Thursday, March 26, 2009

The urinary estrogen theory. Part III

In a previous post, I suggested that something in the environment had begun to alter male sexual development in Western countries by the turn of the 20th century. Among a small minority of men, probably those already weakly predisposed to heterosexuality, the result was a shift to exclusive male homosexuality, i.e., development of a female-like sexual orientation in terms of search image and desired self-image.

To a lesser degree, there seems to have been a similar shift among men in general. The feminine ideal became that of the ‘flapper’ or garçonne: a woman with long legs, a flat chest, narrow hips, large shoulders, and tanned skin, like a young boy on the brink of puberty (Bard, 1998; Marchand, 1997, 1988). This look is described in a history of British fashion:

The Masculine Silhouette of 1920's Females

After the first world war (1914-18) when women's dress became more mannish, … [f]emale clothes became looser and more shapeless in fit. The bust was suppressed, the waist disappeared, the shoulders became broader and hair shorter and shorter. Narrow boyish hips were preferred. The silhouette emphasised a flattened chest and womanly curves were eliminated as the line became more simplified.

The Flat Chest of the Twenties

The slender flat-chested tanned body and face of a 15 year old became the desired silhouette of the bright young things of the 1920s. Health and beauty clubs helped women refine their silhouettes whilst getting fitter and healthier. It was a difficult time for the former matrons of Edwardian society, the previous leaders of fashion whose style of dressing became as passé as their rounded figures and older faces. More youthful women who could party all night and carry the boyish fashions well were all the rage.

Such androgyny is sometimes put down to the social impacts of World War I, either the wartime entry of women into previously male jobs or the postwar shortage of men. Yet the ‘boyish look’ was being mentioned as early as 1914, in the United States, three years before that country entered the war:

The new ideal in feminine figure, dress, and hair styles was all semi-masculine. The “1914 Girl” with her “slim hips and boy-carriage” was a “slim, boylike creature”. The “new figure is Amazonian, rather than Miloan. It is boyish rather than womanly. It is strong rather than soft.” Her dress styles, meanwhile, de-emphasized both hips and bust while they permitted the large waist. (McGovern, 1968)

It looks as though the male search image had been developing imperfectly, with some algorithms receiving the wrong parameters. Was the cause something new in the environment? And could this something have been estrogen-rich wastewater from modern sewer systems—then scarcely a generation old?

Well, there were a lot of other new things at the turn of the 20th century. Can we look elsewhere in history for cases that link environmental estrogens to a change in the male search image? One might be Japan from the 17th century onward, specifically the effects of increased soybean consumption.

Soybeans are rich in isoflavones, which have estrogenic effects. Such ‘phytoestrogens’ exist in many plant species and may have evolved as a form of biological warfare to prevent overgrazing. Indeed, they have been shown to cause infertility in herbivores (Cassidy & Setchell, 1998; Hughes, 1988; Hughes & Tansey, 1998). In humans, research has focused on the beneficial effects of isoflavones, notably their usefulness in preventing heart disease in both sexes, breast cancer, osteoporosis, and menopausal symptoms in women, and prostate cancer in men (Cassidy & Setchell, 1998; Knight & Eden, 1996).

Much less is known about their effects on male sexual development. On average, Japanese men ingest 20 mg of isoflavones per day, an amount that seems too low to have acute hormonal effects (Cassidy & Setchell, 1998). Nonetheless, when infants ingest the same amount through soy formula, they attain plasma isoflavone concentrations that are ten times those of Japanese adults (Cassidy & Setchell, 1998). The effects on children remain uncertain but have raised much concern (Santti et al., 1998).

In Japan, high soy consumption began during the Tokugawa period (1603-1867, also called the Edo period). This period saw a sharp rise in population that reduced meat consumption per capita. In coastal areas, people had to obtain protein mainly from seafood. Elsewhere, they turned to soy products:

Inland, the main source of protein was the soy bean, which has a much higher calorie output per acre than animal flesh, an inefficient source of protein in terms of the amount of land and grain needed to produce it. Thus tofu and other soybean products became a major source of both protein and calcium during the Tokugawa period. (Hanley, 1997, pp. 67-68).

