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The Riddle of Gender - Deborah Rudacille [141]

By Root 2011 0
cancer in men by suppressing the production of testosterone, which stimulates tumor growth in the prostate. “DES also feminizes these patients,” Apfel and Fisher note. A fact sheet on DES produced by the National Toxicology Program notes transsexualism as one of many effects of DES, and the Dictionary of Organic Compounds, a standard reference book for organic chemists, notes that DES “causes male impotence and transsexual changes particularly in offspring exposed in utero.” Far more potent than natural estrogen, DES was sometimes prescribed to induce feminization in male-to-female transsexuals. This super-potency has ominous implications for those exposed in utero. In recent decades, researchers have learned that “fetal tissues are even more sensitive to DES than to natural estrogens because the fetus has to use other biochemical pathways to deactivate the synthetic substance,” say Drs. Apfel and Fisher in To Do No Harm.

The chemical structure of DES is very different from the chemical structure of natural estrogens, and metabolizing DES thus forces fetal tissue to perform a task for which it is not naturally primed. Even more important, researchers have discovered that “the fetus probably becomes sensitized to all estrogens by DES exposure, a sensitization that may become important later in life.” In other words, DES exposure in utero causes the fetus (whether male or female) to become more than usually responsive to the effects of later estrogen or estrogen-mimicking substances. Prenatal exposure to DES primes an individual to be supersensitive to estrogens, whether endogenous (produced within the body) or exogenous (outside the body) for the remainder of his or her life. This sensitivity has major implications for DES mothers and daughters, who are exposed to their own (endogenous) estrogens throughout most of their lives and who may also be exposed to exogenous estrogens through the use of birth control pills and hormone replacement therapy in menopause.

To understand how DES produces this range of effects requires a brief lesson in embryology and endocrinology. The human embryo, like that of other mammals, has the potential to become either male or female. Each embryo develops two paired sets of germinal ducts—the mullerian duct and the wolffian duct. Without the influence of the Y chromosome and its chemical messengers, the wolffian ducts will begin to regress in the sixth week of pregnancy, and the primitive gonad will differentiate into an estrogen-producing ovary. Under the influence of the Y chromosome (and the androgen receptor gene on the male fetus’s X chromosome), the mullerian ducts will atrophy, and the gonads differentiate into androgen-producing testicles. The sexual differentiation of a fetus is an exquisitely choreographed ballet, and the Balanchine directing this intricate dance is the endocrine system. Testis-determining factor is released on day fifty-six of human gestation. As researcher Lindsey Berkson notes in her book Hormone Deception, “If the timed sequence of hormone signals is disrupted, development of the male reproductive organs can be skewed, resulting in undescended testicles or other problems.”

It is often said that the “default” sex in mammals is female, because even in the absence of ovaries, the fetus will develop a female reproductive anatomy unless exposed to sufficient levels of circulating testosterone. Many women object to this way of phrasing the biological reality that females are the basic model and males the frill. “The term default sex has such a passive ring to it, suggesting that girls just happen, that making them is as easy as unrolling a carpet downhill; you don’t even have to kick it to get it going,” science journalist Natalie Angier writes in Woman: An Intimate Geography. “A number of women in biology have objected to the terminology and the reasoning behind it…. Just because hormones don’t appear to be responsible for female sex determination doesn’t mean that nothing is responsible; other signaling systems exist and participate in fetal growth, though they’re

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