<< Extra Supply of Gonadal Hormones >>

The administration of an extra supply of male hormone to an animal, female or male, which has intact gonads, may increase its sexual responsiveness. This may appear to contradict the data on the effects of a castration, but the two bodies of data are not actually in conflict.

Excessive Gonadal Hormones in Young Animals
The administration of androgenic hormones to a young, non-castrated male, whether infrahuman or human, ordinarily speeds up its physical development and the development of its sexual responsiveness and overt sexual activity. 46 There are similar results when estrogens are given to young females. 47 There is considerable work on laboratory animals which establishes this fact. In the case of the human male, the clinical administration of testosterone to a pre-adolescent is ordinarily avoided because of the probability that it will start precocious development. But when adolescent development seems to be delayed, and particularly when there seems to be an under-development of the gonads, some physicians do administer testosterone. There may be complications, however, if more than the optimum dose is given, for an excessive supply of gonadal hormones may inhibit the secretory activity of the anterior lobe of the pituitary.
Experimental and clinical data on the administration of male hormones to young, non-castrated males are cited in: Beach 1942d. Hoffman 1944:157-159. Heller and Maddock 1947:417. Beach 1948:206-207. Burrows 1949:169. Howard and Scott in Williams 1950:339. Experimental data on the administration of female hormones to young, lower mammalian females, are cited in: Beach 1948:196, 203-204. Corner 1951: 57-58.

Precocious adolescent development sometimes, although rarely, may occur in children at five or six, or even at two or three years of age. In some of these cases there may be an endocrine imbalance which sometimes involves an androgen disturbance; but there are other cases in which clinical studies fail to show any sort of endocrine disturbance. Such children may show physical developments equal to those of a normal thirteen- or fourteen-year-old. However, the sexual responses and overt activities of such precocious children are ordinarily typical of those among normal pre-adolescent children of the same age. Investigators are inclined to emphasize that such a child masturbates, shows sexual curiosity, or engages in some form of socio-sexual play, and they are likely to conclude that these activities are a product of the precociousness. But it should not be forgotten that such activities are ordinarily found in the histories of normal pre-adolescent children.

In the several cases which we have of precocious adolescent development, we have rarely found sexual activities which exceeded those ordinarily found among normal children of the same age. We have the history of a five-year-old with the physical development of a fourteen-year-old, but with sexual responses which were normal or even lower than normal for a five-year-old. We have one group of four related cases in which hereditary factors seem to have been involved, for precociousness had appeared among the males of at least two generations in separated branches of the family. We have the history of another boy who turned adolescent at seven, and he was highly responsive and exceedingly active in socio-sexual contacts. Since cases of very early adolescent development are relatively rare, it is highly important that more extensive data be accumulated on the responses and overt sexual activity of such children.
Summaries of published eases of precocious adolescent development in which there are data on sexual behavior, may be found in: Doe-Kulmann and Stone 1927:319 (adult sexuality not present in most precocious cases). Singer 1940:19-22 (summary of published reports on 59 females, 48 males). Stotijn 1946:56 (a Dutch study). Dennis in Carmichael 1946:656-658. Sandblom 1948:110 (one case of a precocious three-year-old male, aggressive sexually).

The administration of androgens to a pre-adolescent human female may do considerable damage because of their over-stimulation of physical development. There seem to be no data on the effects of such an early administration of androgens on the sexual responsiveness and the overt sexual activity of the human female.
Discussion of dosages of androgens affecting precocious physical development in young females is found in: Selye 1949:614. Mazer and Israel 1951:126. Talbot et al. 1952:381, 440-441, 484.

Excessive Androgens in Adults
When an extra supply of androgens is given an adult animal that has not been castrated, there may be an increase in the general level of its physical activity, its aggressiveness, and its frequency of sexual response and overt sexual performance. This is true of laboratory and farm animals, and it is equally true of the human male. It is also true when androgens are given females, whether they are lower mammalian or human females.
Effects of androgens on non-castrate adult male animals is described in: Beach 1942b: 181-182, 193-194. Beach 1942c:227-247. Beach 1948:34, 36. Cheng et al. 1950:452 (increased sex activity in male rabbit).

