The Riddle of Gender

by Deborah Rudacille

  As a result of this focused research program over the past decade, scientific understanding of the mechanisms by which estrogenic chemicals exert their effects has grown dramatically. Studies have shown that environmental estrogens may alter production of normal hormones, disrupt the transport of hormones, affect the metabolism of hormones, interfere with hormone signaling at the receptor level, or modify hormone-regulated gene transcription. Adverse effects include reproductive failure, developmental effects, immune system dysfunction, and cognitive and behavioral pathologies of various types. The types of chemicals that may produce these effects include pesticides, organocholorines, plasticizers, heavy metals, and plant estrogens. In Our Stolen Future, Theo Colborn and her coauthors list eighty-five chemicals known to be estrogen disrupters, many of them ubiquitious in the environment. We are living, scientists now say, “in a sea of estrogens.” Does this have any relevance to the issues discussed earlier in this book? Some people say that it does.

  “Is it a coincidence that since the introduction of the chlorinated pesticides around 1935—1940 the rate of transsexualism has been climbing steadily? The first generation born after the introduction of pesticides was also the first generation to have significant numbers of transsexuals. The condition is virtually absent from the U.S. historical record prior to 1952, when Christine Jorgensen made headlines,” Christine Johnson writes in a brief posted on the TransAdvocate website. “Every generation since then has had higher and higher rates. Clearly researchers knew that sexual developmental changes were observed with DDT in animals as early as 1950, yet this information was ignored, deliberately or not. Fifty years later, large numbers and quantities of EDCs are being distributed around the globe without adequate consideration of the consequences.”

  I met with Christine Johnson in May 2002, in Philadelphia. As I soon discovered, Johnson is passionate about this subject. She speaks eloquently about the damage that she believes has been inflicted on transsexual people who have been told for years that their gender variance is a mental health problem, when the scientific literature shows quite clearly in animals that in utero exposure to exogenous hormones and hormone mimics affects the brain and behavior. “When I saw the words ‘endocrine disrupter’ a lightbulb went off in my head. Because for years and years I had been reading what all these shrinks have been telling us—that in theory transsexuality could be due to hormonal problems, but they don’t measure any natural hormonal variations [in adults]. That’s been commonly reported throughout the literature. Diamond showed in ‘57 in guinea pigs that when exposed to opposite sex hormones [they] would develop in the opposite gendered way,” she says, describing her realization that rising rates of transsexualism might be linked to EDCs. “So I knew that hormonally active chemicals, anything that modifies the function or behavior of the endocrine system, is going to have this kind of effect, whether it’s a natural hormone or a hormone mimic—the body can’t tell. As far as the body is concerned, it’s all information.”

  In 2002, Johnson submitted the results of her research on endocrine-disrupting chemicals and transsexualism to the peer-reviewed International Journal of Transgenderism, published online. The journal rejected it in a somewhat cavalier fashion, Johnson says. She believes that the psychiatric profession in general and the HBIGDA “establishment” in particular don’t want to promote discussion of the endocrine-disruption hypothesis because it poses a direct challenge to their power and authority as gatekeepers of services for trans people. “They are arguing from their paradigm against our paradigm, but the paradigm is what is in question,” she says. “So they can’t use their paradigm to argue against the endocrine-disruption paradigm. Their attitude is ‘we’re not going to talk about this.’ That is in violation of the scientific tradition.” In her view, the scientific community and the trans community are so blinded by traditional ways of viewing gender variance that they are failing to see the obvious. “If you look at the evidence that Benjamin presented, he acknowledged that 45 percent of his patients had hypogonadism. That’s another thing they don’t explain.”

  Scott Kerlin recently uncovered a provocative lead suggesting that Benjamin was aware of a possible correlation between prenatal DES exposure and transsexuality. A new member of the DES Trans online discussion list, completing her transition from male to female in 2004, told Kerlin that in 1971 she and her mother had actually seen Benjamin and discussed the mother’s belief that DES was implicated in her child’s gender dysphoria. According to the list member, Benjamin had indicated that he too suspected that prenatal DES exposure was a likely culprit.