This period also saw a shift in male aesthetic preferences:

Gen Itasaka has described the change in taste during the Edo period as the transition between the styles of woodblock print artists Moronobu and Harunobu. Moronobu’s women are pleasantly plump, Marilyn Monroe-type beauties with round faces, ample bosoms and hips. Harunobu’s women are less sensual, androgynous beauties with slender faces and delicate, willowy figures. (Kurokawa, 1994)

Changes occurred in the ideals of feminine beauty during this period of continuing peace. Gradually, slim and fragile women with slender faces and up-turned eyes began to be preferred to the plump, pear-shaped ideal that remained dominant until the middle of the eighteenth century. (Wagatsuma, 1967)

The shift in search image thus seems to resemble what occurred in the Western world at the turn of the 20th century. Are we looking at the same underlying phenomenon?


Bard, C. (1998). Les garçonnes. Modes et fantasmes des Années folles. Paris: Flammarion.

Cassidy, A., & Setchell, K.D.R. (1998). Clinical experiences in assessing dietary effects of phytoestrogens on the human endocrine system, in: Dunaif, G., Olin, S., Scimeca, J., & Thomas, J. (eds.) Human Diet and Endocrine Modulation, Washington, DC: ILSI Press, pp. 155-165.

Hanley, S.B. (1997). Everyday Things in Premodern Japan. The Hidden Legacy of Material Culture. Berkeley: University of California Press.

Hughes, C.L. Jr. (1988). Phytochemical mimicry of reproductive hormones and modulation of herbivore fertility by phytoestrogens, Environmental Health Perspectives, 78, 171-175.

Hughes, C.L. Jr, & Tansey, G. (1998). Phytoestrogens and reproductive medicine, in: Korach, K. (ed.) Reproductive and Developmental Toxicology, New York: Marcel Dekker Inc., pp. 277-298.

Knight, D.C., & Eden, J.A. (1996). A review of the clinical effects of phytoestrogens, Obstetrics & Gynecology, 87, 897-904.

Kurokawa, K. (1994). Rikyu grey and the art of ambiguity (chap. 6), in The Philosophy of Symbiosis. London: Academy Ed.

Marchand, S. (1997). Rouge à lèvres et pantalon. Des pratiques esthétiques féminines controversées au Québec 1920-1939, Montréal: Éditions Hurtubise HMH.

Marchand, S. (1988). La « Garçonne », un nouveau modèle féminin (1920-1929), Cap-aux-Diamants, 4, 19-20.

McGovern, J.R. (1968). The American woman's pre-World War I freedom in manners and morals, Journal of American History, 55, 315-333.

Santti, R., Makela, S., Strauss, L., Korkman, J., & Kostian, M-L. (1998). Phytoestrogens: potential endocrine disruptors in males, Toxicology and Industrial Health, 14, 223-237.

Wagatsuma, H. (1967). The social perception of skin color in Japan, Daedalus, 96, 407-443.

Wednesday, March 18, 2009

The urinary estrogen theory. Part II

In my last post, I argued that large quantities of estrogen were flushed into lakes and rivers across North America and northern Europe between the introduction of modern sewer systems in the late 19th century and the shift to secondary and tertiary sewage treatment after the 1960s. By separating out solid fecal waste and rapidly discharging the fluid component into nearby cold bodies of water, we unwittingly created ideal conditions for the preservation of urinary estrogen, which then came back to us via water for drinking and bathing.

Did this estrogen affect the sexual development of young boys? It probably had few effects prenatally. For one thing, there is the placental barrier. For another, the developing human fetus is already adapted to the high levels of estrogen in the mother’s body.

But there may have been effects outside the womb. The human infant is adapted to external environments that have very little urinary estrogen. Until the late 1800s, urine was discharged into warm aqueous media with plenty of organic matter, e.g., privies, cesspools, ditch sewers … or the nearest bushes. Any estrogen would have been quickly biodegraded by nitrifying bacteria. All of this changed, however, with the advent of modern sewer systems and the ensuing estrogen contamination of the public water supply.

