By 1915 three book-length treatises on reproduction, hormones, and the sexes had been published. The Physiology of Reproduction, by Francis H. A. Mar­shall, which appeared in 1910, summarized more than a decade of work and became the founding text of the new field of reproductive biology. Marshall, a university lecturer in agricultural physiology, studied the breeding cycles of farm animals and the effects of ovarian secretions on the health and physiology of reproductive organs such as the uterus. His work on what he sometimes called ‘‘generative physiology’’ (the physiology of reproduction) had far – reaching influence, not only forming the basis of new techniques in animal breeding but also shaping the theory and practice of the field of gynecology. Marshall hoped to draw together previously unrelated accounts of reproduc­tion, and in doing so freely consulted and cited works of ‘‘zoology and anat­omy, obstetrics and gynaecology, physiology and agriculture, anthropology and statistics.’’36

The Physiology of Reproduction examined every known aspect of generation: fertilization, reproductive anatomy, pregnancy, lactation, and, of special in­terest for the history of hormone research, chapters on ‘‘The Testicle and Ovary as Organs of Internal Secretion’’ and ‘‘The Factors Which Determine Sex.’’ In the former section, Marshall massed scientific evidence, which had accumulated rapidly during the first decade of the twentieth-century, showing that ovaries and testes secreted ‘‘stuff’’ that influenced other organs in the body. The idea of sex hormones had, at this moment, taken its baby steps.37

Marshall’s tone is dry and factual, his text filled with detailed descriptions of experiments reporting the effects of gonadal extracts on mammalian devel­opment. He seems entirely uninterested in the social implications of his work, yet he relies heavily on scholarship that was itself explicitly concerned with the connections between biology and gender. For example, without endors­ing their social views, he notes the ‘‘special help’’ provided by Patrick Geddes and J. Arthur Thomson’s 1889 book The Evolution of Sex, a compendium of sex in the animal world that sets up the active sperm and the sluggish egg as exemplars of essential biological truths about sex differences: ‘‘It is generally true that the males are more active, energetic, eager, passionate and variable; the females more passive, conservative, sluggish and stable. The more active males, with a consequently wider range of experience, may have bigger brains and more intelligence; but the females, especially as mothers, have indubita­bly a larger and more habitual share of the altruistic emotions.’’38

Despite the book’s detached tone, Marshall did not entirely ignore the social metaphysics of gender. In discussing ‘‘Factors Which Determine Sex,’’ he considered Weininger’s ideas in some detail, noting the latter’s thoughts on the biology of ‘‘the Sapphist and the virago to the most effeminate male.’’ The general idea that animals—including humans—contain both masculine and feminine traits attracted Marshall. He was less sanguine that the sources of masculinity and femininity lay within individual cells, as Weininger hy­pothesized, suggesting instead that his ‘‘physiological mode of thought re­quires one to associate the characters of an organism with its particular me­tabolism,’’39 including, by implication, hormonal physiology. In a footnote Marshall explicitly linked the world of animal experiments on reproduction and hormones to the human social world studied by sexologists, citing key texts by Krafft-Ebing, Havelock Ellis, August Forel, and Iwan Bloch (see ta­ble 6. i).

If Marshall was coy about the social ramifications of reproductive biology, the biologist Walter Heape—a colleague, to whom he dedicated The Physiology of Reproduction—left no doubt about where he stood when he published his influential Sex Antagonism in 1913. Heape had conducted fundamental research in reproductive biology, studying the estrus cycle in mammals, proving that mating stimulated ovulation in rabbits, and more generally making a place for reproductive science within the field of agriculture.40 By 1913, he was applying his knowledge of the animal world to the human condition.