  Kerlin then searched Benjamin’s publications, and although he was unable to find a direct reference to DES, he did find this intriguing statement in a 1971 American Journal of Psychotherapy article titled “Should Surgery Be Performed on Transsexuals?”: “A discussion of the etiology of this syndrome is not my subject here, but I do not want to ignore it entirely. Let me state, therefore, that my clinical impressions suggest to me more and more a prenatal neuroendocrine anomaly as perhaps the foremost causative factor for a majority of cases.”

  Two years later, in an article published in the American Journal of Nursing, Benjamin stated more firmly that “in many respects, transsex-ualism in the anatomic male might be regarded as an incomplete expression of testicular feminization syndrome (AIS, CAIS or PAIS) with the defect affecting only sex-specific areas of the hypothalamus…. Recent research indicates that in the genetic male the hypothalamus is masculinized by fetal androgen at a specific period somewhat after the masculinization of the genitourinary tract. The genetic female, with her XX chromosome complement, lacks fetal androgen and therefore develops along typically female patterns. The important principle here is that effective androgen is necessary for masculinization. Without androgen, masculinization will not occur. Thus, the prenatal hormonal environment is critically important for all future development.”

  Over the past three years, as I’ve researched this book, I’ve been struck by the fact that most of my sources trace their feelings of gender dysphoria to their earliest childhood. Sometimes their intuition of the disjunction between their bodies and their sense of themselves as boys or girls is their very first memory. They can recount exactly where they were and what they were doing when they first admitted to themselves that they were not the children that others assumed them to be—usually before the age of five. Many transgendered people believe that these feelings (which in the case of transsexuals are so overwhelming that those who experience them eventually seek surgical and hormonal sex reassignment) are the result of “hormone surges” in prenatal life that somehow alter the link between their physical sex and their gender identity. More than one person I interviewed compared transsexuality to a cleft palate—characterizing both as “birth defects” that require surgical intervention. A few mentioned the increased incidence of reproductive deformities and “transsexualism” (feminized males, masculinized females) in wildlife and wondered if there might not be some connection to their own situation. But few are willing to state as bluntly as Christine Johnson that their lives and gender identities may have been turned inside out by an environmental toxin.

  In March 2002, I asked the subscribers of the National Trans Advocacy Coalition’s online discussion list what they thought of the environmental endocrine hypothesis as a possible explanation for their gender variance. I received some interesting replies. Rozlyn Manley, a Vietnam veteran who worked as a claims adjuster prior to her transition, posted the following response.My former career was in the insurance industry, where I handled high-exposure claims on behalf of the international insurance market. Among those claims were pollution, environmental, and product liability claims. In addition to managing the defense and negotiation of existing litigation, I was also in constant contact with the Fortune 500 companies regarding potential litigation they were concerned with. This is because they self-insure the first five or ten million of coverage and have a duty to keep the excess insurers fu
lly informed of what was in the pipeline. Before I left, I began hearing from the pharmaceutical and petro-chemical companies about “gender bender” claims. Each have waste by-products that they dispose of in settling ponds, mostly in Puerto Rico, Germany and our Gulf Coast. They were becoming aware of animals displaying homosexual behavior and transsexual changes. For example, female birds in the Gulf Coast were nesting with each other and non-mating with the male birds. Marine and land animals were displaying distinct transsexual changes in their external genitalia and internal organs. We, of course, are all aware that human male sperm count has been rapidly declining during the last few decades. There are claims being filed against these companies, and they are concerned. At least when I left, they had a working hypothesis but no specific proof of what was going on. None of this says that our trans condition is solely the result of someone’s negligence, but it may indicate that something occured that may have trigged our propensity.Another example might be my hometown of Huntingdon Beach, California. When I graduated in 1964, the population was about 10,000 and there were 2,000 students in the high school which served the surrounding counties. I can now identify 18 post-op transsexuals that graduated between 1964 and 1975. Clearly, this rate is far beyond the generally expected incidence of transsexuality. Is this simply an example of the rule of large numbers, or could it be that Huntingdon Beach had its own aquifer, and it is severely polluted from oil drilling and is no longer used for drinking? I won’t begin to state that one led to the other. I simply do not know. I do believe, however, that by sharing these occasional tidbits, some biochemist or geneticist just might have their “idea bell” ring. What follows will be for the next generation to benefit from.

