Etiological Conjectures, Part 2

As 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

 

Etiological Conjectures, Part 1

We 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

 

Lucy!!!

~LUCY!!!~  …Oops, I meant, ~Ethel !!!!~

Ethel Spector Person, of “Person and Oversey” fame, died on October 16th of this year.  Her obituary in the New York Times said that her work was influential in demonstrating that there was more than one type of transsexual.  To that, I would have to agree…

… but, I can’t agree that she was “totally right”, because, in fact, she was not.  To understand why, we need to examine both the times in which she worked, and her own words.

First, where she was right.  Ethel Person did correctly recognize that there were at least two types of transsexual.  She recognized that one type was related to transvestites, and had a transvestic career before seeking sex reassignment.  She described them quite well, when she stuck to pure observation.  She also discussed another type, that was related to homosexuals.  Here, she failed miserably.

Incredibly, she described both of these types as “secondary transsexuals”.  Why?

Why?  Largely because she too was caught up in the pseudo-science of psycho-analysis.  She accepted as revealed truth that sexuality developed during, and was shaped by, early childhood experiences, and not just a little bit,  but root and branch.  She can be forgiven for accepting such, since after all, so did everyone else during the middle of the 20th Century.  Today, with our knowledge of neurological correlates of sexual orientation, the fraternal birth order effect, and of epigenetics, it is easy to forget how even our recent fore bearers struggled to understand the likely biological origins of sexual orientation.

In her book, The Sexual Century, published in 1999, she recapitulated her earlier work.  In 1974, she theorized a “primary transsexual” would be an individual who had developed directly to being an asexual transsexual without having first been either homosexual or heterosexual transvestite.  This is because both homosexuality and transvestism, in her psycho-analytically informed world view, are both primary disorders, so– obviously, their transsexuality must be viewed as “secondary” to their primary disorder.  Thus we read,

Primary transsexuals, as we have seen, are essentially asexual and progress toward a transsexual resolution without significant deviation, whether heterosexual or homosexual.

This naturally begs the question, resolution of what?  The resolution of psycho-analytically hypothesized childhood sexual anxieties, of course.   It is interesting that in her book, a tiny print footnote appears on page 97, “… I no longer regard homosexuality as a disorder…”  So, perhaps we should forgive her for her earlier opinion?

Person’s “primary transsexual” is easily recognized today as being asexual autogynephilic transsexuals, as was specifically pointed out by Blanchard.  Her description is quite detailed and accurate, but her analysis is flawed in that she failed to note the autogynephilia driving them.

On another page, we read,

We have concluded from a study of female transsexuals that there is no female equivalent of primary male transsexualism.  In our opinion, the transsexual syndrome in women develops only in the homosexuals with a masculine gender role identity.  Female transsexualism, therefore, can be classified as another form of secondary (homosexual) transsexualism.

In her equating FtM and MTF transkids as being alike, we see that she was quite right, despite the silly notion of “secondary transsexualism”.  But, as alluded earlier, in her case histories she included descriptions of two individuals who she put forward as exemplifying male “homosexual transsexuals”, which as a modern reader will recognize, one was clearly not, while the other was what Kiira Triea so aptly described as an “in-betweenie”, a 25 year old individual that was right at the borderline between a classic transkid and a feminine gay man / drag queen, and unlikely to actually transition.  This may be understood in the context of presenting not a middle-of-the-road example or two, but the most dysfunctional?  After all, if one is a psychiatrist (as Dr. Person was) describing the course of a disease, one may present a particularly serious case so as to make its characteristics abundantly clear, rather than than a mild one?  If so, she misjudged.  From her book:

Case 1. C. is a fat, effeminate 32 year-old man who lives with his parents.  He is compliant, nonassertive, and unable to mobilize much anger.  Despite these inhibitions, he is engaging, affectively responsive, and easy to talk to .  His adaptive competence is of a very low order.  Although extremely bright and articulate, he failed to complete high school, dropping out in his senior year.  He has worked only a total of two years in his entire life.  His mother has always slipped him money, while both pretend to the father that he is working.  …  C. has been an exclusive homosexual as far back as he can remember.  He now wants sex reassignment so that he can marry his current lover and live with him as his wife.   …

…We interviewed C.’s mother who confirmed the familial history.  …  She had always known of C.’s homosexuality and fully accepted it, but refused to acknowledge his wish for a sex change.  …  As she saw it, his sole problem was his inability to work.

C. was an effeminate child.  He played with girls and pursued girlish interests.  He cross-dressed regularly with parental approval from early child-hood until the age of fifteen.  The cross-dressing was theatrical and used to enhance C.’s fantasies of being a girl.  It was never erotic, as in the transvestite, nor did it provide a feeling of comfort, as in the primary transsexual.  His parents thought it was amusing that they often asked him to entertain.  Once, when he was seven, they took him to relatives for Easter dinner dressed as a girl.

C. began a very active and pleasurable sex life when he was twelve.  He engaged in various homosexual activities with peers, older boys, and adults.  His sexual preference is passive anal intercourse, although he will reluctantly engage in other sexual transactions in order to please a partner.  In such circumstances, he is capable of assuming the active role, but does not enjoy it.  His sexual relationships have been mostly transient contacts with partners picked up while cruising.  Prior to his present involvement, he had only one long-term affair.  This occurred ten years ago and lasted for one year.  C. was so upset when the affair ended that he became suicidal and had to be hospitalized.