For this period (late 1800s – 1970s), we have no direct data on estrogen levels in the environment. Indirect evidence, however, is provided by male reproductive illnesses that are linked to estrogenic exposure, notably lower sperm counts and higher rates of testicular cancer, cryptorchidism, and hypospadias (Carlsen et al., 1992; Carlsen et al., 1995; Colborn et al., 1996; Klotz, 1999; Sharpe, 1998). These illnesses arise from impeded development of Sertoli cells that eventually produce spermatozoa in adult males. In particular, the impediment seems to happen while these cells are dividing and replicating during the fetal stage or infancy, although some replication also occurs during early puberty (Sharpe, 1998).

Prior to 1940, we have reliable data only on testicular cancer—an important consideration if we wish to distinguish between post-late-1800s exposure to urinary estrogen and post-1940s exposure to synthetic estrogenic compounds (Colborn et al., 1996). In the United States, the Connecticut Tumor Registry (CTR) gives the incidence of testicular cancer as far back as 1935 and victim birth cohorts as far back as 1910 (Brown et al., 1986; Schottenfeld et al., 1980). Birth cohorts are more informative than year of tumor diagnosis because testicular cancer seems to originate early in life (Bergström et al., 1996; Brown et al., 1986; Østerlind, 1986). Outside the U.S., long‑running registries have been kept in England and Wales and in other northern European countries (Adami, et al., 1994; Bergström et al., 1996; Davies, 1981; Østerlind, 1986).

The CTR shows a steadily increasing incidence of testicular cancer since the earliest cohort of men born in 1910‑14 (Brown et al., 1986; Schottenfeld et al., 1980). The registry for England and Wales goes further back and reveals that the increase began among men born in 1891‑1900 (Davies, 1981). Registries in northern Europe (Denmark, Norway, Sweden, former East Germany, Finland, and Poland) show an absence of decade-to-decade change in cohorts born between 1880 and 1920, followed by a steady increase in later cohorts (Bergström et al., 1996). In North America and northern Europe, then, the increase seems to predate the post‑1940s entry of synthetic estrogenic compounds into the environment. It is also worth noting that exposure to industrial estrogenic chemicals has been worse in Poland and the former East Germany than in Denmark and Norway, yet the latter countries have much higher incidences of testicular cancer (Adami et al., 1994).

Thus, over the 20th century, the rising incidence of testicular cancer seems to track the growing volume of untreated wastewater if we allow a mean time lag of 35 years between the initial cancer‑inducing event and tumor development [1]. Given the marked decline in untreated wastewater following the 1972 Clean Water Act in the U.S. and similar efforts in other countries, should we now be seeing a parallel decline in the incidence of testicular cancer?

There has in fact been a plateauing of U.S. incidence rates since the 1990s (Holmes et al., 2008; Pharris‑Ciurej, 1999). A similar leveling off has been noted in England and Wales among men born since 1960 and in Scotland among men born since 1965 (Dos Santos, et al., 1999; Swerdlow et al., 1998; see also Cancer Research UK). Denmark has reported a leveling off in post-1963 cohorts and even a decrease in the 1968 cohort, although incidence rates are still rising in the other Nordic countries (Jacobsen et al., 2006; Møller, 2001).

In addition to the plateauing of recent age cohorts, testicular cancer is much less common among men born during World War II in Denmark and, to a lesser extent, in Norway and Sweden (Jacobsen et al., 2006; Møller, 2001). The reason is still a mystery, all the more so because these countries were largely spared the horrors of WWII.

It does seem, then, that the incidence of testicular cancer mirrors rising and falling levels of urinary estrogen in the environment. In my next post, I will return to the possibility of a correlation with changes to male sexual orientation, particularly in terms of search image and desired self-image.