When testosterone, for instance, is given the normal human male, there may be an increase in the frequency of his morning erections, the frequency of his erotic response to various stimuli, the frequency of his masturbation, and the frequency of his socio-sexual contacts. This is ordinarily true of adult males of ages ranging at least from the twenties into the fifties or sixties.
While there is a general use of androgen therapy on intact, normal males in clinical practice, there are few published accounts; but see: Miller, Hubert and Hamilton 1938:538-540. Kenyon et al. 1940:35. Barahal 1940:319 (increased drive in homosexual males). Heller and Maddock 1947:419 (says “normal” men fail to have an increase in sex drive, but on p. 422 agrees that such treatment seems to increase “the power of the sex drive in both normal and homosexual males . . .”). Burrows 1949:169 (excessive masculine urges in “normal” male adults). Perloff 1949:133 ff. H. H. Turner 1950: 38-43 (a survey; indicates contradictions in data).

Testosterone has also been used clinically to increase the levels of sexual response in cases in which a failure to have offspring appears to depend on low rates of coitus. We have several histories of males who had had their coital frequencies increased by such clinical treatment. Sperm counts may also be increased by the administration of testosterone, and this may contribute to the relief of the sterility.
Surveys and studies on the effect of testosterone on sperm count include: Weisman 1941:240-242 (concludes small doses stimulate sperm production, large doses inhibit it). Heller and Maddock 1947:419 (temporary reduction of sperm). C. D. Turner 1948:344 (considers evidence for increase in sperm inconclusive; lack of sperm if dosage is excessive). H. H. Turner 1950:24-25, 53-54 (no change in sperm production, although recognizes that other reports are contradictory). Cheng et al. 1950:447-452 (increases volume of ejaculate in rabbit, but total number of sperm unchanged). Heckel and McDonald 1952:725-733 (reduces sperm production in 72 men; a return to a higher level after treatment stopped in twenty-three out of forty-five men).

The indiscriminate use of testosterone, however, may involve some danger, for if the dose exceeds the amount necessary for optimum effectiveness, pituitary functions may be inhibited, and this may do damage to various structures, including the gonads themselves, and there may be negative effects on sexual activities. In laboratory animals, excessive doses of testosterone may reduce the gonads to more or less vestigial structures.
The harmful effects of various doses of testosterone are pointed out in: Moore 1942:40-41. Heller and Maddock 1947:415-416. Ludwig 1950:453, 465 (small doses more injurious than large doses in male rats).

There is some clinical experience in administering testosterone to normal human females, and the results obtained are quite similar to those obtained in males. Once again, the levels of physical activity may be increased, and the general level of aggressiveness may be increased. In the case of the lower mammals, this increase of aggressiveness increases the frequency with which the female mounts other animals, either females or males. Because males are normally more aggressive than females, normal females usually find few opportunities to mount males; but females who have been given testosterone may become so aggressive that they succeed in mounting a larger number of males.
For clinical use of androgens to increase sex drive in human females, see: Geist 1941. Salmon 1941 (survey of animal and clinical experiments). Salmon and Geist 1943. Greenblatt 1947:177-178. Hyman 1946(3):2406. Carter, Cohen and Shorr 1947:361-364 (a comprehensive survey). Beach 1948:62. Selye 1949:619. Increased aggressiveness among females of lower mammalian species after treatment with testosterone dosage are reported in: Stone 1939. Ball 1940:151-165. Young 1941:135. Birch and Clark 1946 (chimpanzee).

The increased responsiveness of a normal female or male who has received an increased supply of testosterone has ordinarily been taken as evidence that the hormone plays a prime part in controlling sexual behavior. Such an interpretation, however, ignores the evidence of the castration experiments on adult females and males. It seems more correct to conclude that androgens, at every level which does not exceed the point of optimum effectiveness, are among the physiologic agents which step up the general level of metabolic activity in an animal’s body, including the level of its nervous function and therefore of its sexual activity. For instance, as an example of the effect of testosterone on other physiologic activities, it may be noted that dairy breeders sometimes administer it to cattle in order to increase their food utilization. Thereby the breeder may increase the amount of meat which he secures when he gives the animal a given quantity of food.