After his release, he hung around with a drag crowd for about six months.  Once again he cross-dressed, but only in public to be seen, never in private.  …  He received no narcissistic reinforcement as a woman since he lacked beauty, and the masculine homosexuals whom he was really after paid little attention to him since most of them wanted another man, not a drag queen.  Thoroughly discouraged, C. gave up drag and returned to his previous existence, with its characteristic cruising. …

… Last year he went to Spain and met a presumed heterosexual with whom he lived.  He engaged in face-to-face intrafemoral intercourse with this lover and fantasized himself as a woman.  For the first time in his life he began to think seriously of sex reassignment:  “I’ve known about transsexualism since Jorgensen.  I could relate to this guy in Spain better if I were female.  He wants me to stay in the the house and play the whole thing, be subservient.”   …   He is still hesitant, however, because he is skeptical that the lover will, in fact, marry him. …

This man is, in the common vernacular, a “Loser” and a “Bum”.  He is an unattractive 32 year old gay man who has only recently thought of sex reassignment, and then only because a lover he met while on vacation has promised to marry him if he does.  Ummm… yeah… and the check is in the mail!  This man is representative of transkids?  Seriously Ethel?  Seriously?

~ETHEL !!!! You’ve got some ‘splainin’ to do!!!~

 

 

The Wonderful Wizard of Oz

Book Review:  “Men Trapped in Men’s Bodies”

From Seattle, the wonderful Emerald City, Anne Lawrence has published what I hope will soon become the most talked about book on the topic of autogynephilic transsexuality, “Men Trapped in Men’s Bodies“.  I just finished reading Chapter 2, which is available for free download.  None of the material she includes will be a surprise to those that have read my blog in its entirety, but she presents the material in a very cogent and compellingly straight-forward manner.  I will be buying the book and look forward to reading the rest.

http://www.annelawrence.com/mtimb.html

You may read Ray Blanchard’s poignant forward to the book here:

http://link.springer.com/content/pdf/bfm%3A978-1-4614-5182-2%2F1

Addendum 1/30/2013:

I just finished reading the book, cover to cover.  It was well worth the read.

BRAVA!  BRAVA!  Anne, BRAVA!!

Over the course of a little over a decade, Dr. Lawrence had been collecting personal narratives from 249 AGP TS informants.  From these, she analyzed and presents in the book, a breakdown on the common themes found in those narratives.  From them, one can get a sense of both the wide range of expression, yet the common underlying theme of the longing to be feminine and the confusion and pain of these transwomen as they struggle as individuals to come to terms with their sexuality and changing gender identity.

This book is clearly aimed at the clinician whose clients include “late transitioning” male-to-female transsexuals.  After reading it, I strongly recommend that this book should be read and reviewed by every gender therapist, physician, and surgeon.  Hopefully this will serve to dispel the mistaken belief that at least some clinicians have about the suitability of AGP transwomen for HRT and SRS, which from some of the narratives still exists, as Dr. Lawrence explains,

Other autogynephilic transsexuals similarly concluded that the safest approach to take with the psychotherapists was to present themselves as “textbook cases” of MtF transssexualism, not only refusing to disclose their history of sexual arousal with cross-dressing or cross-gender fantasy but lying about this if necessary.  Their attitude is consistent with data from Walworth’s (1997) survey of 52 MtF transsexuals, who reported that sexual arousal with cross-dressing was the single most common topic about which they had lied to or misled their psychotherapists.  … Explanations like these might partly explain why many psychotherapists who specialize in gender issues report that they rarely encounter clients for whom autogynephilia is a significant issue.

For the older transitioning transsexual, reading this book may also help in understanding oneself, and more importantly, know that despite others’ denial, autogynephilic sexuality and motivation for transition and SRS is not only common, but  are found in the majority of transsexuals in the Western countries, that quite literally, they are not alone.

One of the themes common among the narratives was the need to downplay, rationalize, or reinterpret autogynephilic experiences.

One such belief would be that he really has a “woman’s brain” in his male body.  Another would be that autogynephilia is not a paraphilia at all but merely a normal element of female sexuality.  Yet another would be that he really had been destined to be attracted to men all along, but that his natural inclinations were suppressed by social conditioning and homophobia.  Still another would be that the cross-gender fantasies that he found so exciting earlier in life no longer hold any erotic interest for him, but were merely a temporary mechanism for coping with his gender dysphoria.  A final such belief would be that autogynephilia is merely an effect of his cross-gender identification, not the cause of that identification.  Personally, I consider such explanatory beliefs to be implausible at best, but I understand their appeal.

In the end of the book, Dr. Lawrence makes a plea for more transwomen to come out as autogynephilic, to own their sexuality, to stand as role models for self-honesty.  I too would encourage such.  Yet, and I think this may surprise many of her critics, she doesn’t demand that all autogynephilic transsexual women face and acknowledge their sexuality, who use alternative defense mechanisms that downplay or even deny autogynephilic motivations and experiences, saying,

I’m not ordinarily an advocate for self-deception, but if explanatory beliefs like these make it easier for autogynephilic men who are good candidates for sex reassignment to move forward, I’m willing to condone them.  …  If implausible explanatory beliefs make it easier for these transsexuals to justify sex reassignment to themselves or others, I’m not inclined to argue too strenuously.

I came away with a greater appreciation of the uninvited dilemma that faces autogynephilic transfolk.  Even for the androphilic MTF transwoman, FtM transman, and even gay, lesbian, and bisexual, I recommend buying and reading this important book.  We can’t say that we embrace and support our diverse community until we truly understand that diversity.

Download complete book here: Men-trapped-in-mens-bodies_BOOK

You can purchase the book through Amazon.com

 

The Sound of Your Voice…

♫♫…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