An Open Letter to Physicians

Copyright þ 1991 - Sarah Seton M.D.

Sarah Seton M.D.

An Open Letter to Physicians Copyright þ 1991 - Sarah Seton M.D.

Conservatively speaking, transsexualism affects an estimated 1:30,000 males and 1:100,000 females in our society, with recent estimates as low as 1:18,000 in Europe. Others estimate that there are about 200,000 afflicted in this country, out of which less than 10% have had sex reassignment. The condition is global in scope and can be found in virtually all countries, cultures, and through out history. They are called the Acault in Burma, the Xanith in Oman, the Hijera in India, the Berdache among the American Indians from Alaska to South America, the Mahu amongst the Polynesians, the Sarombavy of Madagascar, and they are found amongst aboriginal peoples of Siberia and Africa. In tribal cultures, transsexuals with few exceptions are revered by their societies for spiritual powers and frequently hold a special place as shaman.

In Western antiquity, persons such as the Phrygian and Scythian "non-men" (recorded by Hippocrates) were seers and considered holy -- affecting the "Hermaphroditic Marriage" of alchemy; Venus Castina was the goddess of female souls trapped in male bodies. Frequently in history, the cross gendered drives of afflicted transsexuals extended to primitive physical alteration of their bodies to conform to the characteristics of the sex of choice; one of the earliest reported sex-reassignment surgeries was done in ancient Rome. With the spread of medical knowledge world-wide, sex reassignment procedures have been instituted in Mainland China, USSR, Eastern Europe, Turkey, Egypt, South-East Asia, Philippines, India, and Africa along with already established Western Nations like Australia, New Zealand, Western Europe, Scandinavia, South America, Canada, and the USA. The phenomenon can not be ignored and will be a medical concern into the future. Chances are that transsexuals are unrecognized members of your communities. At sometime in your careers you will have them as patients. The way they are treated by the medical profession not only affects them but their families and friends as well. As a physician, I try to keep my patients from falling through the cracks in the health care system.

Transsexual patients are medical orphans, receive sub-standard medical care and have precious few doctors willing to serve as their advocates. I am endeavoring to educate professionals about gender dysphoria and the transsexual's need for compassionate and appropriate diagnosis, treatment and support. Other professionals like yourselves need to be informed and develop a compassionate response. Before beginning, I must tell you that the views I express here do not necessarily reflect the views of my university medical center or its Department of Psychiatry; nor the views of Geraldo Rivera, Joan Rivers, Sally Jessy Raphael, Phil Donahue, Oprah Winfree, or the Media generally.

You see your family practitioner who knows you very well; she thinks you should have elective surgery and wants you to see a specialist. The specialist sees you once and says he will do the surgery on Tuesday. You check into the hospital on Monday morning and go to your room. You are NPO after midnight and given a sleeper. You wake up at 6:00 am and the nurse takes your vitals and gives you pre-op medications. Another nurse comes in and gives you a shot in the hip to help you relax.

You are transferred from your bed to a gurney and you are wheeled into a well lit basement where the operating suites are. You become sedated; the surgical nurse reads your wrist band and wheels you into an operating theater. A surgeon checks your chart and leaves. The anesthesiologist connects you to the blood pressure cuff, pulse oximeter, and cardiac monitor and gives you the anesthetic. As you drift off you are confident that you are in good hands. As you come out of the anesthesia in the post-operative recovery room, you realize that something is dreadfully wrong. You are hurting where you shouldn't be hurting; when you look underneath the sheets you are horrified. Whereas, you were once a male before the surgery you are now a female, or if you were once a female, you are now a male. Your aspirations to become the Archbishop of Canterbury just went out the window with the histopathology specimens.

