It has long been hypothesized that prenatal or perinatal hormone levels influence sexually dimorphic behavior in humans. The evidence from studies of people with Disorders of Sexual Development and in numerous animals studies lends strong evidence that this is true. So it would seem natural that we should ask if sexual orientation and gendered behavior in otherwise phenotypically normal individuals could also have been affected by hormones. The ultimate study would be one that longitudinally follows a large cohort of individuals from conception to adulthood, taking extensive hormonal assays while evaluating gendered behavior and sexual orientation. The problems of doing such a study for transsexuality is obvious… the cohort would have to be in the hundreds of thousands to ensure statistically significant numbers of transsexual individuals were included.
Thus, researchers are interested in finding sexually dimorphic markers that record historical hormone environments. That is to say, something that is an organizational and not an activational effect, preferably one that becomes fixed at the same period in prenatal development as organizational effects in the brain. It must be something that is observable at birth and remains stable long enough to allow us to use it to retrospectively determine ones hormonal environment after we have found our gender atypical population of interest.
I’ve already blogged about one such putative measure, the 2D:4D ratio, which is mildly sexually dimorphic, and in at least some population has a recognizably large enough effect size that we can hope that we can use it. Sadly, the results have been contradictory so far. But despair not, another such sexually dimorphic marker is available, though it requires specialized equipment to measure.
In individuals with normal, unimpaired hearing, a curious effect is found in which our inner ears respond to external sounds with sounds of their own, which is known to be mildly sexually dimorphic, as described in the abstract from a recent paper out of Europe, the first known to explore this effect as a potential probe of the role of androgens in gender dysphoria,
“Click-evoked otoacoustic emissions (CEOAEs) are echo-like sounds that are produced by the inner ear in response to click-stimuli. CEOAEs generally have a higher amplitude in women compared to men and neonates already show a similar sex difference in CEOAEs. Weaker responses in males are proposed to originate from elevated levels of testosterone during perinatal sexual differentiation. Therefore, CEOAEs may be used as a retrospective indicator of someone’s perinatal androgen environment.”
Before we get too excited about this marker, we need to look at the effect size, with is quite small at only d=0.30 in the left ear and was better in the right ear at d=0.60. You may recall that this is of the same order as the 2D:4D finger length ratios at d=0.63. This is large enough to be useful, but only if enough subjects are available to achieve significant statistical power. Sadly, this lack of enough subjects seems to be the case in this study. Too bad, because there is a hint at some exciting results in that looking at a group of gender atypical and gender dysphoric children and teens, the natal males seem to show a shift in the female-like direction, but oddly, the natal females do NOT,
“In the present study, we retrospectively investigated possible organizational effects of prenatal androgens on CEOAEs in relation to gender identity. We found that boyswith GID had sex-atypical (hypomasculinized) emissions. Their mean response amplitudes, though, were not significantly different from either the male or female controls. Thus, boys with GID had an intermediate position between the sexes in terms of CEOAE response amplitudes. By contrast, girls with GID showed emissions in the same range as female controls. Consistent with several earlier studies, sex differences in emission strengths were observed in the control group, with girls having significantly stronger emission amplitudes than boys. Our finding that boys with GID showed stronger, more female-typical emissions compared to control boys suggests that boys with GID might have been exposed to relatively lower amounts of androgens during early development. The effect sizes for the comparison boys with GID versus control boys were similar to those for control girls versus control boys, supporting the notion of a hypomasculinized early sexual differentiation in boys with GID. However, considering the lack of statistically significant differences between the control boys and the boys with GID and the relatively small sample size of subjects with GID, this conclusion may still be premature and our results therefore need to be interpreted with caution. Furthermore, our findings did not support the hypothesis of an increased exposure to androgens in girls with GID during prenatal development. Though speculative, this might reflect that GID in girls does not develop under the influence of prenatal androgens or at least not during the same critical time window as when androgens exert influences over OAEs.”
