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.
Note
[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)
References
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 18, 2009
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
References
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), http://eerc.ra.utk.edu/insites/ins7-1.htm#Something
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.
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
References
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), http://eerc.ra.utk.edu/insites/ins7-1.htm#Something
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:
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:
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?
Yes.
(to be cont’d in my next post)
References
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. http://www.fordham.edu/halsall/pwh/gaymidages.html
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 .
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?
Yes.
(to be cont’d in my next post)
References
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. http://www.fordham.edu/halsall/pwh/gaymidages.html
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 .
Labels:
estrogen,
germ theory,
Greg Cochran,
male homosexuality
Thursday, February 26, 2009
More on the origins of male homosexuality
Are there other theories on the origins of male homosexuality? Yes, quite a few. These theories generally fall into two categories: those that explain the relatively small variance due to genetic factors (30-45%) and those that explain the larger variance due to some environmental factor. Conceivably, we could be looking at an interaction between the two, i.e., an environmental factor (a pathogen, prenatal trauma, or perhaps environmental estrogens) interacting with a genetic predisposition (partly feminized male brains, as postulated by Ed Miller).
This week, we will look at another theory. Like Miller, Zietsch et al. (2008) postulate a genetic predisposition maintained by a balanced polymorphism. Unlike Miller, they believe this predisposition somehow increases mating success, rather than offspring survival.
Using twin data, they found that heterosexuals tend to have more sexual partners over a lifetime if they have a homosexual twin than if they have a heterosexual twin. This increased mating success, however, was significant only when the heterosexual was female. The authors attribute these findings to a genetically influenced behavioral trait.
The authors attribute this hypothesis to Ed Miller, although Miller’s theory has more to do with increased offspring survival (due to increased paternal investment) than to increased success on the mate market.
Does this hypothesis explain the authors' findings? Does it predict that hetero women with gay or lesbian siblings have more lifetime sexual partners? No. First, it doesn’t explain why such an effect is confined to female heterosexuals. Nor is it clear why this hypothesis should account equally well for hetero women with gay brothers and for hetero women with lesbian sisters. The authors seem to be arguing that these women have more lifetime partners than do other women because they’re more feminine in some cases and more masculine in others.
Hmm … Could we be looking at a shared family environment effect? Parental attitudes toward homosexuality in offspring tend to correlate with parental attitudes toward promiscuity in offspring, especially in daughters. This correlation is especially high if we compare religious families with non-religious ones. If a mother and father accept expression of homosexuality in their children, they would probably also accept their daughters having more sexual partners. On these grounds alone, a gay or lesbian child is likelier to have a sister who has more sexual partners on average. But this correlation would not be a cause-and-effect one. It would flow from a common cause: parental permissiveness.
One could shoot back: “Homosexuals are not made by permissive parents. They’re born that way.” True, but the participants in this study were asked to self-identify as heterosexual or homosexual (on a scale of 1 to 6). Even if family environment doesn’t determine latent sexual orientation, this factor would probably influence one’s willingness to affirm it, both to oneself and to others.
References
Zietsch, B.P., Morley, K.I., Shekar, S.N., Verweij, J.H., Keller, M.C., Macgregor, S. Wright, M.J., Bailey, J.M., & Martin, N.G. (2008). Genetic factors predisposing to homosexuality may increase mating success in heterosexuals. Evolution & Human Behavior, 29, 424-433.
This week, we will look at another theory. Like Miller, Zietsch et al. (2008) postulate a genetic predisposition maintained by a balanced polymorphism. Unlike Miller, they believe this predisposition somehow increases mating success, rather than offspring survival.
Using twin data, they found that heterosexuals tend to have more sexual partners over a lifetime if they have a homosexual twin than if they have a heterosexual twin. This increased mating success, however, was significant only when the heterosexual was female. The authors attribute these findings to a genetically influenced behavioral trait.