Okay, how would you feel about that? Would you be a female or male then simply on the basis of your new genitals? What would you do? Ask to be changed back? Ah ha, you can't be changed back; what would you do then? (If you say you would like it, I have some surgeons I can refer you to.) You probably would say you were not a member of the other sex. So how would you adjust to living as a member of the opposite sex? How would you deal with being called "he" when you are a "she." Think about the psychic pain of your genital sex being opposite to your gender identity. In fact, this alienation between mind and body is what transsexuals experience from the earliest years of their lives. This scenario of mistaken identity actually happened with three non-transsexual patients during 1987 in Germany and Mexico. It points out how important and immutable gender identity is. Gender is not what is between the legs; gender is between the ears. Think about how important gender identity is for all of us: it is the first datum we establish before we relate to another human being. Throughout my professional relationship with the transsexual community, I have been impressed by their evident intelligence and talent. My impression was confirmed by documented psychological testing in research literature which shows an average of at least 15 IQ points above the general populus. I was further impressed by the overwhelming burden of suffering they have been forced to endure due to being raised as the opposite sex. I say "opposite sex" in that I believe, with many other professionals who have worked with transsexuals over long periods, their problem is biological more than psychological. They have been misassigned their gender in society based upon incomplete medical knowledge of what constitutes a male or female. The consequences of this ignorance has resulted in wasted lives, needless suffering, and the loss of an important human resource for society.

Until fairly recently, an infant's sex assignment at birth has been based on a cursory glance at the infant's genitals. Science has learned in the past 35 years that we can no longer singularly determine a person's assigned sex solely on the basis of superficial genital appearance; in fact, we can no longer determine sex solely on the basis of chromosomes either, as I will shortly explain. Gender dimorphism, or the ability of the nascent organism to develop into two distinct gender types, can be looked at in several ways via genes, chromosomes, gonads, hormones, internal and external reproductive systems other than gonads, secondary sex characteristics, sex of rearing, and behavioral sex (gender identity and gender role). Who we are as sexual adults is a result of a multi-determined cascade of events beginning at conception and continuing throughout the rearing of the child, involving all the preceding factors. It is the product of this cascade that matters not how we got here. We all have become men and women by factors of which we are seldom aware or in control. As I will try to show here, from a medical viewpoint, we have no right criticize another's sexuality because all of us are intersexed at some level; Nature has made females and males interconvertible at conception.

Current models of psychosexual development avoid dichotomies as to nature versus nurture, genetics versus environment, innate versus acquired, biological versus psychologic, or instinct versus learning, in favor of a sequential and interactional view. The medical model can be likened somewhat to a relay race or decision tree in which something can go awry at each level and affect all later levels of integration; a small change at the genetic level has devastating effects at the level of the person in society. As you will see, transsexualism is part of a spectrum of intersexed disorders in humans and it is frequently a strategy for survival amongst lower animals. I will briefly go over this model now.

The first stage is chromosomal. It is based on what sperm wins the swimming race amongst the sperm. As there is survival of the fittest amongst animals, so there is amongst chromosomes and genes. It has long been known that sex errors of the body exist at this level. There are numerous intersexed disorders reflecting differing mixes of X and Y chromosomes and their parts. The most common and well-known of these intersexes are the disorders known as Turner's and Klinefelter's Syndromes. With Turner's children, there is only one X chromosome. Traditionally, two X chromosomes are necessary for full femaleness and at least one Y for maleness. These patients have no significant male or female sex hormones in fetal or later life. Lacking adequate estrogens, they develop no secondary sexual characteristics and have inadequate female anatomy. However, Turner's children are identified at birth as females and raised as girls. When grown, they have no gender conflicts because prenatally their brain is in the female resting state which we will discuss shortly. Other syndromes do not have such a fortuitous destiny with respect to their gender. A child with Klinefelter's syndrome has extra X chromosomes in addition to the XY pair usually found in males. The presence of the extra X chromosome tends to weaken the effect of the virilizing Y chromosome, lessening the androgen production, and resulting in a fetal hypogonadal state. As these children mature, they do not complete the brain organization that should underlie masculine behavior. They often have gender disturbances ranging from complete reversal of gender identity -- similar to transsexuals -- to desire to wear women's clothes, to effeminate homosexuality.

By way of passing, rarely children suffer with Chimerism or true hermaphroditism, 46XX-46XY mosaic genotype. About 75% of these children are raised as boys but have both genital structures in various combinations like the mythical beast Chimera. They frequently menstruate at puberty if not discovered before then. Gender assignment, many times, depends on their gender identity which is usually male due to the presence of a testis which secretes testosterone; rather than have decisive surgery, some decide to remain as two sexes and float between them like the transsexual, experiencing both sides.