There are so many other factors which affect the levels of metabolic activity in a fully mature animal that the loss of the usual supply of androgens, as in a castration, does not make it impossible for an animal to hold its metabolism at something approaching a normal level. This, however, does not preclude the possibility that supplies of male hormones in excess of those normally provided by the gonads, may raise the metabolic levels and consequently the levels of sexual response and performance. But male hormones are not the only agents that step up the levels of activity, including the levels of sexual activity, for the administration of pituitary extracts, of thyroid, and of some other substances may have similar effects. In fact, good health, sufficient exercise, and plenty of sleep still remain the most effective of the aphrodisiacs known to man.

Excessive Estrogens in Adults
What effect the administration of an extra supply of estrogens may have on the sexual behavior of the human or lower mammalian female or male, is a matter which may not be asserted with assurance in our present state of knowledge. Some clinicians assert that they have raised the levels of sexual responsiveness in female patients by administering estrogens, while other clinicians make just as positive statements that they have never secured such a result. Animal breeders and students experimenting with laboratory animals, female and male, give similarly contradictory reports. The contradictions may mean that there is no simple and direct relationship between estrogens and sexual behavior, or they may mean that the effectiveness of an increased supply of estrogens depends upon the concomitance of a variety of factors, including such things as the general metabolic level, the general physical health, the levels of the other hormones in the body, the age, the point in the estrus cycle at which the estrogens are administered, and probably still other factors.
Various effects of estrogen therapy are reported in: Frank 1940:1509. Soule and Bortnick 1941. Mazer and Israel 1946:34. Greenblatt 1947:177-178. Emmens and Parkes 1947:240-241. Kimbrough and Israel 1948:1217-1219. Perloff 1949:135. Ford and Beach 1951:225-226. Mazer and Israel 1951:33. Masters in Cowdry 1952:669. For estrogen effects on the behavior and physical structures of mammalian males, see: Clark and Birch 1945:328 (loss of dominance in chimpanzee). Emmens and Parkes 1947:236 ff. (atrophy of testis, prostate, Cowper's glands, spermatogenesis). Beach 1948:61-62. Selye 1949:360 (decreases sexual responsiveness). Goldzieher and Goldzieher 1949:1156 (male impotence). Howard and Scott in Williams 1950:342 (depresses spermatogenesis). Paschkis and Rakoff 1950:137-138 (testicular degeneration). Howard et al. 1950:134. Lynch 1952:734-741 (atrophy of rat testis, depresses spermatogenesis).

There is a theory that estrogens counteract the effectiveness of androgens. The theory is as yet unsubstantiated by adequate experiment, and is confused by the fact that both androgens and estrogens occur simultaneously in both the female and male bodies.
The lack of any antagonistic effect between androgens and estrogens is noted in: Koch 1937:206-208. Hartman 1940:449-471 (female monkey). Hoffman 1944:42-43. Burrows 1949:122. Selye 1949:64-65.

However, some clinicians in this country, in Denmark, and in Holland are using estrogens in an effort to reduce the levels of sexual responsiveness of males convicted as sex offenders. It is possible that estrogens do reduce the amount of androgen which is secreted, but the attempt to control sexual behavior by lowering androgens depends, of course, on a misinterpretation of the role of the androgens in the sexual activities of the male. There are optimistic reports of “good results” from the estrogen injections, but, as usual, the reports are not supported by adequate details of what the “good results” are supposed to be. Since an excessive supply of estrogens may affect many body functions besides sexual behavior, and since an excessive supply may do irreparable damage to other glandular structures, several research endocrinologists assert that they consider the use of estrogens to lower the sexual responsiveness of a male nothing less than medical malpractice.
The use of estrogens on male sex offenders and others to reduce sex drive is discussed or reported in: Dunn 1940:2263-2264 (a single case, 96 day treatment, resulting in loss of sex drive and degeneration of genitalia). Dunn 1941: 643 (later report on same case. Some effects disappeared after stopping therapy, but sexual levels still reduced). Rosenzweig and Hoskins 1941:87-88 (massive doses, no effect on one homosexual male). Greenblatt 1947:279-280. Golla and Hodge 1949 (13 males, uncontrollable sex urge, treated with estrone successfully). Perloff 1949:135. Brown 1950:52-53 (cites 300 male homosexuals, unsuccessful treatment with androgens). Tappan 1951:247-248 (in Holland).

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