This result is surprising, in that previous studies involving gay men and women, researchers saw the opposite pattern, in that gay men showed no shift from control men, but lesbians showed a shift from the female to the male response. The most exciting times in science are when you hear, “That’s strange!” This is one of those times. Several possibilities exist. This result could just be spurious, with not enough subjects to have seen the real signal. It could be that there is an additional activational effect that occurs as children mature, that causes a shift for both gay men and gay women toward the masculine response. We may be seeing the effect of heterosexual “tomboys” swamping out the FtM signal. Or, we could be witnessing the first hint that there is a difference between transkids, both MTF and FtM, and conventionally gay men and lesbian women. Time and additional studies will tell.
Sarah M. Burke, Willeke M. Menks, Peggy T. Cohen-Kettenis, Daniel T. Klink, Julie Bakker, “Click-Evoked Otoacoustic Emissions in Children and Adolescents with Gender Identity Disorder” Archives of Sexual Behavior, DOI 10.1007/s10508-014-0278-2
Dennis McFadden, Edward G. Pasanen, “Spontaneous otoacoustic emissions in heterosexuals, homosexuals, and bisexuals” Journal of the Acoustic Society of America, http://dx.doi.org/10.1121/1.426845
A recent paper seemed to be lending weight to the hypothesis that prenatal androgen exposure dose may influence transsexuality. The papers concern the use of 2D:4D finger length ratio as a proxy measurement of prenatal androgen dose exposure. I’ve written about this before, but please allow me to cover the basics again.
The 2D:4D ratio is mildly sexually dimorphic based on the androgen/estrogen ratio during fetal development. The conventionally approved method of measuring the 2D:4D ratio is from the middle of the crease between the finger and the palm to the middle of the tip of the finger. When I measure mine, I find that for the left hand, they measure 67mm:62mm giving a 2D:4D ratio of 1.08. For my right hand, I measure 67mm:63mm, giving a 2D:4D ratio of 1.06. If you are wondering, this is an extremely feminine (hypomasculine) 2D:4D ratio, which would be very unusual to find in a western european male (mostly Irish descent).
When we do this measurement for a large population and graph it as a histogram, as shown on the right, we see that the average male hand has a 2D:4D ratio of 0.975, and the average female hand has a 2D:4D ratio of 0.995. One also notices that there is a range, a classic bell curve, of ratios. Note that they are highly overlapping, but still recognizably separate (effect size d=0.63). Thus, for any given individual, the ratio is essentially meaningless. It is only when we look at large numbers, can we average out the noise, the random factors that push the measurement one direction or the other, that we can see a real signal that might give us interesting clues to scientific questions. Different ethnic populations show different average and effect sizes, so it is important that when conducting a study of this type, that the controls be from the same ethnic population as the subjects.
In the Vujovic paper, they compared a group of FtM and MTF transsexuals to controls, all of whom were ethnic Serbs. The paper was very confusing in that in the text, they use the conventional 2D:4D ratio. But the accompanying bar chart, shown on the left, appear to have flipped this for some, but not all, to use 4D:2D ratios ! This kind of error should have been spotted during peer review. (I’ve seen exactly this kind of error in the papers that I’ve reviewed for journals… it is common to find mislabeling of figures, etc. due to multiple contributing authors.) So, let’s ignore the bar graph and look at the numbers?
“Our study found larger 2D : 4D for right hand in control males, compared to left hand (0.928 versus 0.935). Control female exhibited, as well, larger 2D : 4D for right hand, compared to left hand (0.921 versus 0.945). Control males left hand ratio 2D : 4D is lower (0.935) than in female left hand control (0.945) while there were no differences for the right hand (0.928 versus 0.921).”
Oh dear… if you follow that text carefully, one realizes that once again, something is messed up. The larger numbers were supposed to be for the right hands in the first two sentences, but now it appears, from the third sentence, that the opposite is true. Once again, it appears that the ratios have been flipped from 2D:4D, to 4D:2D in the numbers in the text, but that the original writer of the words had intended to use the conventional 2D:4D ratio… but someone inserted the flipped numbers at some point. (Again, this should have been caught at peer review!)