Twenty years ago, following the discovery of trans-sexing and sex reversal in the animal domain, human males and females were found with the opposite chromosomal sex, e.g., XX-males and XY-females. This occurs in 1:20,000 births. These individuals have been studied with genetic probes. This research has revealed that one's sex is determined by a cascade of genes initiated by one gene called the Testicular Determining Factor (TDF). It is the presence of the TDF gene, alone, that determines one's sex and fetal gonadal development. This gene can be on the X or the Y chromosome, rendering the X or Y chromosomal sex technically irrelevant. In fact, researchers have recently succeeded in changing the sex of mice simply by altering this gene biochemically.

The TDF gene is believed to be responsible for the vanishing-testes syndrome or pure gonadal dysgenesis. Faulty expression of the gene in genetic males causes a regression of the developing testes before 8 to 12 weeks post-conception so that all sex structures become female. After 10 to 12 weeks, there is partial regression resulting in testicular failure and male pseudo-hermaphrodism. With the isolation of a candidate TDF gene this past year, research has been initiated with transsexuals to ascertain the absence or presence of certain genes in the TDF cascade using genetic probes. Transsexualism may be understood ultimately at the molecular genetic level as has been the case with the intersexes -- an intersex at the genetic level rather than the chromosomes. Several transsexual twin concordances have been found which further support a genetic cause: two identical twins reared independently developed as transsexuals and triplets in one family all wound up as transsexual.

The next step in the decision tree is fetal gonadal sex. Up until this point the fetus is bi-potentiated and can develop as either male or female. Nature without the TDF gene produces females by default. It is the presence of the TDF genetic cascade that causes the undifferentiated gonads to become testes, which in turn initiate production of fetal androgen. Fetal androgen changes the genitalia. What would have developed as a clitoris becomes a penis. Labia minora form the penile sheath. What would have been labia majora fuse to become the scrotum. Developing from the medulla of the primitive gonads, the testes descend through the peritoneal sheath into the scrotum. Otherwise, the cortex of the primitive gonads develop as ovaries. Under the influence of Mullerian Inhibiting Factor secreted by the Sertoli cells of the testes, the female Mullerian paramesonephric ducts regress and the male Wolffian mesonephric ducts develop into vas, seminal vesicles, epididymis, etc. Dimorphic changes also occur in the fetal brain to shape gender identity. Ovaries are not essential for female development since this is the default pathway for the fetus, whereas testes are necessary for male development. Both males and females have testosterone and estrogen in their blood stream, produced by the gonads and adrenal cortex. It is the ratio of the two that determines whether you will be a "little girl" or a "big boy." A high testosterone to estrogen level is essential for the development of male genitalia. In the genetic female with virilizing congenital adrenal hyperplasia (adreno-genital syndrome), an autosomal recessive trait located on the short-arm of chromosome 6, the ratio favors testosterone due to excess secretion of androgens by an hyperplastic fetal adrenal cortex. Deficiency in any of six enzymes (21-à, 11-þ, 17-à hydroxylases; 3-þ hydroxysteroid dehydrogenase; delta-5 isomerase; and cholesterol side-chain cleavage enzyme desmolase) is responsible. These enzymes catalyze pathways in steroid synthesis. Their absence creates an increase in adrenocorticotropin, accumulation of steroid precursors and diversion to the sex hormones, much as water flows around a watershed. The result is a grossly enlarged clitoris or even normal looking penis and scrotal sack with testes absent in the female. Behind these external male genitalia there are normal Mullerian (female internal) structures. In some cases these girls are raised as boys until, to the surprise of their family, they begin to menstruate at puberty and develop a extreme tom-boyish personality. This is an example of female pseudohermaphrodism. Another cause is fetal exposure to virilizing progestins (found in oral contraceptive pills), danazol (an antigonadotropin) given for endometriosis, diethylstilbestrol (which inhibits 3-þ hydroxysteroid dehydrogenase), exogenous testosterone, and virilizing ovarian tumors.