Heape was disturbed by the social upheavals around him, particularly the dramatic and highly visible suffrage and labor movements. Women activists in the U. S. and Britain took to the streets in the early twentieth-century to pro­test their inferior social, economic, and political status. Women garment workers walked in picket lines across the U. S.,41 and in 1909 abroad coalition of labor, older suffragists, organizations of black women activists,42 and immi­grant housewives pushed for enfranchisement in new and militant combina – tions.43 The movement had broad appeal, as ‘‘women at both ends of the eco­nomic spectrum had new appetite for political organization.’’44 Meanwhile, in England, suffragettes disrupted Parliament by unfurling banners from the galleries, smashing windows, and assaulting guards at 10 Downing Street.45

Heape began his book by attributing ‘‘the condition of unrest, which per­meates society… to three sources. Racial antagonism, Class antagonism, and Sex antagonism.’’46 These antagonisms, he felt, particularly sex antago­nism, were rooted in the social mismanagement of biological difference. Men and women had fundamentally different generative roles. If woman lived ‘‘in accord with her physiological organization,’’47 he insisted, by attending to home and hearth and leaving public affairs to men (whose sexuality naturally rendered them more restless and outward-reaching), she would be able to avoid the evils ofmental derangement, spinsterhood and its implied masculin –


ity, and general ill health.48 Interestingly, Heape acknowledged a certain mea­sure of biological overlap between male and female bodies. But this didn’t lead him to question his assumptions about the fundamental nature of sex difference. Rather, he saw the mix of sex characteristics in each body as a metaphor for how gender difference functioned in the body politic. Sex antag­onism, he wrote, was present within ‘‘every individual of one sex. . . Thus both sexes are represented in every individual of each sex, and while the male qualities are most prominent in the man and the female qualities are most prominent in the woman, they each have qualities of the other sex more or less hidden away within them.’’ Each individual, then, carried a mixture of dominant and subordinate factors that were, ‘‘in reality, though more or less feebly, antagonistic.’’49

It was the British gynecologist William Blair Bell who took the step of linking social sex differences to hormones. He thought that the internal secre­tions of individual organs ought not be considered in isolation, but rather as part of a whole-body system of interactions among the various endocrine or­gans. Whereas scientists had generally thought that ‘‘a woman was a woman because of her ovaries alone,’’ Bell believed that ‘‘femininity itself is dependent on all the internal secretions.” To support his theory, Bell noted the existence of women with testes and individuals with ovaries ‘‘who are not women in the strict sense of the word.’’50 Bell’s views helped dethrone the gonad as the sole determinant of sex, thus changing medical understanding and treatments of intersexuality.51 They also completely recast scientific ideas about the nature and origins of ‘‘normal’’ sexuality.

Bell believed that women’s ovaries and other endocrine glands inclined them toward ‘‘womanly’’ pursuits and sexuality; those women who were ‘‘unwomanly,’’ he believed, were living contrary to the tendencies of their own bodies. Those he considered ‘‘nearest to nature’’ or ‘‘untouched by civili­zation’’ were women ‘‘who enjoy sexual intercourse, and who are, perhaps, somewhat promiscuous. . . yet their maternal instincts are strong.’’ Women ‘‘touched by civilization’’ ranged from those who eschewed sexual desire but wanted maternity, and those who delighted in sexual pleasures but had no maternal instincts (and who were ‘‘not strictly speaking normal’’), to women who wanted neither sex nor motherhood. These latter were ‘‘on the fringe of masculinity. . . usually flat-chested and plain. . . their metabolism is often for the most part masculine in character: indications of this are seen… in the aggressive character of the mind.’’ Bell concluded that ‘‘the normal psy­chology of every woman is dependent on the state of her internal secretions, and that unless driven by force of circumstances—economic and social—she will have no inherent wish to leave her normal sphere of action.’’52 As in so

much of the endocrinological literature from this period, the social concern for women who wanted out of their ‘‘normal sphere of action’’ loomed large.

