Biology contrasted the traditional toxicological approach based on carcinogenesis and acute toxicity, with the endocrine-disrupter approach, which “relies on a developmental model and delayed dysfunction.” A fetus exposed to an endocrine disrupter might not show any effect at all until puberty— like the first cases of cancer in DES daughters. The delayed effects of DES, DDT, and other estrogenic compounds allowed potential problems to escape detection for many years. Not until the mid-eighties did scientists begin to link the kinds of reproductive anomalies that had been observed for years in wildlife with possible human health effects. In 1990, pharmacist- turned-zoologist Theo Colborn published the results of an extensive literature search on the Great Lakes ecosystem, which revealed signs of reproductive anomalies in eleven of the fourteen species previously identified to be declining in population. Colborn found that though adult animals seemed unharmed by pollutants, “some of their offspring were not surviving, and those that did were afflicted with a variety of abnormalities of reproduction, metabolism, thyroid function, and sexual development.”
Around the same time, a reproductive physiologist named Frederick vom Saal published studies on what he called “the positioning effect,” showing that male mice positioned in the womb between two female fetuses receive extra doses of estrogen, and female fetuses positioned between two males receive extra doses of testosterone just prior to delivery, as the hormone circulates in the amniotic fluid. “The differences in hormone exposure caused by the positioning effect of the mice in the uterus were quite small, yet the behavioral and physiological effects were nonetheless significant,” writes Krimsky in Hormonal Chaos. “Some animals that experienced the positioning effect become more aggressive and territorial—the result of one-time exposures to additional estrogen (or testosterone) that seemed to have made imprints in their brains. These experiments revealed that even minute changes in the hormone exposure of the developing fetus during certain sensitive stages could result in measurable effects.”
Colborn, vom Saal, and other researchers began sharing data, “a unique cross-fertilization of scientific disciplines,” says Krimsky, which soon produced provocative results. Toxicologists were forced to rethink the dose- response paradigm and to consider the possibility that barely detectable doses of estrogenic chemicals could disrupt the functioning of the exquisitely sensitive, self-regulating endocrine system—a system that engages in “cross talk” with every other system in the body, including the nervous system. In July 1991, researchers from a number of different disciplines met at a seminal scientific meeting to discuss “Chemically Induced Alterations in Functional Development: The Wildlife/Human Connection” at the Wingspread Conference Center in Racine, Wisconsin. The consensus statement signed by twenty-one scientists at the meeting laid the groundwork for future research and marked the start of public debate on the subject of environmental estrogens.
This debate was given added impetus by Danish researcher Niels Skakkebaek and British researcher Richard Sharpe, who, working independently, had both identified spiking rates of male reproductive problems. Together, the two wrote a paper, published in the British medical journal The Lancet in 1993, linking fetal exposure to estrogens or estrogen mimics to declining sperm counts, sperm quality, and motility. The threads of the environmental estrogen hypothesis began coming together in the mid-nineties, as scientists in various disciplines who had been working separately began meeting and pooling their data. Funding agencies, too, began taking notice, and as more money became available to study the problem, generating more data, the environmental endocrine hypothesis achieved a greater degree of scientific legitimacy. “Additional research funds to study different components of the environmental endocrine hypothesis soon became available. Scientists in a variety of subfields of molecular and cellular biology, toxicology, and enviromental sciences, taking notice of the new funding opportunities, began to reorient their model systems to compete for a share of the newly available grant money,” writes Krim-sky. “Once it enters America’s network of biomedical and environmental funding streams and is incorporated within program requests for proposals, a scientific hypothesis gains new constituencies.”
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
