Biological Underpinnings of Transvestism

The original source of this article is unknown however It is one of the more understandable explanations for the causes of transvestism that I have read. Republished from Suzi Jet’s blog. This thesis is further supported by a recent study from the University of Vienna on brain networks and how they effect gender identity

causes of tranvestismHow does a transvestite become a transvestite or a transsexual become a transsexual? How does a gay man become gay for that matter?  These disorders are all very different but may share to some extent the same cause.  There have been many theories regarding these disorders, most of which have related to environmental factors during one’s upbringing.   For instance, one old school of thought was that a man becomes a transvestite because he was humiliated as a boy by being cross dressed.  More recent evidence has suggested more biological causes, however.   In my opinion, a cross dresser’s interest in women’s clothing is every bit as biologically determined as his interest in women.   It is the interest itself that defines the cross dresser, not the practice, as most men obviously would have no interest in wearing women’s clothing and would feel rather peculiar if cross dressed.  The scientific community has discovered much about how these interests develop.  What follows is a very short and somewhat simplistic discussion of some of their findings.

It’s really no secret that all males have the genetic information required to make them either male or female.  It is during (normal) fetal development that either one set of blueprints or the other is selected for our development.  Of course many parts of our genetic code are common to both blueprints, while other parts are specific to only one gender.  It is those parts of our genetic code that are activated, as appropriate, according to the presence or absence of a Y chromosome. Let’s examine briefly how this works.

When fetuses are first formed, they have _both_ male (Wolffian) and female (Mullerian) duct systems and a single pair of undifferentiated gonads.  At that stage, a male fetus differs from a female fetus only by the presence of a Y chromosome.  Among other things, the Y chromosome has the genetic code for a peptide called Mullerian-inhibiting hormone (MIH). MIH is manufactured by the male fetus (and never the female fetus) according to this code.  This hormone has three important functions: (1) it preserves the Wolffian duct system. (2) It causes the Mullerian duct system to degenerate. And (3) it causes the gonads to differentiate into testes. Without the presence of MIH, the Wolffian duct system would spontaneously degenerate, the Mullerian duct system would continue developing, and the gonads would differentiate into ovaries. For this reason, it is said that the “default sex” is female.

Once our gonads have differentiated into testes or ovaries, they produce either testosterone or estrogen, respectively. Both of these hormones are steroids, which are a fat-soluble class of hormones derived from cholesterol that readily pass through all barriers, including the placenta. The remainder of the fetus differentiates into either a male or a female pattern (or both) according to which steroids are present. As Dr. Prince pointed out in her article, the high levels of estrogen produced by the mother readily cross into the fetal bloodstream. So why then don’t all fetuses develop into girls (apart from their ductwork)? In fact, it is not estrogen that feminizes a fetus but testosterone that masculinizes it. Again, the default blueprint is that of a girl. Once testosterone is present, the feminine blueprint is disregarded, and the male blueprint is used. One peculiar problem remains, though. In order for testosterone to achieve its effects, it has to be converted to estrogen after it enters each target cell. It is then the estrogen that binds to receptors inside the cell and the estrogen/receptor complex that activates the genetic codes of the male blueprint. This may seem quite strange, but it makes sense when one considers that estrogen and testosterone are chemically very similar and are readily converted. Estrogen is ultimately the hormone that achieves either masculinization or feminization of the body and brain after birth, depending on the developmental events that occurred in utero (with the exception of a few target organs that are feminized in both sexes by estrogen and not testosterone — e.g. the breasts).

If testosterone must be converted to estrogen to achieve its effects anyway, then why have two different hormones? Why not use just estrogen? The answer has to do with the mother. Since the mother’s estrogen passes readily to the fetus, and since that estrogen can freely enter the cells of the fetus, it would seem that the mother’s estrogen would result in the male blueprint being activated. Furthermore, it would seem that either testosterone or estrogen produced by the fetus would achieve the same effect. In fact, nature has provided a cleaver mechanism for dealing with this problem. Both male and female fetuses produce a substance in large quantity called alpha-feto-protein (AFP). AFP circulates in the fetal bloodstream and binds up the estrogen there, essentially neutralizing it. Thus, regardless of the gender of the fetus, and irrespective of the mother’s high circulating estrogen levels, the only sexual steroid that can circulate freely in the fetal bloodstream is testosterone. Testosterone, therefore, is like estrogen traveling incognito. Once it enters a target cell, it can shed its disguise (i.e. by being converted to estrogen) and do its work. (Does this sound perhaps just a bit too much like cross-dressing?) Once fetal development is completed, all of the cells in the body have been made either male or female, depending on the presence or absence of circulating testosterone. After birth, the need for this apparently strange system is gone, as male fetuses no longer have to contend with circulating estrogen. At that point, the child stops manufacturing AFP, and its body becomes responsive to estrogen (converted from testosterone in the case of the male) in a manner consistent with its fetal development.

How then can this system fail? One common failure occurred in the “bad old days” of obstetrics when androgens (testosterone-like hormones) were given to some women to prevent miscarriages and premature labor. These androgens were not bound up by AFP, readily entered fetal cells, were converted to estrogen, and masculinized female fetuses. The primary result wasn’t so much the production of male genitalia. Remember that the basic pattern of ductwork has nothing to do with sexual steroids. There was some degree of masculinization of the external genitalia, resulting in an almost penis-like structure. The primary effect, however, was upon the sexual orientation and gender identity of the girl. Most commonly, these girls were quite “tom-boyish” and often were homosexual. A similar effect sometimes occurs when more estrogen enters the female fetal bloodstream than can be bound up by AFP. The estrogen that escapes binding then enters fetal cells and masculinizes them.

