Traditionally, scientists address such crises, which often plague new and rap­idly expanding fields, by agreeing to standardize. If only everyone used the same method of measurement, if only everyone quantified their products in the same manner, and if only all could agree on what to call these proliferating substances that had somehow escaped the boundaries of the bodies to which they were supposed to belong—then finally, scientists hoped, they could straighten out what had become a messy situation. In the 1930s, standardiza­tion became central to the agenda of sex hormone experts.

During the first three decades of the twentieth century, scientists had used a bewildering variety of methods to test for the presence of female hormones. Generally speaking, they removed the ovaries from test animals and then in­jected or implanted test substances or tissue parts and looked for the restora­tion of some missing function. But what missing function were they to look for, and how accurately could it be measured? Gynecologists focused on the organ dearest to their hearts—the uterus— measuring the impact of test substances on the increase in uterine weight in test animals following ovariec­tomy. Laboratory scientists, however, used a much wider variety of tests. They measured muscular activity, basal metabolism, blood levels of calcium and sugar, the feather coloration of domestic fowl, and the growth of mammary glands and the vulva.63 Not to be outdone, psychologists used a variety of behaviors to assess the presence of hormonal activity: maternal nest building, sexual vigor and drive, and maternal behavior toward newborn pups.64

The question of how to measure and standardize the presence and strength of the female hormone was not merely academic. Many of the early research reports on measurement and standardization explicitly addressed the ques­tion of pharmaceutical preparations.65 Drug companies, leaping on the op­portunities presented by the advances in hormone research, began hawking preparations made from male or female sex glands. Especially popular was the idea that testicular hormones could slow or even reverse the aging process. One report on the extraction and measurement of testicular hormones at­tacked the use of preparations in humans, writing: ‘‘Thus far there is no indi­cation that this product can be of any value in restoring ‘vigor’ to the aged or neurasthenic. However, if there is an indication for its use and if the dosage in man is comparable to that found in the capon, the daily injection equivalent for a 150 pound man would have to be an amount equivalent to at least 5 pounds of bulls’ testes tissue or 2 gallons of normal male urine.’’66

This initial scientific skepticism had little impact on the hormone market. As late as 1939, companies such as Squibb, Hoffman-LaRoche, Parke-Davis, Ciba, and Bayer were marketing approximately sixty different ovarian prepa­rations of doubtful activity.67 Mindful of the debacle in 1889, in which the scientist Edouard Brown-Sequard (see chapter 6) had insisted that testicular extracts made him feel younger and more vigorous, only to withdraw his claims a few years later, gynecologists wanted to make sure such preparations had genuine therapeutic value.68 So too did the pharmaceutical companies that funded basic research aimed at standardizing hormone preparations.69 Finally, in 1932, an international group of gynecologists and physiologists met under the auspices of the Health Organization of the League of Nations to develop a standard measure and definition of the female sex hormone.

As one of the participants, A. S. Parkes, later noted, ‘‘the proceedings were unexpectedly smooth.’’70 Participants in the First Conference on Stan­dardization of Sex Hormones, held in London, agreed, for instance, that the term ‘‘specific oestrus-producing activity’’ is to be understood as the power of producing, in the adult female animal completely deprived of its ovaries, an accurately recognizable degree of the changes characteristic of normal oes­trus. For the present, the only such change regarded by the Conference as providing a suitable basis for quantitative determination of activity in compar­ison with the standard preparation is the series of changes in the cellular con­tents of the vaginal secretion of the rat or mouse.71 Amusingly, the tradition of using mice in America and rats in Europe led to two standard units: the M. U.(mouse unit) andtheR. U. (rat unit).

Despite this agreement, the standardization conference did not satisfy everyone. By narrowing the definition of the female hormone to its actions in the estrus cycle, conference members had rendered less visible the hormone’s other physiological effects. Dutch scientists, who had played a key role in the processes of identification and hormone purification, criticized what they called the ‘‘unitary school’’ of sex endocrinology.72 A 1938 publication by Korenchevsky and Hall at the Lister Institute of London underscored their point. Estrogens could stunt growth, produce fat depositions, accelerate the degeneration of the thymus gland, and decrease kidney weight, the authors pointed out. These were, then, ‘‘not merely sex hormones, but. . . hormones also possessing manifold important effects on non-sexual organs.’’73 Was it biologically correct to define the female hormone solely in terms of the mam­malian estrus cycle? Didn’t that divert attention from the many nonsexual roles in the body? Indeed, given that ‘‘sex hormones are not sex specific,’’74 could they legitimately continue to call these hormones sex hormones? Did sex hormones really exist?