Heape and Bell spoke about sex antagonism in a social sense, and believed that internal secretions helped create masculine and feminine minds and bod­ies. The Viennese physician and physiologist Eugen Steinach, however, be­lieved the hormones themselves displayed antagonism. As a physician and re­searcher in Prague, and then as Director of the Physiology Division of the Viennese Institute for Experimental Biology, he worked in the growing tradi­tion of animal transplantation studies, transferring testes into female rats and guinea pigs, and ovaries into male rodents (of which more in a moment).53 Steinach’s interventionist style of experimentation embodied the spirit of a new, authoritative analytical approach that was sweeping both Europe and the United States.54 Masculine and feminine bodies and behaviors, he felt, re­sulted from the activities of sex hormones, and his animal experiments pro­vided evidence for the antagonistic nature of the sex hormones. In Steinach’s hands, hormones themselves acquired masculine and feminine characteris­tics. Sex became chemical, and body chemistry became sexed. The drama of sex difference didn’t just stem from internal secretions; it was already being played out in them.55

Steinach believed hormones patrolled the borders dividing male from fe­male and homosexual from heterosexual. His research on rats and guinea pigs and the importation of his results into humans illustrate the complex ways in which gender belief systems become part of scientific knowledge. He began his career as an experimentalist in 1884, working on a variety of problems in physiology—none obviously related to sex. In 1894, however, he published a paper on the comparative anatomy of male sex organs, foreshadowing his experimental turn toward sexual physiology. Ten papers and sixteen years later, he returned to the physiology of sex. His article ‘‘The Development of Complete Functional and Somatic Masculinity in Mammals as a Particular Effect of Internal Secretion of the Testicle’’ marked the beginning of modern experiments on the role of hormones in sexual differentiation.56

Indeed, his entire life’s work was premised on the unexamined idea that there must be a sharp ‘‘natural’’ distinction between maleness and femaleness. Despite the rather gender-bending experiments he performed, the highly an­thropomorphic way he described his results speaks to how deeply his assump­tions about sexual difference shaped his science. First, he concluded that the hormonal products of ovaries and testes, which he called the ‘‘puberty glands,’’ had sex-specific effects. Testes produced substances so powerful that they could cause young female rats and guinea pigs to develop both the physi­cal and psychical characters of males. He reasoned that hormonal effects on the psyche must work through changes in the brain in a process he dubbed the ‘‘erotization of the central nervous system.’’57 Steinach thought that all mammals contained rudimentary structures (Anlage) for both sexes. Puberty gland secretions promoted the development of either ovaries, influencing feminine growth, or testes, for masculine. But this was only part of the story. He also believed that the sex glands actively inhibited the Anlage of the ‘‘oppo­site’’ sex. Thus, ovarian substances in the female not only produced feminine growth but inhibited masculine growth. Meanwhile, testicular secretions in the male inhibited feminine development. Steinach called this process of sex – specific growth inhibition ‘‘sex hormone antagonism.’’

What experimental evidence led Steinach to describe physical growth pro­cesses in such militaristic terms as ‘‘battles of the antagonistic actions of sex hormones’’ and ‘‘sharp antagonisms’’?58 He transplanted ovaries into new­born, castrated male rats and guinea pigs (see table 6.2). Over time, these males developed many feminine characteristics. Their bone and hair structure became typical of the well-groomed female rodent; they developed functional mammary glands, willingly suckled infants, and presented their rumps to male suitors in a suitably feminine manner. Ovaries, it seemed, produced a specifically feminizing substance. But there was more. First, ovarian trans­plants would not ‘‘take’’ in the male body unless the testes were removed. Second, Steinach compared the growth of the penis in males with ovarian transplants to males that had been castrated but received no implants. Re­markably, to him, the penis seemed to shrink under the influence ofthe female puberty gland, until it was smaller than a penis from plain old castrates. Fi­nally, Steinach observed, the feminized, castrated males were even smaller than their unoperated sisters. The ovarian implants had not only prevented them from growing into larger, heavier males; they seemed actually to have inhibited their growth (see figure 6.2).