A defect in genetic males causes a reversal of the fetal testosterone-estrogen ratio which produces feminization of the external genitals or male pseudohermaphrodism. Congenital adrenal hyperplasia occurs here too with the same six varieties of enzyme deficiency (especially 11-þ hydroxylase) and autosomal recessive inheritance. The same watershed phenomenon with diversion of steroid precursors to sex hormone production happens as in females with the disease. In addition, two other deficiencies of 17,20 lyase and 17-þ hydroxy-oxidoreductase are autosomal recessive and also tip the scales for a reversed hormone ratio.

These boys are raised as girls because of the difficulty reconstructing the genitals and fortunately grow up with female gender identity due to lack of testosterone's influence on their brains (which I will discuss). To point out how potent a small change at the molecular level can be, boys are sometimes born with a uterus, fallopian tubes, and internal vagina (Mullerian structures) but with cryptorchid testes where the ovaries should be and normal male external genitalia. Failure of the Sertoli cell to secrete Mullerian Inhibiting Factor prevents regression of Mullerian structures (uterus, fallopian tubes, internal one thirds vagina). Due to the presence of normal male genitalia, these infants have total hysterectomies perinatally and grow up as normal boys with male gender identity intact. There are defects in androgen receptor glycoproteins, resulting in testicular feminization syndrome (androgen insensitivity) in 46,XY males. It is called Rokitansky syndrome in 46,XX females, an X linked recessive disorder. These are genetic males with normal androgen levels in the blood stream, but they differentiate with normal appearing female external genitalia and undescended testes at birth. Androgen has absolutely no effect on the cells of these individuals. Since the testes produce some estrogen anyway, they grow up as phenotypic females indistinguishable from normal females. They have female gender identities because there is no receptor protein for testosterone in the brain to tell it to be other than female. Male infertility has been explained as partial androgen insensitivity of this type -- possibly incomplete penetrance of the genes responsible for synthesis of androgen receptor proteins. An important enzyme deficiency in 5-à reductase has led to insight into gender development in recent years. This enzyme catalyzes the conversion of testosterone to dihydrotestosterone. The latter hormone activates development of male external genitalia. Testosterone differentiates male internal genitalia (Wolffian structures such as the Vas, prostate, seminal vesicles) and adult secondary sex characteristics. Boys with 5-à reductase deficiency have normal female external genitalia at birth and are assigned and raised as girls. The index case is 38 children in the Dominican Republic who made history by spontaneously "changing sex." The surprise arrived with puberty in these children when Nature played catch-up. Their undescended testes began to flood their blood with testosterone causing the testes to descend, labia to fuse as scrotum and clitoris to enlarge into a penis. Thereby Nature completed the job it left unfinished. These boys adapted easily to the "sex-change" and became well-adjusted men with families. Based on follow-up study, these boys, thought to be girls at birth and raised as such, differentiated masculine gender identities well before puberty. How could this happen? In all vertebrates, the presence of estradiol, a female sex hormone, in brain tissues causes a marked enlargement of sexually dimorphic nuclei in the brain. The hormone converts the brain from its female resting state to that of the male. The aromatase enzyme found inside brain cells converts testosterone arriving from the blood into the female sex hormone estradiol catalyzing the path to male sexual behavior. In the presence of testosterone, an aromatase enzyme deficiency causes the brain to behave as a female. In the Dominican Republic case cited, while the 5-à reductase deficiency produced the lack of male external genitalia, the presence of the aromatase enzyme in the brain did give the children their male gender identities. This experimental question has not been answered yet: if conversely 5-à reductase and all the other proteins previously described are present except aromatase then might not the fetus develop normal male genitalia but have the brain of the opposite sex? This may explain male-to-female transsexualism and the 3:1 prevalence over female-to-male transsexuals. Female-to-male transsexuals probably occur by a different mechanism with a final common path; many have histories of virilizing polycystic ovarian disease and progestin/androgen hormone exposure in utero.

Thus errors in fetal hormones produce errors in genital dimorphism which can be misread by the doctor at birth. A girl may be read as a boy and a boy may be read as a girl. The odds of this happening are roughly 1: 2000 births -- fairly common. This innocent guessing affects how society will influence the child from that point on. The infant's perceived or assigned sex from birth will constitute the person in the eyes of society. For example, pink or blue clothing, choice of name, pronouns used, legal status, social conventions and a myriad of other distinctions relentlessly remind and reinforce in the child's mind that he is a boy or she is a girl. These pervasive and barely conscious cultural forces mutually reinforce the biologic forces in normal children.