So what is going on? Clearly this paper could NOT have been peer reviewed, since if it had, these simple and inexcusable errors would not have been allowed in the final version of the paper. The answer is simple. The journal in which this paper was published is NOT peer reviewed. In fact, it is an egregious example of what many in the scientific community are calling “predatory publishing”, as Jeffrey Beall explains,
“An example of a gold open-access journal is The Scientific World Journal, currently published by Cairo-based Hindawi Publishing Corporation. This megajournal covers virtually all scientific fields and imposes an article processing charge of $1,000 for each accepted article. “
As Beall has pointed out, because this is not a peer reviewed journal, not even a subject focused journal, quite literally (not figuratively) anyone can publish ANYTHING in these journals, most especially this one, as long as you pay the publishing fee. The process of academic science depends upon peer review to keep everyone honest, to keep junk science, non-science, erroneous and, most especially, fake data out of the publications. This “journal” does none of that.
Thus, this paper is of questionable value to the scientific community… and especially to the trans-science-skeptic like me. How can I trust the data presented? How can anybody? We can’t. I don’t.
Addendum 1/16/2015: In doing a bit more research into this journal, its publisher claims that it uses a single-blinded peer review process. But, I’m still convinced that it could NOT have been properly reviewed. It took me only a few minutes to realize that the graphs, text, and numerical values were messed up. One would NOT need to be a specialist to see the error, merely scientifically literate.
Addendum 2/17/2015: I wrote to the lead author of this study asking for the correct data. She didn’t bother to read my letter, nor this blog post, with any depth, because her response was non-nonsensical, starting with misgendering me, likely not understanding that the name “Kay” in English denotes a woman’s name, not a man’s. But in any case, it means that she hadn’t bothered to look at my blog post, nor my “about” page:
Thank You for Your kind email.
Figure 1 was excluded from the paper because men created it made a mistake (incidentaly he took data from another study).
I am sorry for this mistake. All other data in the text are correct.
We followed up transsexuals since 1989. and have many interesting data. So, if You have any interest we can have further successfull cooperation.
Vujovic et al., “Finger Length Ratios in Serbian Transsexuals”, The Scientific World Journal
A new argument was presented to me just yesterday involving the well documented fact that among those who transitioned as teenagers, far fewer report having experienced autogynephilia. What made the line of argument ironic was that the proponent had started out in absolute denial of any of the science and most especially of the the notion that autogynephilia existed in some transsexuals, “autogynephilia my ass!” However as the debate developed, she presented a novel take on the Nuttbrock data that I presented, to wit that in that study, 82% of self-reported exclusive gynephiles reported sexual arousal to cross-dressing, while only 14% of those who had begun HRT as adolescents (defined in the Nuttbrock study as before one’s 20th birthday) reported such arousal.
Here’s where it gets interesting: In an effort to win ANY point she could, she took the position that I was twisting the data to suit my position… yet in so doing she had to take the position, for her arguments’ logic to work, that autogynephilia is a UNIVERSAL phenomena among MTF transsexuals. I had to laugh privately, since this reversal of her position would obviate all of her previous positions and support some (but not all) of mine. Interestingly, this argument of universal autogynephilia mirrors the argument proposed by another contingent of autogynephilic transwomen, that autogynephilia is also normal and expected in natal women. I find it doubly ironic that there is such an extreme reaction to the two type taxonomy, but from two camps, those that deny any autogynephilia in transwomen, and those who insist that their autogynephilia is just part of being a woman, and thus, all transwomen must also be autogynephilic.
Her argument also starts with several assumptions that are not supported by the data, nor by community observation. She assumed first that HRT in these teens meant “puberty blockers” and that such blockers would preclude an individual from experiencing any sexual arousal. It wasn’t made explicit, but she may also have been making the false assumption that even traditional HRT precludes any sexual arousal. (I’ve heard several “late transitioning” transwomen make this statement, likely due to their own personal experience, while real for these individuals, is neither universal nor inevitable. From casual observation, it seems to occur more frequently in more senior transwomen than younger “late transitioning” transwomen. And from personal conversations with a fair number of transkids, not one had experienced this phenomena.)
