these gender atypical boys are also gender dysphoric.  And a subset of those that are gender dysphoric will persist being so to become transkids.

In the Crocker and Munson study, they showed that older gender atypical boys had even more feminine voices than younger atypical boys.  As I showed in my essay on persisting and desisting gender dysphoria in children, those who desist in being gender atypical and gender dysphoric seem to be doing so just before the age of 10 or so.  Thus, I believe that we can surmise that Crocker& Munson’s older boys would have a higher percentage of ‘persisters’, transkids, than their younger test group.  So, I hypothesize that the increased perceived femininity of voice production in the older group is an artifact of the desisters having dropped out of the potential pool of older boys, leaving the more naturally feminine transkids.

One working assumption is that a sizable subset of gay men have significantly feminized brain structures that influence both erotic target (sexual orientation) and vocal production.  This is supplanting the hypothesis that the “gay voice” is the result of community wide agreement upon a ‘code’, a voice that helps gay men identify each other.  The evidence supports the former, rather than the latter, as pre-adolescent boys are unlikely to have self-identified as gay, and to have deliberately learned a community code.

I hypothesize that the feminization of the brain is more extensive in ‘persisters’, transkids, and that the voice production is similarly more feminized.  This is in keeping with the conceptualization that (at least some) gay men are somewhat feminized, more like women than straight men, and that HSTS transkids are “so gay they’re women”, as James Cantor has quipped.

I think it would be interesting for researchers to compare the “gay voice” to the “transkid voice”.  From my own experience, they are similar, but not identical.  The gay voice is trending towards the transkid voice, but doesn’t reach it.  The average transkid voice is trending toward the female voice, but also doesn’t quite reach it, though, with just a tiny effort, it can allow the average transkids to pass as female to most listeners.  Some transkids have voices so like the typical female voice that no effort is needed.

Again, as I pointed out in the field guide, the untrained AGP voice is typically masculine.  A great conscious effort must be made if an AGP wishes to achieve a passably female voice.  I think it would be interesting to compare and contrast the HSTS and AGP voice.

Addendum 1/4/2013:

Lal Zimman has conducted an interesting bit of research on FtM transmen’s voice, which I now reference.  He has a couple sound clips that may be of interest.

References:

Crocker, L., & Munson, B., “Speech Patterns of Gender Non-Conforming Boys”
http://www.tc.umn.edu/~munso005/Crocker&Munson_NWAV2006_PostConference.pdf

Peter Renn, “Speech, male sexual orientation, and childhood gender nonconformity”
http://homepage.psy.utexas.edu/homepage/class/psy158h/prevhonors/z111/project.htm

Deborah Günzburger, “Acoustic and perceptual implications of the transsexual voice”
http://link.springer.com/article/10.1007/BF01541604

Lal Zimman, “Pronunciation of ‘s’ sounds impacts perception of gender, CU-Boulder researcher finds”
http://www.colorado.edu/news/releases/2013/01/03/pronunciation-%E2%80%98s%E2%80%99-sounds-impacts-perception-gender-cu-boulder-researcher

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Out of the Frying Pan…

Posted in Transsexual Theory by Kay Brown on January 14, 2010

… Into the Fire.    Or, how to lose even more friends.

androgynous faceI believe that it has now been convincingly demonstrated that there are two and only two major types of MTF transsexuals, that one type is autogynephilic (AGP) and the other is exclusively androphilic. We’ve mostly been talking about the AGP type.  That’s typical of the dialog in the “community” since most transsexuals are AGP and many of them are extremely uncomfortable with the fact.  But, I would now like to turn my attention to the non-AGP, the feminine androphilic type.

It has been noted by a number of people, but most clearly, if not flatteringly, portrayed by Michael Bailey, that the feminine androphilic type transsexual is possibly an extremely feminine form of the more conventionally understood homosexual man.  This too is not a popular notion, both among AGPs, many of whom would otherwise like to identify as a member of the feminine androphilic type, and even among those who would clearly be understood to be members of this feminine androphilic type.  After all, these are people who clearly identify as women, are socially accepted as women, who often marry, and even occasionally adopt and raise children, as women.  But, we are not talking about social or personal identities.  We are talking about biological etiologies.  And there is evidence to support the hypothesis that feminine androphilic transsexuals have the same, or at least similar, etiologies.