What happens if the child's gender identity is contrary to the sex of rearing? There is an anecdote a colleague told me about a boy who grew up telling his parents he felt like a girl. The parents thought he was crazy and sent him to a psychiatrist who for years tried to cure the child of his gender identity conflict. When the boy entered puberty, one day he came screaming to his parents with blood all over his underpants. The parents took him to the emergency room where a doctor examined the child and announced that their boy had just had his first menses: she was intersexed but nobody ever thought to listen to her. All evidence so far points to the fact that the fundamental direction toward masculine or feminine behavior is laid down before birth. It is true however that, like language acquisition, the prenatal thrust towards gender identity is a state of functional preparedness that will be unable to mature unless it finds and is found by the social environment. To refute this prenatal thesis, the only case that social learning theorists can point to is the one in which a male twin had his penis ablated during electrocautery while being circumcised. It was decided to reassign the boy surgically and raise him as his brother's sister. His brother was brought up normally. This girl in adolescence was given estrogens to feminize her as in normal puberty. Long term follow-up by Diamond clearly indicates the girl is having severe gender identity conflict adjusting as a girl and recent information indicates she has already been reassigned surgically as a male. In the transsexual, the individual's inner sense of who they are as males or females is constantly in conflict with the contradictory messages given them based on the superficial regard for the body habitus in which these children mature. The tension or gender dysphoria produced by these contradictory messages creates many psychological adjustment problems, needless suffering, and wasted lives.

Our physical self is the way we visualize our bodies, and sexuality is an important component of this. It is the most concrete expression of gender. Body image is co-determined by genital and brain dimorphism in our psychosexual decision tree. With the genitals in agreement with the brain's gender, the person's genitals appear to determine what the person's body image will be. However, this is only an apparent distinction. When the genitals do not conform to the brain's gender, the primacy of the brain in forming body image comes to the fore. For example, some genetic females with adreno-genital syndrome who had been subjected to fetal androgen, discussed earlier, were discovered at birth and surgically corrected as girls. They looked and were reared as girls but still behaved as tom-boys -- more assertive, functional in dress, athletic, interested in boys games rather than doll-play, achievement-oriented rather than romance-oriented. The boys with 5-à reductase deficiency syndrome revealed the opposite picture -- they were raised completely as girls but sensed themselves as males and became masculine. With transsexuals, body-image is opposed to genital sex because the brain has differentiated somehow as female in male-to-females and as male in female-to-males. Why this is, brings us to a discussion of brain dimorphism, the next stop on the decision tree.

In animal ethology, the work of Lorenz, Tinbergen and others have discovered critical periods in learning behavior. With Greylag geese, shortly after hatching, the goslings will follow their mother. If the gosling is taken into human care immediately, it will follow the initial object presented to it, rather than its own species, whether the object is human or wooden. This phenomenon is called imprinting.

Evidence from matched control studies of gender reassignment in infants who had ambiguous genitalia indicates that the destiny of gender in early childhood is locked at a critical period similar to imprinting in lower animals; this period is partially determined by thyroid hormone levels. The window of opportunity closes between 18 and 36 months; the same period in which language acquisition occurs. Both windows are probably effects of myelination, dendritification, and vascularization of the central nervous system completed at about 18 months. In children brought up contrary to their biologic sex due to the presence of ambiguous genitalia at birth, the further away from this critical period, the more difficult is the attempt to reassign gender. Furthermore, in lower animals it has been shown that a critical level of testosterone will produce imprinting on a neuro-physiological level resulting in cross-gender behavior. For example, barbiturates increase the breakdown of testosterone in the liver of the fetal male animal. When developed without testosterone, the male will exhibit lordosis and other female sexual behavior. A testosterone pellet placed surgically in the fetal ewe causes it to grow up behaving as a ram with mounting behavior towards other ewes. Similar trans-sexing phenomena have been discovered in bird-song, fish, frogs and other vertebrate species, even as a natural phenomenon in the wild. The target sites for this cross-gender behavior have been mapped using radioactive hormones in the hypothalamus.