[1]. Although testicular cancer can occur in teenagers, it is much more common in adulthood. “Unlike most other cancers, testicular cancer, with a peak incidence in the third decade of life, suggests a latency period that involves some pre or postnatal stimulatory event that influences subsequent tumor development. The widespread observation of a birth cohort correlation for testicular cancer suggests that early or prolonged exposure to some carcinogenic stimuli might be required for the subsequent development of testicular cancer.” (McKiernan et al., 2000)


Adami, H‑O., Bergström, R., Möhner, M., Zatonski, W., Storm, H., Ekbom, A., Tretli, S., Teppo, L. Ziegler, H., Rahu, M., Gurevicius, R., and Stengrevics, A. (1994). Testicular cancer in nine northern European countries. Int. J. Cancer, 59, 33‑38.

Bergström, R., Adami, H‑O., Möhner, M., Zatonski, W., Storm, H., Ekbom, A., Tretli, S., Teppo, L., Akre, O., and Hakulinen, T. (1996). Increase in testicular cancer incidence in six European countries: a birth cohort phenomenon. J. Natl. Cancer Inst., 88, 727‑733.

Brown, L.M., Pottern, L.M., Hoover, R.N., Devesa, S.S., Aselton, P., and Flannery, J.T. (1986). Testicular cancer in the United States: trends in incidence and mortality. Int. J. Epidemiol., 15, 164‑170.

Carlsen, E., Giwercman, A., Keiding, N., and Skakkebaek, N.E. (1995). Declining semen quality and increasing incidence of testicular cancer: is there a common cause? Environ. Health Perspect., 103(suppl. 7), 137‑139.

Carlsen, E., Giwercman, A., Keiding, N., and Skakkebaek, N.E. (1992). Evidence for decreasing quality of semen during past 50 years. BMJ, 305, 609‑13.

Colborn, T., Dumanoski, D., and Peterson Myers, J. (1996). Our stolen future. New York: Dutton.

Davies, J.M. (1981). Testicular cancer in England and Wales: some epidemiological aspects. Lancet, 1, 928‑32.

Dos Santos Silva, I., Swerdlow, A.J., Stiller, C.A., and Reid, A. (1999). Incidence of testicular germ-cell malignancies in England and Wales: Trends in children compared with adults. Int. J. Cancer, 83, 630-634.

Holmes, L. Jr., Escalante, C., Garrison, O., Foldi, BX., Ogungbade, G.O., Essien, E.J., and Ward, D. (2008). Testicular cancer incidence trends in the USA (1975-2004) : Plateau or shifting racial paradigm? Public Health, 122(9), 862-872.

Jacobsen, R., Møller, H., Thoresen, S.Ø., Pukkala, E., Kruger Kjaer, S., and Johansen, C. (2006). Trends in testicular cancer incidence in the Nordic countries, focusing on the recent decrease in Denmark. International Journal of Andrology, 29, 199-204.

Klotz, L.H. (1999). Why is the rate of testicular cancer increasing? CMAJ, 160, 213-4.

McKiernan, J.M., Hensle, T.W., and Fisch, H. (2000). Increasing risk of developing testicular cancer by birth cohort in the United States, Dialogues in Pediatric Urology, 23, 7-8.

Møller, H. (2001). Trends in incidence of testicular cancer and prostate cancer in Denmark. Human Reproduction, 16, 1007-1011.

Østerlind, A. (1986). Diverging trends in incidence and mortality of testicular cancer in Denmark, 1943‑1982. Br. J. Cancer, 53, 501‑5.

Pharris‑Ciurej, N.D., Cook, L.S., and Weiss, N.S. (1999). Incidence of testicular cancer in the United States: has the epidemic begun to abate? Am. J. Epidemiol., 150, 45‑6.

Schottenfeld, D., Warshauer, M.E., Sherlock, S., Zauber, A.G., Leder, M., and Payne, R. (1980). The epidemiology of testicular cancer in young adults. Am. J. Epidemiol., 112, 232‑246.

