Johnson also rejected the notion that the growing visibility of trans-gender and transsexual people was due to greater social tolerance of gender diversity. “Ts find increased acceptance inside the T community, and to a lesser extent within the larger GLBT community, but to extend that acceptance to the general population is a bit disingenuous. Where is the evidence that society is more accepting of Ts? It seems to be that most people claim increased social benevolence, but in general are unable to identify in what tangible ways this benevolence is manifested. We have not achieved many basic civil rights, and if you ask the average (non-TG) person to name a single TG, they would be hard pressed to name anyone, because we are, in essence, the invisible ones. Also to be noted is the fact that Ts are excluded in most cases for insurance reimbursement—this is decidedly not benevolent. So while I see relatively large increases in the number of teen Ts, I see no significant increase in benevolence, at least in the U.S., towards transpeople.”
Regarding the environmental endocrine hypothesis itself and its relationship to transsexuality, Johnson points out that the scientific literature “makes it abundantly clear that it is possible to feminize males and masculinize females by application of exogenous hormones. This is reproduced reliably in the lab on animals, so there should be little argument over the potential of hormonal compounds to alter the ‘normal’ path of development. For the last 40 years, gender researchers have been saying that hormonal variations can indeed cause altered development of the anatomy of the genitals and the brain. And so now we find endocrine disrupters all over the place, and yet we still take the incredibly naive view that somehow we develop independently from our hormonal environment? I find this view totally inconsistent with my understanding of how natural systems work.”
We agreed to meet in the spring, to discuss these issues in more detail. In the meantime, I learned that colleagues at the Johns Hopkins
Bloomberg School of Public Health were holding a workshop on endocrine disrupters in February 2002. The workshop would bring together scientists from industry, academia, and regulatory agencies from the United States and abroad to discuss progress in identifying and testing hormonally active substances, and ways to implement those goals that would not require a massive animal testing program. I was particularly interested to see that one of the speakers at the meeting was Dr. John McLachlan, the Tulane University researcher considered one of the primary architects of the environmental estrogen hypothesis. McLachlan has been studying the effects of endocrine-disrupting chemicals for over thirty years. I approached him after his presentation at the February 2002 meeting and asked him, with some trepidation, if it was possible for endocrine-disrupting chemicals to affect human gender identity and sexual orientation, and to increase the prevalence of intersex conditions.
“Absolutely,” he replied, pointing out an already documented increase in the incidence of hypospadias (incompletely differentiated penis) in baby boys. Having studied the effects of endocrine-disrupting chemicals on one-celled organisms, fish, reptiles, and mammals for more than two decades, McLachlan said that he can predict with some certainty what effects endocrine-disrupting chemicals will produce when administered in sufficient doses to animals at critical stages in fetal development. But he also said that no one has yet linked these effects, which have been confirmed in laboratory animals and wildlife, to the development of gender identity or sexual orientation in humans. “You should have a look at the DES literature,” he said. Soon after the meeting, I did so. What I discovered astonished me.
DES was first synthesized in 1938, in the laboratory of Sir Charles Dodds, a professor of biochemistry at the Middlesex Hospital Medical School at the University of London. Researchers working independently in England and Germany had succeeded in isolating natural estrogens for the first time in 1929, but natural estrogens were very expensive and difficult to produce. Further, the supply of natural estrogens could not meet the demand; Dodds’s discovery of a synthetic estrogen that could be easily and cheaply produced was hailed as a great boon. Dodds and his colleagues tested the effects of this new synthetic estrogen on female rats that had first undergone ovariectomy (removal of the ovaries). The ovariectomized rats responded to DES as though it were an endogenous estrogen produced by their own bodies—even though DES, manufactured from coal tar products, is not at all chemically similar in structure to natural estrogens. Indeed, DES appeared to be even more potent than natural estrogen, mimicking its biological effects when ingested in much smaller doses.
Within a year, DES was being manufactured and marketed in mass quantities by drug companies in Europe and North America. Never patented, the drug was sold under more than 400 different brand names by 257 pharmaceutical companies in the United States alone. DES was used as “hormone replacement therapy” for women, and was approved by the U.S. Food and Drug Administration for that purpose (among others) in 1941. DES was also initially prescribed to suppress lactation in the growing number of women who did not wish to breast-feed their infants, to treat amenorrhea (failure to menstruate) and vaginitis, and (surreptitiously) to prevent miscarriage, though it was not approved for the last purpose in the United States until 1947.
The use of DES to prevent miscarriage was strongly advocated by a husband-and-wife team of researchers from the Harvard Medical Schooclass="underline" George Smith, an obstetrician-gynecologist, and Olive Wat-kins Smith, a biochemist. In 1945, Smith and Smith asked 119 obstetricians in the United States and Europe to participate in a clinical trial on the use of DES in high-risk pregnancies. Seven published papers subsequently reported that DES not only reduced miscarriage but also produced bigger babies in high-risk pregnancies. It was later noted that three of the seven studies that reported the efficacy of DES to prevent miscarriage had used no controls at all, and none of the control participants was treated with the experimental cohort or by the same physician. A larger, controlled study at the University of Chicago in 1953 showed that DES had no beneficial effect whatsoever on the prevention of miscarriage; this finding was reinforced by six other controlled studies done in the fifties. Nonetheless, more than three million pregnant women in the United States alone were prescribed DES between 1941 and 1971. Many more mothers and fetuses were exposed to the drug in pregnancy vitamins in which DES was the active ingredient. Ads that appeared in medical journals and women’s magazines promised “a healthy pregnancy” through the use of DES. “DES became a routine part of the quality care that private practitioners gave their predominantly middle-class patients, including their own wives,” write Drs. Roberta J. Apfel and Susan M. Fisher in their 1984 history of DES, To Do No Harm: DES and the Dilemmas of Modern Medicine. “DES was considered the best possible pregnancy enhancer and it was even included in vitamin tablets for pregnant mothers.”
Beginning in the early forties, DES was also used in commercial agriculture, added to the feed given to livestock and chickens in pellets—a practice given added impetus when, in 1947, researchers at the Purdue University Agricultural Station discovered that DES was a potent growth stimulant in cattle. In 1959, high levels of DES in meat were discovered to produce “disturbing symptoms” in agricultural workers and consumers, including sterility, impotence, and gyneco-mastia (breast growth) in men. As a result, the FDA banned the use of DES pellets in chicken and lamb feed in 1959. However, the use of DES in cattle feed was not prohibited by the USDA until 1979, after nearly a decade of wrangling between cattle breeders and regulatory agencies.