Gorski at UCLA, Dorner in East Germany, and others have demonstrated that male and female brains are anatomically different. The medial preoptic area, ventromedial nucleus, suprachiasmatic nucleus, anteroventral periventricular area, tubero-hypothalamus, amygdaloid nucleus, stria terminalis, corpus callosum, limbic cortex and the lumbar spinal cord differ in size between the male and female in virtually all mammalian species including humans. The amygdala, part of the limbic system, is involved in male aggression in response to testosterone. The medial preoptic area is five times bigger in males than females. Conversely, the ventromedial nucleus is larger in females than males. Testosterone actually increases the size of the preoptic area in female rats and castration of males causes regression of this structure. Testosterone enlarges the lumbar spinal cord so that it can control penile erection in the male.

Changes in size of these sexually dimorphic structures correlate with changes in sexual behavior. Grafting of female ventromedian tissue into the corresponding male's site results in female behavior in the male rat. Similarly, grafting of the male preoptic area onto a corresponding female's site causes the emergence of male behavior. In females, exogenous testosterone stimulates the preoptic area to suppress the growth of the normally enlarged ventromedial and suprachiasmatic nuclei. The stimulus in turn eliminates the pulsatile Gonadotropin Releasing Hormone (GnRH) necessary for cyclic estrous, and establishes male tonic GnRH. Further, the suprachiasmatic nucleus is implicated in female sexual behavior by stimulating the pituitary's pulsatile secretion of Luteinizing Hormone. Lesions in this nucleus cause tonic secretion of LH and lack of ovulation. A congenital absence of GnRH in Prader-Willi syndrome is characterized by mental retardation, obesity and hypogonadism. In the hypogonadic state, sex hormones are poorly secreted. Lack of male sex hormone causes the suprachiasmatic nucleus to enlarge severely during fetal sexual maturity. Study of post-mortem transsexual brains reveals an extremely large suprachiasmatic nucleus (twice the age-matched controls) just like Prader-Willi; this lends support that the male transsexual's brain may be formed in the absence of male sex hormones during development and is structurally like the larger suprachiasmatic nucleus of the normal female brain.

The Dorner hypothesis proposed that transsexualism is the result of this imprinting in utero. Contrary variation in the testosterone-estrogen ratio causes contrary differentiation of the hypothalamus and related structures in the brain. This results in gender identity and later body-image opposite to gonadal sex. As the sex hormone ratio influences errors of genital dimorphism, transsexualism appears to be a sex error at the level of brain dimorphism. A transsexual's neurological pathways have been laid down opposite to the vector of gonadal differentiation. Once the neuro-endocrine critical period is closed, the pathways reify and it is impossible to change them. Many professionals have noted that transsexuals are notoriously refractory to psycho-therapy. They pursue their cross-gender drives in snow-ball fashion to the point of sex reassignment with a motivation and determination that is hard to explain as other than a biological imperative.

To summarize so far, transsexualism probably is a sex error of the body at the level of brain dimorphism. It is not a matter of choice. It is probably caused by previous stages of neurosexual differentiation; at the level of fetal hormones, testosterone-estrogen ratio is imbalanced due to a defect in fetal gonadal development at the molecular level. This may be determined by the absence or presence of certain genes in the TDF cascade.

Each gene produces an enzyme responsible for correct genetic transcription of instructions for gonadal, hormonal, and neurosexual pathways. When these are disturbed, a small change at the level of the genes can have devastating consequences at the level of the person in society. Correct understanding of this phenomenon will probably be at the molecular genetic level.