Although at first Steinach referred to these last processes simply as ‘‘inhibi­tions,’’59 he soon began to describe them with the stronger language of the battle between the sexes. Did his initial data demand such strong language? It would seem not. In a 1912 study on rats, when he first reported the data on penile shrinkage, for example, he found no such effect on the prostate or seminal vesicles—facts that Steinach explained by noting how small these organs already were at the time of ovarian implant. In 1913, however, he de­scribed seminal vesicle shrinkage—above and beyond the level of control cas­trates—in castrated guinea pigs with ovarian transplants.60 Thus, the data on organ development were weak and contradictory. Nor does reciprocal inhibi­tion obviously show why feminized males were smaller than their intact sis­ters; one can imagine other explanations for the fact that gonadal implants

Подпись: 091table 6.2 Steinach’s Experiments






Ovaries transplanted into young, male castrates


• Transplant only ‘‘takes’’ in castrated males

• ovary does not promote growth of penis, prostate, and other secondary characteristics

• ovary causes penis to shrink (R but not GP)

• ovary stimulates mammary growth (GP)

• implanted males smaller and have more ‘‘feminine’’ hair structure (R & GP)

• implanted males show female mating reflexes, maternal responses, and lack of masculine mating or aggressive impulses

• Sex hormone antagonism

• since testis does promote such growth, a ovary and testis secrete different substances

• ovary inhibits male development

• secretes female-specific substance

• ovary inhibits male growth (size, hair quality)

• hormones cause an ‘‘eroticization of the central nervous system”


Testes transplanted into spayed female


• Mammaries and uterus remain undeveloped

• indifferent anlage develop in a masculine direction

• body and hair type more masculine

• implanted females more aggressive, make sexual advances to females in heat

• Testis implants inhibit female characteristics

• testis promotes male development

• testis masculinizes growth patterns

• hormones cause an “eroticization of the central nervous system’’ (p. 723)


Simultaneous trans­plant of ovaries and testes into castrated juvenile males


• Many masculine secondary sex characteristics develop

• functioning mammary glands develop

• Growth-inhibiting influences of ovary cannot assert self in presence of testes

• ovaries can influence the development of female anlage and testes the development of male anlage


R = rats GP = Guinea Pigs a. Steinach 1910. b. Steinach 1912. c. Steinach 1913. Thispaper alsomentions the feminizingeffectsofX ray—inducedovarian

hypertrophy in females later reportedwith Holznecht (1916), which is the nearest Steinach ever comes to examining the effects of ovaries in females. d. Steinach 1913.

Enter Hormones, Center Stage

figure 6.2 : Steinbach’s hormonally transformed guinea pigs.

A (above): Feminized nursing male guinea pig. Top: full profile of the animal; demonstration of its male sex characters. Bottom: feeding a young guinea-pig; feeding two young guinea pigs. B (below): Masculinization series: Left to right: masculinized sister, castrated sister, normal sister, normal brother (Source: Steinach 1940)

Enter Hormones, Center Stage

wouldn’t ‘‘take’’ in the presence of their ‘‘opposite’’ number. For example, perhaps testes stimulated the activity of some other gland, thus producing an environment unfavorable to ovarian growth (and vice versa).61

Steinach’s language of conflict not only reflected preexisting ideas about the natural relationship between male and female; it also set up an analytical framework that shaped his ongoing research interests and experimental de­signs. What would happen, he wondered, if both gonads were transplanted into a neutered host and ‘‘under equal and indeed equally unfavorable. . . conditions forced to battle it out’’?62 In some cases the ovary and testis blended into a single ‘‘ovo-testis’’ and when Steinach examined these tissues under the microscope he had ‘‘the impression that a battle raged between the two tissues.’’63 When he turned to secondary sex characters, he found that bisexual animals, created via double transplants, looked like super-males: larger and

stronger than their normal brothers. Steinach concluded that the growth – inhibiting influence of the female puberty gland, so evident in earlier experi­ments, could not assert itself with a male gland in place. That did not mean, however, that the testes neutralized the ovaries (this was not a rock-paper – scissors scenario). The bisexual animals had strong and masculine builds, but they also grew ‘‘strong, long, ready-to-suckle teats.’’64 Steinach concluded that in his double transplants, all signs of the cross-gender inhibitory actions of the gonads had disappeared. The testis promoted male development, the ovaries promoted female organs, and ‘‘the inhibiting forces were unable to assert themselves.’’65