  Vanessa Edwards Foster, the chair of the NTAC Board, responded:Wonderful! For years, I lived just Vi mile from a lot of those settling ponds and 1 block from petroleum gathering tanks next to the ship channel in Corpus. My dad used to bring the family when he’d go fishing … along the ship channel! And a lot of those places around the Tule Basin, and back in the Tuloso area, and in the back side of Nue-ces Bay all had settling pools of whatever variety (besides eight oil refineries, we also had a PPG chemical plant as well). While my dad fished, we had to entertain ourselves—usually playing next to or around those pools, and on a rare occasion, stepping or falling partially in them. Other than stinking a bit, and being a little messy, I really don’t think they did anything though. It never affected my brother…. Truthfully, though, I really don’t give a crap about litigation or suing anyone over it. We’re resourceful and resilient, and don’t look for handouts or anything. If the worst health issue I ever have from living around this chemical soup all my life (San Diego, L.A., Corpus, and now chemical and smog-laden Houston) is gender dysphoria, then I came out of it all right, from a health aspect. My only request would be that general society—from political to religious to corporate—would just simply understand what happened and just allow us to live, to work and to enjoy our lives to the fullest without having to be further penalized (by systemic discrimination, ostraciza-tion, ridicule, violence and persecution) for something that may have had no bearing on any free will on our part, save for choosing not to repress what innately compels us to be ourselves.

  Julie Maverick, the university professor who chairs the National Transgender Advocacy Coalition’s research committee, told me that there are valid scientific hypotheses that link transsexual behavior and physiology in many animals to endocrine-disrupting chemicals and hormones in the environment. “These include fish, frogs, and alligators,” says Maverick. “Endocrine-disrupting chemicals have also been linked to malformation and malfunction of sexual organs in these animals and there is some evidence, though not much and mostly anecdotal, to suggest a higher incidence of transsexualism in humans due to elevated exposure to various organic chemicals, particularly DES.” However, Maverick said that at present it would be rash to assert a causal relationship between these chemicals and transsexuality, cross-dressing, or any other form of anomalous gender identity or expression. “To claim any causal link is decidedly premature. Rather, it [existing data] should foster research in this area.”

  The science of endocrine disruption is still in its infancy, so it is not surprising that no one has investigated possible links between human gender variance and exposure to EDCs. In some ways, “the concept is ahead of the science,” says my friend Jim Yager, senior associate dean for academic affairs at the Bloomberg School of Public Health at Johns Hopkins University. Yager, a toxicologist, has been studying the relationship between estrogens and breast cancer for more than two decades, and even in that well-studied endeavor there have been no definitive data establishing causality between exposure to EDCs and rising rates of breast cancer. Yager says that one of the challenges researchers have encountered in EDC research is that “we’re seeing [biological] effects at concentrations that we couldn’t even detect ten years ago.” Much of the laboratory research thus far has been carried out in vitro, and while it is clear that there are measurable biological effects on cells exposed to various EDCs, and on gene expression within those cells, “you can see an effect, but is it a biologically meaningful effect?”