Sharpe, R.M. (1998). Natural and anthropogenic environmental oestrogens: the scientific basis for risk assessment. Environmental oestrogens and male infertility. Pure & Appl. Chem., 70, 1685‑1701.

Surveillance, Epidemiology, and End Results (SEER) Program Public‑Use Data (1973­-1998), National Cancer Institute, DCCPS, Surveillance Research Program, Cancer Statistics Branch,

Swerdlow, A.J., Dos Santos Silva, I., Reid, A., Qiao, Z., Brewster, D.H., and Arrundale, J. (1998). Trends in cancer incidence and mortality in Scotland: description and possible explanations. Br. J. Cancer, 77(supplement 3), 1-16.

Wednesday, March 11, 2009

The urinary estrogen theory. Part I

What is the main source of estrogen in the environment? Birth control pills? An industrial compound with estrogenic properties, like DDT, PCBs, and dioxins?

No, it’s women’s urine. The stuff that gets flushed down toilets millions of times a day. There is also testosterone in wastewater but at much lower levels, being less water‑soluble (Tabak et al., 1981). What happens, then, to this estrogen as it wends it way through the environment?

The question has attracted little interest. And perhaps we have no cause for worry. On the one hand, natural estrogen is quickly consumed by nitrifying bacteria if left in a warm stagnant medium with organic matter (Vader et al., 2000). These were the conditions of traditional wastewater disposal, i.e., privies, cesspools, and ditch sewers (Rockefeller, 1996). On the other hand, modern wastewater disposal is very good at removing urinary estrogen. Primary treatment alone removes 35‑55 percent and the proportion rises to 50‑70 percent for primary and secondary treatment combined (Tabak et al., 1981). Today, state‑of‑the­-art treatment plants remove 90 percent of all natural and synthetic estrogenic compounds (LeQuire, 1999).

If there had existed only a traditional system of disposal and a modern system, we would indeed have no cause for worry. But there was a long transitional period with a third system: central collection of wastewater and separation from fecal waste, followed by discharge into local bodies of water without treatment. This kind of sewage system was available to one million Americans in 1860. By 1900, the total had risen to over twenty‑four million, including a million served by primary wastewater treatment (Hyde, 1938). By 1960, untreated wastewater was being produced by 70 million Americans—an all-time high that fell to 2 million after passage of the Clean Water Act in 1972 and subsequent upgrading to secondary treatment of almost all U.S. sewer systems (Copeland, 1993; U.S. Council on Environment Quality, 1984).

As stated above, wastewater treatment currently removes 50 to 90 percent of all wastewater estrogen. Such removal is impaired by two factors: cold temperatures, as shown by seasonal variation in estrogen removal, and lack of bacteria due to short sludge retention (Desbrow et al., 1998; Ternes et al., 1999; Belfroid et al., 1999; Vader et al., 2000). Thus, urinary estrogen persists in the environment only when wastewater is untreated and rapidly discharged into a cold, clear, and largely aqueous medium. From the late 19th century to the 1970s, this was the way we dealt with wastewater in North America and northern Europe.

Cold bodies of water were not just destinations for sewage. They were also sources of drinking and bathing water. Did this situation pose a serious risk of estrogen exposure? No one seems to know. But there is some suggestive evidence.

Estrogen feminizes male rainbow trout (as measured by production of female egg yolk protein) at levels as low as 10 ng per liter of water for estradiol and 25 ng per liter for estrone; above these thresholds the response follows a dose-related curve (Routledge et al., 1998). By comparison, treated wastewater in Great Britain contains 1 to 10 ng of estrogen (either estradiol or estrone) per liter, with levels exceeding 30 ng at the outflow from some sewage treatment plants (Desbrow et al., 1998). Drinking water generally has low or undetectable concentrations. To date, the record seems to be 14 to 22 ng/L for drinking water from Lake Kinneret, Israel (Desbrow et al., 1998, Shore et al., 1993). It should be noted, however, that before the 1980s no one was testing drinking water or wastewater for estrogen pollution (Tabak et al., 1981).