First, there is the noted similarity of the obvious behavioral femininity exhibited by the majority of conventional homosexual men before the age of seven and the obvious behavioral femininity seen in feminine androphilic transsexuals at that same age.  In fact, one would be hard pressed to separate them at that age.  Richard Green, testing the hypothesis that feminine boys grow up to be transsexuals, recruited a cohort of such feminine boys in the late 1960s to follow as they grew up, as a longitudinal study.  Of the fifty feminine boys, only one grew up to be transsexual, most grew up to be conventionally homosexual or bisexual.  Interestingly, one grew up to be a heterosexual transvestite.

Other studies involving retrospective reports of childhood behavior of homosexual men have shown the same pattern, that the majority were notably behaviorally feminine as small children.  Thus, not only do most notably feminine boys grow up to be conventional homosexual men, but most gay men were feminine boys.  Similarly, homosexual women have shown the same pattern with respect to behavioral masculinity in early childhood, a trait shared with gynephilic FtM transsexuals, I might add.

So, as young children the two groups, gay men and feminine androphilic transsexuals, are nearly indistinguishable, but by the time they are in puberty, they begin to look quite different in behavior, and often, even physically.  Thus, it could be argued that they are not the same, nor even similar in etiology, given the difference in development pattern between seven and adolescence.

However, there are many other phenomena that suggest a similar, if not the same, etiology.

One of these shared phenomena is the Fraternal Birth Order effect.  Both conventional homosexual men and feminine androphilic transsexuals, as groups, have more older brothers than random chance.  That is to say, that the likelyhood that a male child will be gay or be feminine androphilic transsexual increases by 30% for each older brother that his or her mother has given birth to.  This is not a family constellation effect, as studies have shown that older step-brothers do not influence the odds of being either gay or feminine androphilic transsexual.

Interestingly there is the maternal uncle to aunt ratio mismatch that is shared by both gay men and feminine androphilic transsexuals.  Both groups have more maternal aunts then uncles compared to straight men, significantly more.

Finally, the chance of having a gay brother, for both gay men and feminine androphilic transsexuals is higher than for straight men.

Thus, there are three distinct similarities in family make-up that both conventionally homosexual men and feminine androphilic transsexuals share.

Another similarity is that both gay men and feminine androphilic transsexuals have female like responses to the introduction and sudden reduction of exogenous estrogens, but gynephilic transsexuals do not!  Thus, we have yet more strong evidence for two types of transsexuals, and evidence that the feminine androphilic transsexual is similar to most homosexual men.

The evidence that conventionally homosexual men are neurologically feminized, more like females than straight men, is growing. The most famous is that a certain part of the brain is notably female like in gay men.  But this is only available postmortem.   Other studies using fMRI have shown that when gay men perform certain cognitive tasks that are known to show sexually dimorphic differences in topical brain activation between men and women, the gay men look more like typical women.

Thus, the preponderance of the evidence suggests that feminine androphilic transsexuals are similar to gay men in that both are neurologically feminized, while the AGP transsexuals are not!

One hypothesis is that gay men show a range of femininity and that feminine androphilic transsexuals are the extreme tail end of a distribution that is mostly centered on only mildly feminized.  Indeed, there the are the ranges of femininity exhibited in the gay male population, from unremarkably masculine to feminine, to those who relish joining the ranks of pre-op feminine androphilic transsexuals for short periods, through being drag queens.  Indeed this would parallel the range of autogynephilic behavior, from occasional cross-dresser, to full-time, to post-op transsexual.

Another hypothesis is that there is a dissimilar etiology, but one that causes femininization in similar ways in a neonate, that in gay men, the cause of the femininization is no longer operating in later childhood, allowing the child to masculinize from endogenous hormones, while for feminine androphilic transsexuals, the cause of the feminization is still operating.  For example, if the conventional gay male is caused by the prenatal environment, but postnatally no further developmental interference occurs, then the brain may be further masculinized by endogenous androgens as puberty and adolescence nears.  While for the feminine androphilic transsexual, the effect is from within, perhaps epigenetic inactivation of genes that code for specific androgen receptors in the brain, and possibly elsewhere.  This would explain the observation that feminine androphilic transsexuals are more feminine physically, smaller in stature and slimmer for their height than average males.