  Then, too, “estrogens are considered reversible cellular signals,” as John McLachlan writes in a 2002 review titled “Environmental Signaling and Endocrine Disruption,” meaning that when the estrogen is withdrawn, the effects of the estrogen fade—as any trans person who has gone on and off hormones could testify. “On the other hand, when estrogens are given to newborn mice, at least one gene under estrogen control is expressed persistently, even in the absence of estrogen,” McLachlan notes in the paper. “This leads to the question, how does a reversible signal became irreversible in the absence of a detectable gene mutation?” McLachlan says that “the actual mechanism underlying the molecular feminization of genes by estrogen still has not been elucidated.” Nonetheless, studies have shown that estrogen can “imprint” genes in such a way that “when a gene programmed to respond to estradiol at puberty is misprogrammed or reimprinted by developmental exposure to a hormonally active chemical, it will respond abnormally to the secondary cue, resulting in a functional cellular abnormality.” This process has been elucidated most clearly in chicken and frogs. But it does lead one to wonder what might be the effects on human fetuses whose gene expression may have been chemically altered by exposure to estrogens in the womb and who are then re-exposed again and again to estrogenic chemicals in the environment?

  It’s a long way from cells in a dish to a complex human trait such as gender identity, but the path from cell to animal to human in biomed-ical research is a well-traveled one. The neurological basis of psychiatric conditions once considered the result of inadequate parenting (schizophrenia) or insufficient willpower (alcoholism and other addictions) is now recognized, even if the mechanisms that produce the condition remain incompletely understood. McLachlan points to one interesting example of a behavioral disorder gradually revealed to be a signaling problem in “Environmental Signaling and Endocrine Disruption.” The condition, once called “St. Anthony’s fire,” is today called ergotism and is recognized as a consequence of “the human body’s misreading of a fungal signal.” In the Middle Ages, individuals exhibiting the bizarre symptoms of St. Anthony’s fire were thought to be possessed by the devil. “This level of knowledge was consistent with the unpleasant consequences usually visited on such individuals,” McLachlan notes dryly. In later centuries, they were incarcerated in mental institutions. Eventually, the disorder was shown to result from eating moldy rye bread, and an understanding of the biochemical etiology of the condition led to a public health solution—“prevent mold from developing in rye flour or, if it does, don’t make bread from it.”

  No one believes that an understanding of the manner in which gender identity develops will be so simple—nor do many believe that gender variance itself is a problem requiring a solution. Milton Diamond, for example, objects to the characterization of the d
ifferent forms of gender variance as “anomalies” and prefers to term them simple variations. Still, science liberated the victims of St. Anthony’s fire from the stigma of mental illness, just as I am certain it will eventually reveal the actual biological mechanisms that produce the wide range of anatomical and neurological intersex conditions. Many of the anatomical conditions, of course, have already been elucidated. The “natural” genetic and/or biochemical mechanisms that produce Klinefelter’s syndrome, CAH, Turner’s syndrome, AIS, and various enzyme deficiencies that produce anomalously sexed bodies were identified decades ago. Yet there is still resistance in some quarters to accepting that many individuals born with these conditions are fine as they are—that they don’t need to be “fixed” to conform to some rigid aesthetic or medical concept of what “normal” genitals or “normal” human beings look like.

  “More people are coming around,” says Milton Diamond. “They have to. The data is accumulating. I gave a talk at the American Academy of Pediatrics in ‘98 and I really thought they would throw stones at me. I was telling them that, first, I thought that what they were doing [intersex surgery on infants and children] was wrong; number two, that they have to do the research to discover the effects of what they were doing; and number three, they have to be honest. Well, they didn’t want to hear any of that. Now I have to give them credit. They did listen. In 2000, they changed the standard procedure. I gave a similar talk in England in 2000 and in 2001 they changed their procedure.” The current guidelines, he points out, “basically say, ‘think twice’” before correcting anomalous genitals. Diamond and legions of intersex activists would like physicians to wait permanently—or at least until the child expresses a gender preference. In many cases, the children might opt to stay exactly as they are.