His data are compatible with the conclusions, but they do not point toward them indisputably. Philosophers call this underdetermination, and it is a com­mon aspect of scientific fact-making. The organism’s response to particular experimental interventions limits the permissible conclusions, but often not uniquely. Hence, scientists have several plausible interpretations from which to choose. Both the final choice and its reception beyond the boundaries of a single laboratory depend in part on nonexperimental, social factors.

Describing the interaction between ovarian and testicular secretions as antagonism (as opposed to inhibition), for instance, was scientifically plausi­ble. At the same time, however, it also superimposed on the chemical pro­cesses of guinea pig and rat gonads a political story about human sex antago­nism that paralleled contemporary social struggles. Physiological functions became political allegory—which, ironically, made them more rather than less credible, because they seemed so compatible with what people already ‘‘knew’’ about the nature of sex difference.

Or consider the choice to do double transplants.66 Why did he not spend more time detailing the growth effects of male and female secretions in male and female bodies, choosing to learn more about what the hormones did in their ‘‘natural’’ locations? Part of the answer certainly lies in his commitment to the new experimental methods that demanded that normal processes be disrupted in order to learn about underlying events. But beyond that, having accepted the language of hormone antagonism, and working in a milieu in which both female masculinity and male femininity threatened social stabil­ity, the double-transplant experiments seemed both obvious and urgent. They spoke to the politics of the day. That Steinach’s interests were shaped by politi­cal debates is made clearest, perhaps, by his focus on homosexuality.67 In his animal studies, he believed he had found evidence that cross-transplantation of testes or ovaries led to altered sexual behavior. His animal research pro­vided him with a foundation for a detailed theory of human homosexuality. Those with ‘‘periodic attacks of the homosexual drive,’’ he argued, had gonads

that alternated between the production of male and female hormones. In con­trast, ‘‘constant homosexuals’’ developed opposite sexual organs when, at pu­berty, their male-hormone-producing tissue degenerated.68 To confirm his theories, Steinach searched for ‘‘female tissue’’ in the testes of male homosex­uals, and found both testicular atrophy and the presence of cells that he called F-cells, which he believed synthesized the female hormone.

Then he performed the ultimate test of his ideas. In collaboration with the Viennese surgeon R. Lichtenstern, he removed one testicle from each of seven homosexual men, implanting in its place testicles from heterosexuals.69 (The implanted testis had been removed for medical reasons—for example they were unilaterally undescended. This left the heterosexual patient with one working testicle.) At first they euphorically reported success: the appearance of sexual interest in the ‘‘opposite’’ sex. As time went on, however, the failure of the operations became evident, and after 1923 no further operations were done.70 Steinach’s choice of experiments and choice of interpretation were influenced in part by the scientific traditions of the time and in part, of course, by the responses of the organisms under study, but also by the social milieu in which he lived, which defined male and female, homosexual and heterosex­ual, as oppositional categories—definitions that seemed both borne out and in need of scientific bolstering, given the political upheavals of the day.

Still, social milieus do not uniquely determine scientific facts. Indeed, in the United States and England, significant scientific opposition to the idea of sex-hormone antagonism emerged.71 By 1913 British physiologists, repre­senting the emerging field ofendocrinology, and American geneticists seemed to have reached an impasse. The geneticists felt that chromosomes defined or controlled the development of sex. The endocrinologists, believed that hormones defined the man (or the woman). An American embryologist, Frank Rattray Lillie (1870—1947) broke the logjam with his work on freemar – tins, the sterile, masculinized female co-twin of a male calf. In 1914, the manager of Lillie’s private farm sent him a pair of dead twin fetal calves, still enveloped in their fetal membranes.72 One was a normal male, but the other’s body seemed to mix together male and female parts. Intrigued, he continued to study the question, obtaining more material from the Chicago stockyards.73 Fifty-five twin pairs later, Lillie concluded, in a now classic 1917 publication, that the freemartin was a genetic female whose development had been altered by hormones from her twin brother, following the commingling of the circu­latory systems after the fusion of their initially separate placentas.74 He thus demonstrated how the genetic view of sex worked in concert with the hor­monal view. Genes started the sex determination ball rolling, but hormones did the follow-through work.