There are many possible studies that could be conducted that could show the similarity and possibly the difference between feminine androphilic transsexuals and homosexual men, and likely at the same time, show the dissimilarity between AGP transsexuals and feminine androphilic transsexuals, but most studies of “transsexuals” have not rigorously, if at all, differentiated between AGP and feminine exclusively androphilic transsexuals.  I for one would like to see such studies, to answer such questions as; Are feminine androphilic transsexuals the same or merely similar to gay men?  I would like to see studies that would answer why, in spite of the similarities, we have such extremely divergent life arcs past mid-childhood.  After all, gay men become more masculine as they reach adolescence, while feminine androphilic transsexuals get more feminine.

Although feminine androphilic transsexuals may not be comfortable with knowing that they may share the same etiology as gay men, gay men may return the favor, themselves being uncomfortable with the knowledge that they are feminized males, in the same category as feminine androphilic transsexuals.

But science is about discovering the nature of reality, not about how we would like things to be.

Further Reading:

Essay on Persisting and Desisting Gender Dysphoria in Gender Atypical Children

Essay on Greater Fraternal Birth Order Effect in androphilic transwomen than in gay men

References:

Bailey, J. M., “The Man Who Would be Queen” 2003

Green R (January 1979). “Childhood cross-gender behavior and subsequent sexual preference”. Am J Psychiatry 136 (1): 106–8. PMID 758811.
http://ajp.psychiatryonline.org/cgi/pmidlookup?view=long&pmid=758811.

Bailey, J. Michael; Zucker, Kenneth J. “Childhood sex-typed behavior and sexual orientation: A conceptual analysis and quantitative review”
Developmental Psychology. Vol 31(1), Jan 1995, 43-55.
http://psycnet.apa.org/index.cfm?fa=search.displayRecord&uid=1995-17028-001

Blanchard, R., & Sheridan, P. M. (1992). Sibship size, sibling sex ratio, birth order, and parental age in homosexual and nonhomosexual gender dysphorics. Journal of Nervous and Mental Diseases, 180, 40–47.

Blanchard, Bogaert, “Homosexuality in men and number of older brothers”
http://ajp.psychiatryonline.org/cgi/content/abstract/153/1/27?ijkey=e186877631aa1c47de8fd859310668c21bcd25ef&keytype2=tf_ipsecsha

Anthony F. Bogaert, “Biological versus nonbiological older brothers and men’s sexual orientation”
http://www.pnas.org/content/103/28/10771.full

Green, R. (2000). Birth order and ratio of brothers to sisters in transsexuals. Psychological Medicine, 30, 789–795.

Blanchard, R., Zucker, K., Cohen-Kettenis, P., Gooren, L., & Bailey, J. (1996). Birth order and sibling sex ratio in two samples of Dutch gender-dysphoric homosexual males. Archives of Sexual Behavior, 25, 495–514.

Poasa, K. H., Blanchard, R., Zucker, K. J. (2004). Birth order in transgendered males from Polynesia: A quantitative study of Samoan fa’afafine. Journal of Sex and Marital Therapy, 30, 13–23.

Blanchard, R., (2017). “Fraternal Birth Order, Family Size, and Male Homosexuality: Meta-Analysis of Studies Spanning 25 Years” Archives of Sexual Behavior, https://link.springer.com/article/10.1007/s10508-017-1007-4

Dorner, G., et al., A neuroendocrine predisposition for homosexuality in men
http://www.springerlink.com/content/g1176x7289822289/

Dorner, G., Neuroendocrine response to estrogen and brain differentiation in heterosexuals, homosexuals, and transsexuals
http://www.springerlink.com/content/l20386114j163331/

LeVay S (August 1991). “A difference in hypothalamic structure between heterosexual and homosexual men”. Science (journal) 253 (5023): 1034–7. doi:10.1126/science.1887219. PMID 1887219.
http://members.aol.com/slevay/hypothalamus.pdf.

A. Elias, L. Valenta, “Are all males equal? Anatomic and functional basis for sexual orientation in males”  Medical Hypotheses, Volume 39, Issue 1, Pages 85-87
http://linkinghub.elsevier.com/retrieve/pii/0306987792901453

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