So, she explains the significant difference between these adolescents (of whom only one had identified as gynephilic and 7% as bisexual, with the remaining 93% identifying as exclusively androphilic) and the gynephilic (all but one of whom had begun HRT as adults or had never had HRT, and yes, that one individual is in both groups… I couldn’t back her out of the data), as the adolescents not experiencing sexual arousal to cross-dressing due to them not experiencing sexual arousal in general.
So, having convinced herself that she had won her point… she began to crow that I was the one who was not willing to look at reality!!!
Ummm… Not so fast.
Hypothesis were meant to be tested.
I’ve already pointed out the canard that HRT stops sexual arousal in all transwomen. If it did, would we be having sex as often as we do post HRT and SRS, especially transkids? It simply isn’t true. Second, it is extremely unlikely that these youngsters were all on puberty blockers (e.g. Lupron) as it is still a fairly rare protocol. It is typically initiated by well meaning parents bringing their extremely gender dysphoric pre-adolescent children to specialists. While I would wish that all parents were so willing to medically intervene and save their transkid from the damaging effects of endogenous hormones, it is still a rare parent who does so. Most transkids have to fight to get medical help… and many never get parental support, either waiting until they are legally of age, running away early, or getting HRT “on the street” surreptitiously.
Although the Nuttbrock study did not give us the fine detail I would have liked regarding the exact ages which folks started HRT, we know that half of those who identified as androphilic and had started HRT did so before the age of 20. That also means that half did NOT. From other studies, we know that the age of 20 is the median and the mode, that most androphilic transwomen start HRT, not right at puberty, but nearer age 20, showing a Gaussian distribution centered on age 20, with the bulk having started HRT between the ages of 17 and 23 inclusive. This is enough after puberty to have allowed them to experience that first flush of sexual awakening that accompanies the onset of puberty and adolescence.
We know from countless personal narritives of autogynephilia that those early years of adolescence are typically when sexual arousal to autogynephilic imagery, most especially to cross-dressing, stereotypically in women’s lingerie, is the most obvious and intense. Thus, IF these youngsters who began HRT as teens were universally autogynephilic, they would have had ample time to experience it in all of its intensity, before begining HRT, even if, as was argued, HRT would preclude experiencing it!
Looking further at the Nuttbrock study, only 40% of the self identified exclusively androphilic population had started HRT before age 20. If this argument that HRT in adolescence explains the reduced number reporting autogynephilic arousal to cross-dressing, we would expect that those who did NOT start HRT as an adolescent to report at the same rate as the other sexual orientations. Of those who self-identified as androphilic, all of those, including adolescent onset HRT, adult onset HRT (40%), and not on HRT (20%), the combined population had 23% report autogynephilic arousal to cross-dressing. A little algebra and a calculator will show that those who were NOT adolescent onset HRT were reporting at the rate of 29%, far lower than the 82% of gynephilic transwomen, and even lower than the bisexually identified transwomen who reported at 67%, and the asexual at 66%.
Thus, even if HRT did what my erstwhile debating partner claimed… the data STILL would NOT show that self-reported exclusive androphiles report less than half the incidence of autogynephilic arousal to cross-dressing. We would instead expect the later onset HRT androphiles to report at rates that were at least similar to the bisexual population.
OH… and a note on why I keep using the term “self-reported”: There is, unfortunately for our research purposes, a well documented phenomena of “late transitioning” transwomen misreporting their sexual orientation. It is quite possible, even probable, that the 29% rate of adult onset HRT and no HRT, is from a number of such misreporting older transitioners.
Thus, I’ve outlined my theoretical and evidence based reasons why this novel hypothesis is not supported by the data. Instead, the data supports the two type taxonomy for MTF transsexuality, namely “exclusively androphilic vs. autogynephilic”.
To those who understand the limitations and implications of sociological and psychological studies, I’m sure that the above explication of the data is sufficient. I’m equally certain that to those who are in denial of this research and of the Fruend/Blanchard transsexual taxonomy, what I’ve outlined above will only back them further into their denial.