The naturally occurring freemartin in many ways resembled Steinach’s gonad-implanted animals a fact that Lillie recognized immediately.75 Lillie, though, was reticent about allowing his calves to speak about the nature of male and female hormones. He wondered, for example, why only the female twins were affected. Why didn’t female secretions feminize the male, as they did in Steinach’s rodents? Lillie proposed two possibilities. Perhaps there was ‘‘a certain natural dominance of male over female hormones,’’ or, alterna­tively, the timing of male and female development differed.76 If the testis be­gan to function earlier in development than the ovary, perhaps in these un­usual twins the male gonad secreted a hormone that transformed the potential ovary into a testis before it ever had the chance to make female hormones. Careful anatomical studies supported the timing hypothesis. ‘‘Hence,’’ Lillie concluded, ‘‘there can be no conflict of hormones.’’77 Finally, Lillie felt unable to conclude much about the nature of male hormone activity. Initially, it sup­pressed ovarian development; but did the later appearance of masculine char­acters such as an enlarged phallus or the growth of sperm-transport systems result from mere absence of ovarian tissue or from the positive stimulation offered by male hormones? He remained unsure.78

Such uncertainty prompted Lillie to ‘‘mildly suggest’’ to his protege, Carl R. Moore, that he repeat Steinach’s work.79 Moore agreed, performing recip­rocal transplants—ovaries into castrated juvenile male rats and testes into spayed juvenile females. Immediately, he encountered gender trouble. ‘‘It is unfortunate that the distinguishing somatic characters of the male and female rat are not more sharply marked,’’ he wrote. ‘‘Steinach has placed considerable emphasis upon these weight and body-length relations of his feminized males and masculinized females as being indicative of maleness and femaleness. It is the opinion of this writer, however, that such slight differences. . . are but poor criteria of maleness and femaleness.’’80 After further critical comments, Moore rejected weight and length as satisfactory measures of rat gender. Simi­larly, he found hair structure, skeletal differences, fat deposits, and mammary glands too variable to indicate gender reliably.81

But although Moore rejected Steinach’s account of physical gender mark­ers in rats, he argued that certain behaviors indicated clear links between hormones and sex differences. Feminized male rats (castrated with ovary transplants), he found, wanted to mother. They positioned themselves to allow newborns to suckle (even though they had no teats!) and aggressively defended the pups against intruders. Normal males and masculinized females showed no interest in the babies. Masculinized females did, however, show unusual behaviors of their own—they tried to mate with normal females— mounting and licking themselves between mounts, as would an intact male.


But even with behavioral markers, Moore observed, gender differences were not always obvious. ‘‘Steinachhas described the docility of the normal female rat (does not fight, is easily handled, not so apt to bite or to resist handling, etc.) but here again the variations are too great to be of any practical value. Many females of this colony are decidely [sic] more pugnacious than males. In several cases, these, after repeated handling, would bite, scratch, and resem­ble any other than a meek and mild-tempered female of the colony.’’82

Moore pushed the issue.83 In a series of papers emerging over a decade, he systematically dismantled Steinach’s work (see table 6.3). Steinach had in­sisted that male rats and guinea pigs were much larger than females, and that castrated females grew larger than their normal sisters (see figure 6.2) if they had implanted testes. In contrast, castrated males with ovarian implants seemed actually to shrink, becoming smaller than even their normal sisters. Moore argued differently. He cited already published work showing that merely removing the ovaries caused female rats to grow larger. In his own experiments on rats, a sex difference in size remained even after gonad re­moval, suggesting that gonads had nothing to do with the fact that male rats were larger. His results with guinea pigs increased his skepticism. While early in development the growth rate of male and female differed, one year after birth males and females were the same size, and as time progressed females became the larger sex. Spayed females grew at the same rate as intact ones, and only the male showed an effect from castration—becoming smaller than intact males, spayed females, and intact females. Moore concluded his 1922 article with a direct jab at Steinach:

Striking as may be the influence of the internal secretions of the sex glands on some characters in certain animal forms, it appears difficult and often impossible to discover characters in ordinary laboratory animals that are of sufficient difference and constancy in the two sexes to be capable of analysis by experimental procedure. And many of the characters cited in the literature supposedly offering a demonstration of the power of sexual secretions to effect modifications in the opposite sex fall to the ground if subjected to critical analysis. In the writer’s opinion the character of weight reactions in guinea pigs belong to this group.84

Steinach, meanwhile, stood by his theories. He wrote that Moore mis­understood his work and that his opposition was ‘‘meaningless.’’ In a last, dra­matic experiment, he took advantage of advances in hormone chemistry (dis­cussed in the next chapter), injecting ovarian and placental extracts containing active female hormone into young male rats (rather than using the

Подпись: 166table 6.з Moore’s Transplantation Experiments






Testis graft into spayed female (F); ovary graft into castrated male (M)


• Weight and hair quality very variable

• M’s with ovaries show maternal behavior

• F’s with testes show no maternal behavior

• aggression present in normal M’s and F’s

• F’s with testes try to mate as M’s

• Unreliable markers of sex differences

• ovaries feminize male parental behavior

• testes masculinize female parental behavior

• aggression is a poor marker for sex differences

• testes masculinize female mating behaviors


Compares growth in castrated M’s and spayed F’s over 180 days


• Castrated M’s always weigh more than spayed F’s

• Sex difference in size not related to gonadal secretions


Graft ovaries into M’s with one intact testis and testes into F’s with intact ovaries


• In grafted ovaries, follicles develop normally, but do not ovulate

• in grafted testes, sperm-forming cells degenerate but not the Sertoli cells

• Both results dispute Steinach’s claim that grafts succeed only when host gonad is removed— a cornerstone of his claim for hormone antagonism


Graft ovaries into M’s with one intact testis and testes into F’s with intact ovaries


• In grafted ovaries, follicles develop normally, but do not ovulate

• in grafted testes, sperm-forming cells degenerate but not the Sertoli cells

• male and implanted ovary develops normal penis, prostrate, and psychical characters (becomes a breeding male)

• Disputes Steinach’s inability to graft ovaries in M’s with testis intact

• ignores result; not clear (to AFS) that the testis grafts truly succeeded

• ‘‘presence of a normal testicle does not prevent. . . growth… of an ovary grafted into a male rat’’ (p. 167)

• ‘‘there is no indication of an antagonism between the ovary or testis’’ (p. 169)


TABLE 6.3 (continued)










Enter Hormones, Center Stage
Подпись: І91

less certain organ transplants). The result: an inhibition of the development of testicular growth, as well as the seminal vesicles, prostate, and penis, con­firmed his view that female hormones antagonized male development.85

But in 1932 Moore and his collaborator, Dorothy Price, had repeated the experiment and gone him one better. First, they concluded that ‘‘contrary to Steinach. . . oestrin [the factor extracted from ovaries] is without effect upon the male accessories. Itneither stimulates nor depresses them.’’ Steinach’s dis­missal was merely the appetizer, however, to the main course: a new vision of hormone function. The debate with Steinach over hormone antagonism, they wrote, ‘‘forced us to extend our interpretations to link gonad hormone action with the activity of the hypophysis.’’86 Moore and Price set forth several principles: (1) in their proper location, hormones stimulate the growth of reproductive accessories, but have no effects on organs of the opposite sex; (2 ) pituitary (hypophysis) secretions stimulate the gonads to make their own hormones; but (3) ‘‘gonads have no direct effect on the gonads of either the same, or the opposite, sex;’’ and (4) gonadal hormones from either sex de­press pituitary activity, diminishing the amount of sex-stimulating substance flowing through the organism.87 In short, Moore and Price demoted the go­nads, making them one of several sets of players in a more complex system in which power was decentered. Gonads and pituitaries controlled one another’s activities by a feedback system analogous to that of a thermostat.88