If the public water supply used to be a significant source of estrogen, either via drinking or bathing, the effects should be more serious in young children, whose body tissues are much less sexually differentiated. If serious enough, such effects ought to show up in statistics on male reproductive health, some of which go back to the late 19th century. What do these statistics tell us?

To be continued in my next post


Belfroid, A.C., Van der Horst, A., Vethaak, A.D., Schäfer, A.J., Rijs, G.B.J., Wegener, J., and Cofino, W.P. (1999). Analysis and occurrence of estrogenic hormones and their glucuronides in surface water and waste water in The Netherlands. Sci. Total Environ., 225, 101‑108.

Copeland, C. (1993). Wastewater Treatment: Overview and Background [93-138 ENR] Washington, D.C.: Congressional Research Service.

Desbrow, C., Routledge, E.J., Brighty, G.C., Sumpter, J.P., and Waldock, M. (1998). Identification of estrogenic chemicals in STW effluent. 1. Chemical fractionation and in vitro biological screening. Environ. Sci. Technol., 32, 1549‑1558.

Hyde, C.G. (1938) A review of progress in sewage treatment during the past fifty years in the United States. In: L. Pearse, (ed.) Modern Sewage Disposal. Anniversary Book of the Federation of Sewage Works Associations, pp. 1‑15.

LeQuire, E. (1999). Something in the Water. InSites, 7(1),

Rockefeller, A.A. (1996). Civilization and sludge: Notes on the history of the management of human excreta. Current World Leaders, 39, 99‑113.

Routledge, E.J., Sheahan, D., Desbrow, C., Brighty, G.C., Waldock, M., and Sumpter, J.P. (1998). Identification of estrogenic chemicals in STW effluent. 2. In vivo responses in trout and roach. Environ. Sci. Technol., 32, 1559-1565.

Shore, L.S., Gurevitz, M., and Shemesh, M. (1993). Estrogen as an environmental pollutant. Bull. Environ. Contam. Toxicol., 51, 361‑366.

Tabak, H.H., Bloomhuff, R.N., and Bunch, R.L. (1981). Steroid hormones as water pollutants II. Studies on the persistence and stability of natural urinary and synthetic ovulation‑inhibiting hormones in untreated and treated wastewaters. Dev. Ind. Microbiol., 22, 497‑519.

Ternes, T.A., Stumpf, M., Mueller, J., Haberer, K., Wilken, R.-D., and Servos, M. (1999). Behavior and occurrence of estrogens in municipal sewage treatment plants ‑ I. Investigations in Germany, Canada and Brazil. Sci. Total Environ., 225, 81‑90.

U.S. Council on Environment Quality. (1984). Annual Report. Washington D.C.

Vader, J.S., van Ginkel, C.G., Sperling, F.M.G.M., de Jong, J., de Boer, W., de Graaf, J.S., van der Most, M., and Stokman, P.G.W. (2000). Degradation of ethinyl estradiol by nitrifying activated sludge. Chemosphere, 41, 1239‑1243.

Thursday, March 5, 2009

Has male homosexuality changed over time?

One point is often raised about male homosexuality: it has always been with us. True, but has it ever changed in its nature or prevalence?

Well, more gays have been ‘coming out of the closet.’ People are practicing openly what used to be done in secret. But have there also been more fundamental changes?

Such a change has been postulated by Michel Foucault and others who argue that European societies originally had plenty of male homosexuality but few male homosexuals (Foucault, 1976; Halsall, 1988; Trumbach, 1977). In the Middle Ages, this behavior was seen as a ‘vice’ of older heterosexual men, typically with young boys or men of a servile status. In contrast, far fewer men were exclusively homosexual in the sense of being uninterested in women and resembling women in their sexual orientation (i.e., having a woman’s search image and desired self-image). This relative rarity is implied by the astonishment that European explorers felt on encountering Amerindian berdaches during the 18th and early 19th centuries (Désy, 1978).