Failure of this system is less understood in the male fetus. In the most extreme case, a male fetus (and child or adult) may have a gene defect that results in nonfunctional testosterone receptors. This results in a condition called androgen insensitivity. Males with this disorder have male ductwork and testes; however, their external genitalia are very poorly developed, appearing little different from female genitalia, and their bodies develop essentially a feminine form. These people mature to become essentially normal (but sterile) women. The same sort of effect could occur, naturally, if for some reason testosterone were not produced by the fetus. Thus, the amount of fetal testosterone activity determines whether the fetus develops functionally into a boy or a girl. It is not hard then to recognize that the male fetus would be incompletely or inadequately masculinized if testosterone activity were sufficiently suppressed or impaired.

One possible cause for suppression of fetal testosterone activity could be maternal stress. When a person is under stress his/her adrenal glands secrete high levels of another steroid called corticosterone (or hydrocortisone). This hormone, being a steroid, readily crosses the placenta and travels to the fetal brain, where it suppresses the release of the pituitary hormones FSH and LH, resulting in turn in a reduction of testosterone production. The first demonstration of a linkage between maternal stress and incomplete fetal masculinization came from a study examining males born in NAZI Germany during the latter stages of World War II. Because of the crumbling of the Third Reich and the intense bombing operations, mothers were under extreme stress throughout their pregnancies. The records reveal an extraordinarily high incidence of male homosexuality in this population, compared with control populations, thus supporting the maternal stress hypothesis.

Of course homosexuality is very different from transvestism, but I believe that both disorders have a similar cause. I believe further that transsexualism is related to these two disorders. What then determines the outcome of perturbation of one’s hormonal environment in utero? I would say that two factors are critical. First, obviously, is the magnitude of the perturbation. Different brain and body systems may require different levels of testosterone in order to be masculinized, and masculinization may not be an all-or-nothing phenomenon. Thus, different testosterone levels may be associated with different magnitudes of masculinization and with different combinations of masculine and feminine development throughout the brain and body. Perhaps more critical is the timing of the testosterone suppression, as different systems develop and sexually differentiate at different times throughout fetal development. Testosterone suppression very early in pregnancy may result, for instance, in a failure to masculinize the hypothalamus, which arguably could result in female-patterned sexual preference, hence homosexuality, during adulthood. Testosterone insufficiency at later stages could result in failure to masculinize numerous other brain systems, including perhaps the cerebral cortex very late in development. As a result, the adult’s cognitive patterns could be very feminine, although socialized artificially into masculine patterns. This condition could underlie gender identity disorders such as transvestism and transsexuality.

Although the maternal stress hypothesis, to my knowledge, has not been applied to gender identity disorders, I see no reason why it would not apply. Of course I am speculating in this regard. Nevertheless, I have taken the opportunity to ask numerous (perhaps 50) transgendered individuals about the possibility that their mothers had stressful pregnancies. The overwhelming majority of those people, including myself, can identify specific events that unquestionably would have caused their mothers great physical or psychological stress. Of course this was not a scientific survey with proper controls and should not be regarded as such. This is certainly an avenue of investigation that needs to be pursued.

Given that there are clear indications of physiological causes of gender identity disorders, why should we care? We are the way we are, after all. The simple answer is that we must all live in the “real” world, a small proportion of which is populated with bigots and other intolerant folks who make our lives very difficult. Among other things, we have to deal with the legal system. For instance, transgendered individuals often find themselves in the throes of hostile divorces with child custody at issue. There is a very big difference legally between arguing that one “chooses” to cross-dress and that she “must” cross-dress. If someone were to believe that a parent’s cross-dressing is somehow harmful to her children, then her “choosing” to cross-dress would indicate that she put her own pleasure higher in importance than the well being of her children. On the other hand, if the courts recognize that it is something she “must” do, that would lead them to conclude she might not be such a bad parent after all. There are also civil rights questions at stake. If cross-dressing is something we “choose” to do simply because we enjoy it, then should we have the right to do it when it offends someone else equally? I would of course argue that we do, for reasons of freedom of expression; however, not everyone would agree with me. On the other hand, it is absolutely, unquestionably unconstitutional for a transgendered person to suffer discrimination if her gender disorder is not a “choice” but a “birth defect” of sorts. Transsexuals face still other issues. As long as transsexuality is considered by enough ill informed individuals to be a matter of choice, then there will never be any guarantee of insurance coverage for HRT, electrolysis, and SRS. If transsexuality is a birth defect, however, then it is clearly defensible that these interventions should be covered just like any other birth defect. Thus, irrespective of how we feel about ourselves and how we personally justify our cross-dressing or gender identity, our legal rights are clearly impacted by the question of whether cross-dressing a manifestation of a congenital biological disorder or whether it is no more than an alternative lifestyle which a few narrow-minded people find offensive.

2 thoughts on “Biological Underpinnings of Transvestism

  1. Interesting article. I admit I don’t like the notion of “birth defect.” I am more inclined to embrace the notion of natural diversity and variation. In either case there is no “choice” being made. The problem with “defect” is that it asserts there is something “wrong” rather than simply “different” or “unusual.” Actually, I like the term “remarkable.”

    Joan Roughgarden makes a compelling case in her book, “Nature’s Rainbow” that variations in gender identity and sexual preference are found in nearly all mammals, fish and birds. The causes of those variations, I believe, are almost certainly biological.

    So, I will agree immediately that I am remarkable and vary in an important way from the most common males. But I certainly don’t accept the label of “defective.” Nature didn’t make a “mistake.” Nature simply provided me with a rare, but normal condition for which I am forever thankful.


  2. Pingback: Essays on Transgenderism | Library

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