In making the diagnosis of transsexualism, the physician has to exclude several mental disorders that may present this way. Obvious thought disorders such as the schizophrenias must be ruled out as well as organic disorders. (There is an association of transsexualism with temporal lobe epilepsy.) Occasionally, schizoid, borderline personality traits can be ruled out on the basis of history. Transsexual patients are not delusional or body dysmorphic. What the patient invariably means when they say they are of the opposite sex is that they feel like it. They do not believe that they are already the opposite sex. As reported above, medicine is investigating to what extent transsexuals can be truly considered as the opposite sex; it is a useful heuristic. From the transsexual's viewpoint however they are treated in society without regard to this distinction. Transsexualism is an identity disorder that happens to involve gender concomitantly. It has nothing whatever to do with sexual preference or life-style as with homosexuality. Most transsexuals are asexual (analloerotic) but hetero- and homosexual transsexuals can frequently be found just as in the general population. It has nothing to do with transvestic fetishism, sexual masochism, or other paraphilias. Transvestites -- exclusively heterosexual men -- gain sexual arousal from wearing woman's clothes as an adjunct to masturbation or coitus. Cross-dressing in transsexuals is never erotic, rather it serves to ameliorate gender dysphoria. Neither the transvestite nor the homosexual has a gender identity conflict. At times they may appear to have one as a defense against being conscience-ridden (e.g., ego-dystonic homosexuality and self-stigmatized transvestism). Less easily differentiated is the Gender Identity Disorder Non-Transsexual Type (DSM-III-R: GIDAANT). Here the patient does not have any history of denial of his genitals and is comfortable as a transgenderist living quietly in the gender role opposite to his gonadal sex without any desire to reassign sex.

There are further contributors to adult gender identity in the decision tree such as pubertal hormonal levels, pubertal eroticism, and pubertal morphology. However, in transsexuals, because of the primacy of brain organization, these pubertal factors have little affect on the transsexual's cross-gender identification. In fact, transsexuals persist to the point of trying to reverse these pubertal factors. Some, by gaining access to sex steroids illicitly, prevent the pubertal effects on body habitus and others physically deny their developing genitals in the form of binding, "gaffing", auto-castration and asexual behavior. In some cases, denial of assigned sex occurs as early as three years. However, most cannot gain access to hormones and at puberty they grow into bodies which they loathe; they further succumb to loneliness and peer pressure to behave according to the societal expectation of heterosexual norms and sex-stereotypes.

While their minds become more and more alienated from their bodies, a severe cognitive dissonance develops which leads to dysphoria, dysthymia, major depression and suicide. It is reasonable to expect these patients to recount a history of mood disorders. In a society less polarized with regard to sexual diversity, transsexuals would have much less psychopathology (observe the Berdache of indigenous peoples who allow transsexuals a third sex).

Human nature steeped in the shame of original sin has always required a scapegoat. As the ancient ritual recounts, the Jews collected the blood of unclean animals and ritually imbued the blood with the sins of their tribes. They took a goat and pored the blood over it so that it may carry their sins. Then they took the goat out far into the desert and tied it to a stake without food or water and left it to die there by expiating their sins. Today we are little more conscious than this -- we persist in projecting our own shame on others, attacking, hating and even destroying that which we do not understand. Jesus was the apotheosis of the scapegoat -- the spring lamb. Transsexuals and other sexual minorities are made to wear the shame of our society's insecurity about gender identity and sexual preference; they are sent out into emotional deserts to die of alienation and loneliness to expiate society's loathing of itself. For, in truth, no one is without stigma -- "let those who are without blame cast the first stone." Some people's stigma are hidden or not obvious and so these people become the normals within society. Those whose stigma is clear for all to see are the ones who are set apart. The normals stigmatize them so as not to call attention to their own hidden stigmata. Normals fear being discovered by others and being set apart themselves so they require scapegoats. And so fear, ignorance and hatred persist. Transsexuals are the new dispossessed, the invisible. While medical science continues to seek answers to the problems at hand, what do we -- as physicians -- do? Will we game play? Or will we, in faith, struggle together in the reality of the present world, actively engaged in healing physical and emotional anguish ... bringing wholeness. How then can we -- as healers -- continue to turn our backs? Our Hippocratic Oath enjoin us to be compassionate, to strive for justice and to respect the dignity of every human being. History has also shown us that it is human nature to hate, attack and destroy that which we do not understand. Are we not, therefore, compelled to stand between the dehumanizing forces within society and people, to strive for compassion born of understanding, coupled with the knowledge of what we can accomplish.

(The author wishes to thank the J2CP Information Services and its director Sr. Mary Elizabeth, SSE, for the opening scenario.)

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