Towards the end of the 19th century and into the early 20th century, this facultative male homosexuality seems to have been overtaken by the exclusive kind throughout northern Europe and North America. Today, at least in these regions, most male homosexuals fall into the second category, as Greg Cochran notes when comparing male and female homosexuality:

Female homosexuality is less common and women who self-label as homosexuals are a lot more likely to have children than gay men. So the overall impact on fitness is less. The distributions are different too: you find a lot more men who are Kinsey 6s, who aren't interested in women at all, than bisexual men: the distribution is J-shaped. It's the other way around in women, more bisexuals than Simon-pure lesbians. (Cochran, 2005)

Thus, around the turn of the 20th century, a shift occurred in the search image of some men, making them homosexual and exclusively so. Interestingly, a similar shift took place among heterosexual men in general, though to a lesser degree. The feminine ideal became that of a woman with long legs, a flat chest, narrow hips, large shoulders, and tanned skin, like a young boy on the brink of puberty (Bard, 1998; Marchand, 1997, 1988). This sort of woman appears in a 1925 novel, The Great Gatsby, where Miss Jordan Baker is described as "a slender, small-breasted girl with an erect carriage which she accentuated by throwing her body backward at the shoulders like a young cadet" (Fitzgerald, 1992, p. 15). Such androgyny is sometimes put down to the social impacts of World War I, either the wartime entry of women into previously male jobs or the postwar shortage of men. Yet the ‘boyish look’ was being mentioned as early as 1914, in the United States, three years before that country entered the war:

The new ideal in feminine figure, dress, and hair styles was all semi-masculine. The “1914 Girl” with her “slim hips and boy-carriage” was a “slim, boylike creature”. The “new figure is Amazonian, rather than Miloan. It is boyish rather than womanly. It is strong rather than soft.” Her dress styles, meanwhile, de-emphasized both hips and bust while they permitted the large waist. (McGovern, 1968)

It is as if something had been altering the male search image, thereby causing a preference for more boyish-looking women and, in a minority of cases, for men. But what could this ‘something’ have been?

From the perspective of Cochran’s germ theory, it may have been a pathogen that became more transmissible with the growth of towns and cities in the late 19th century. Its male hosts may have varied in their degree of susceptibility, being pushed over the threshold of male homosexuality in some cases. In most cases, the psychological change would have been less drastic.

An alternate candidate may be some kind of chemical agent, specifically an estrogen or estrogenic compound that would hinder the masculinization of male brains. There has been much talk about a long-term decline in sperm counts, allegedly because of synthetic compounds that mimic natural estrogens (e.g., contraceptive pills, DDT, PCBs). Most of these compounds, however, date back only to the 1940s. Is there reason to believe that an estrogenic agent began to enter the human environment in the late 19th century—and in large quantities?


(to be cont’d in my next post)


Bard, C. (1998). Les garçonnes. Modes et fantasmes des Années folles. Paris: Flammarion.

Cochran, G.M. (2005). Cause of Homosexuality: Gene or Virus? Cochran Interview. Thrasymachus Online.

Désy, P.P. (1978).
L'homme-femme. (Les berdaches en Amérique du Nord), Libre — politique, anthropologie, philosophie, 78(3), 57-102.

Fitzgerald, F. S. (1992). The Great Gatsby, New York: Collier Books.

Foucault, M. (1976) Histoire de la sexualité. Tome 1. La volonté de savoir. Paris: Gallimard.

Halsall, P. (1988). The Experience of Homosexuality in the Middle Ages.

Marchand, S. (1997). Rouge à lèvres et pantalon. Des pratiques esthétiques féminines controversées au Québec 1920-1939, Montréal: Éditions Hurtubise HMH.

Marchand, S. (1988). La « Garçonne », un nouveau modèle féminin (1920-1929), Cap-aux-Diamants, 4, 19-20.

McGovern, J.R. (1968). The American woman's pre-World War I freedom in manners and morals, Journal of American History, 55, 315-333.

Trumbach, R. (1977). London's sodomites: homosexual behaviour and Western culture in the eighteenth century, Journal of Social History, 11, 1-33 .