What should we make of this moment in hormone history? Did Moore’s ‘‘good science’’ simply win out over Steinach’s sloppy work?89 Or does this dispute about the chemical sexing of the body reveal a more complex relation­ship between scientific and social knowledge? Certainly Moore relied more broadly on previously published work, provided more data, and seemed pre­pared to rule out what he called ‘‘the personal equation’’ by attending to prob­lems of variability.90 He clearly felt that Steinach chose his data to fit his theory, rather than building a theory from neutrally collected information. But Moore, although following a path that ultimately led to what we believe today to be the ‘‘right’’ answer, had his own unexplained experimental lapses. For example, he directly contradicted Steinach by showing that he could implant an ovary into a rat that retained its own testis. But when he extended this work to guinea pigs, he used only castrated or spayed animals to host his implants. Why? Did the guinea pig experiments work less well when he left the host’s gonad intact? Or perhaps this experimental choice reflected Moore’s lower level of interest in questions of sexual intermediacy and homosexuality.91

Or consider his results with testicular implants. These may not have pro­vided a real test of Steinach’s work. Steinach reported that his testicular im­plants contained a lot of interstitial cell growth (now known to be the source


of testosterone production).92 Moore’s implants grew poorly, and seemed not to produce much in the way of interstitial cell growth. In fact, it is not clear that his testicular grafts were physiologically active, yet he concluded that they had no masculinizing effects. It seems possible, however, that the experiment simply failed. Without successful testicular grafts, there could be no test of this aspect of Steinach’s work.

Right or wrong, the idea of sex antagonism, when imported into the arena of hormone biology, stimulated an enormously productive debate.93 Moore and Price ultimately created an account that integrated elements of a ‘‘sepa­rate but equal’’ status with a sexually nonspecific role for gonadal hormones as powerful growth regulators. On the one hand, they argued that testis hor­mone (still unnamed in 1932) had promoted the growth of male accessory glands but had no direct effects on female parts. Similarly, the ovarian hor­mone (named oestrin under circumstances described in the following chap­ter) stimulated certain aspects of female growth but had no direct effects on male differentiation. On the other hand, both hormones could inhibit the pituitary in either sex, thereby indirectly suppressing gonadal hormone pro­duction. Moore and Price offered no socially redolent phrase (analogous to ‘‘hormone antagonism’’) to describe their theory, although they acknowl­edged that their work would be of interest to those concerned with intersexu­ality and hermaphrodites. Perhaps they came from a more cautious scientific tradition;94 perhaps the crises of gender, class, and race had begun to wane by the time Moore and Price reached their conclusions.95 Although answering such questions is a matter for future historical investigation, here I argue that reading gender into and from bodies is a more complex matter than merely allowing the body to speak the truth.

Although defeated by hormone biologists, the idea of hormone antagonism did not die. Steinach, himself, never abandoned it.96 The medical endocrinol­ogist and sexologist Harry Benjamin, who pioneered the idea of surgery as a cure for transsexualism,97 praised the idea of sex hormone antagonism in Steinach’s obituary. ‘‘Opposition to this theory of the physiological antago­nism of sex hormones still exists,’’ he wrote, ‘‘but remains unconvincing in view of many corroborating experiments.’’98 Others also continued to sub­scribe to Steinach’s model. In 1943, our pal de Kruif would refer to sex antag­onism as a ‘‘chemical war between the male and female hormones. . . a chem­ical miniature of the well-known human war between men and women.’’99 A scientific fact, once established, may sometimes be disproved in one field, re­main a ‘‘fact’’ in others, and have a further life in the popular mind.