The establishment of a standard measure and definition of the male sex hormone followed a similar pattern. Again, a wide variety of effects from substances injected after castration presented themselves as potential stan­dards for the male sex hormone. The growth ofthe cockscomb as the standard unit of measure emerged victorious over other contenders—changes in the weight of the prostate, seminal vesicle, and penis to the size of the comb of the fowl, the horns of the stag, the crest of the male salamander, or the pro­duction of mating plumage in certain birds. The Second International Confer­ence on Standardization of Sex Hormones, which took place in London in 193 s, recognized the need for a mammalian assay, but concluded that an ac­ceptable one did not exist. It was therefore ‘‘agreed that the International Standard for the male hormone activity should consist of crystalline andros – terone and the unit of activity was defined as о. 1 mgm [sic]. This weight is approximately the daily dose required to give an easily measurable response in the comb of the capon after 5 days.’’75 As with the female hormone, ‘‘all functions and processes that were unrelated to sexual characteristics and re­production were dropped.’’76

Defining the female hormone in terms of the physiology of the estrus cycle, and the male hormone in terms of a secondary sex characteristic less central to the drama of reproduction, did not necessarily represent what we might call today ‘‘the best science.’’ For both the male and the female hor­mones, more than one potentially accurate, easy-to-use assay contended for the role of standard-bearer. For example, the male Brown Leghorn chicken has black, round-tipped breast feathers, while its saddle feathers are orange, long, and pointed. The female Leghorn has salmon, round-tipped breast feathers and round-tipped, brown saddle feathers. Injecting female hormone into plucked capons produced the growth of new salmon-colored breast or brown saddle feathers. The experiments on this dimorphism ‘‘suggest that the production of brown pigments in the breast feather of the Brown Leghorn capon might be used as an indicator for the female hormone.’’77 The test was easy, did not involve killing any of the test animals, and took only three days. In apparent contrast, the rat estrus assay required great care because of indi­vidual variability—a fact noted at the time it was chosen as the standard measure.78

In the case of the male hormone, a test based on prostate and seminal vesicle growth in castrated rats stood out as an alternative to the comb growth test. Korenchevsky and his colleagues distrusted the comb growth test for a number of reasons. They were especially disturbed that the urine of both pregnant and ‘‘normal’’ women stimulated comb growth to the same degree as did urine from men. ‘‘The specificity of the comb test, therefore, becomes doubtful’’ and should be ‘‘replaced by a test on the sexual and other organs of mammals.’’79 On the other hand, Thomas F. Gallagher and Fred Koch, who developed the comb test, thought the mammalian assays had not proven their mettle. ‘‘We know of no studies,’’ they wrote, ‘‘in which animal variability has been established by means of mammalian tests. Our opinion is that the mammalian tests thus far devised will be found to be either more time­consuming or less accurate or both.’’80

Thus, the choice of a measurement that distanced animal masculinity from reproduction, linked animal femininity directly to the cycle of generation, and made less visible the effects of these hormones on nonreproductive organs in both males and females was not inevitable. Nature did not require that these particular tests become the standard of measurement. Choices for particular measures were probably not made because of the gender views—either con­scious or subconscious—of the main players. That would be far too simplistic an explanation. Being present at the conference may have carried a big advan­tage. Neither Korenchevsky nor Gustavson were present at either of the inter­national standardization conferences, while Doisy and Koch, whose assay sys­tems were chosen, were conference participants. At any rate, the hypothesis that gender ideology caused the particular assay choices would require more in-depth research to confirm or deny. Nevertheless, the choices made, for whatever reasons—rivalries, publication priority, convenience—have pro­foundly influenced our understanding of the biological nature of masculinity and femininity. These decisions shaped the sexing of the sex hormones. The normal processes of science—the drive to standardize, analyze, and accu­rately measure—gave us particular sex hormones at the same time that they proscribed the possible truths about how the body works, about how the body does gender.

From the moment the process of measuring male or female hormones was standardized, a set of molecules of a known chemical composition and struc­ture officially became sex hormones. From that time on, any physiological activity those hormones had were, by definition, sexual, even though the ‘‘male’’ or ‘‘female’’ hormones affected tissues such as bones, nerves, blood, liver, kidneys, and heart (all of which was known at the time). That hormones had such wide-reaching effects didn’t change the association of hormones with sex. Instead, these non-reproductive tissues became sexual by virtue of their interaction with sex hormones. The scientific definitions of standard mouse, rat, and comb units seemed to echo on a molecular level the notion of human makeup that Sigmund Freud had insisted on: sex was at the very center of our beings.