Our hypothesis is that a number of pleiotropic (more than one effect) genes predispose to homosexuality but also contribute to reproductive fitness in heterosexuals. In the case of males, there are a number of alleles that promote femininity: if only a few of these alleles are inherited, reproductive success is enhanced via increased levels of attractive but typically feminine traits such as kindness, sensitivity, empathy, and tenderness. However, if a large number of alleles are inherited, even the feminine characteristic of attraction to males is produced. In females, the converse explanation could be used—a low dose could lead to advantageous typically masculine characteristics such as sexual assertiveness or competitiveness, and a large dose could further lead to attraction to females. (Zietsch et al., 2008)
The authors attribute this hypothesis to Ed Miller, although Miller’s theory has more to do with increased offspring survival (due to increased paternal investment) than to increased success on the mate market.
Does this hypothesis explain the authors' findings? Does it predict that hetero women with gay or lesbian siblings have more lifetime sexual partners? No. First, it doesn’t explain why such an effect is confined to female heterosexuals. Nor is it clear why this hypothesis should account equally well for hetero women with gay brothers and for hetero women with lesbian sisters. The authors seem to be arguing that these women have more lifetime partners than do other women because they’re more feminine in some cases and more masculine in others.
Hmm … Could we be looking at a shared family environment effect? Parental attitudes toward homosexuality in offspring tend to correlate with parental attitudes toward promiscuity in offspring, especially in daughters. This correlation is especially high if we compare religious families with non-religious ones. If a mother and father accept expression of homosexuality in their children, they would probably also accept their daughters having more sexual partners. On these grounds alone, a gay or lesbian child is likelier to have a sister who has more sexual partners on average. But this correlation would not be a cause-and-effect one. It would flow from a common cause: parental permissiveness.
One could shoot back: “Homosexuals are not made by permissive parents. They’re born that way.” True, but the participants in this study were asked to self-identify as heterosexual or homosexual (on a scale of 1 to 6). Even if family environment doesn’t determine latent sexual orientation, this factor would probably influence one’s willingness to affirm it, both to oneself and to others.
References
Zietsch, B.P., Morley, K.I., Shekar, S.N., Verweij, J.H., Keller, M.C., Macgregor, S. Wright, M.J., Bailey, J.M., & Martin, N.G. (2008). Genetic factors predisposing to homosexuality may increase mating success in heterosexuals. Evolution & Human Behavior, 29, 424-433.
Labels:
balanced polymorphism,
Ed Miller,
male homosexuality
Thursday, February 19, 2009
Origins of male homosexuality - The germ theory
How does male homosexuality originate? More to the point, how does it perpetuate itself? According to Ed Miller, it results from a balanced polymorphism—a delicate balancing act where too much feminization of the male brain causes attraction to one’s own sex and too little causes indifference to one’s own children. This week, I will present an alternate explanation: Greg Cochran’s germ theory.
Greg has never published his theory in a peer-reviewed journal, although it is briefly summarized in Cochran et al. (2000). In itself, this is no shortcoming. Most journals seem uninterested nowadays in real debate. But sometimes I wish he would at least pretend he was writing for a journal. He tends to be polemical, as if only political correctness—or sheer stupidity—could motivate his detractors.
His starting point is the same as Miller’s. Male homosexuality makes no sense as a reproductive strategy. It should die out for the same reason that the Shakers did (the Shakers were a Protestant sect dedicated to lifelong celibacy). This point might seem obvious. Or maybe not. The following is an exchange between a germ theory critic and Greg Cochran:
Since natural selection would tend to eliminate male homosexuality, it should be uncommon—like most genetic conditions that impair one’s ability to survive and reproduce.
Since male homosexuality is not rare, it cannot have a genetic cause, at least not principally. There may be a genetic predisposition (with around 30-45% heritability, according to twin studies), but this predisposition is interacting with something in the environment. And this something cannot be a recent environmental change, since male homosexuality has been around for a long time.
The only remaining cause would be some kind of infectious agent that selectively alters certain parts of the brain while leaving the rest intact. There are precedents for this sort of thing.
Such pathogens may be more common than we think. The ones that get our attention—that make us go and see a doctor—are the ones that cause discomfort. But those ones may be a small minority of all pathogens, with most of the others flying under the radar. After all, it is in the pathogen’s own interest to be discrete and not cause too much havoc. It needs a healthy home to live in, until it can spread to another host.
Greg also argues that male homosexuality should be less common in smaller communities than in larger ones—where pathogenic transmission is likelier.
Finally, this pathogen may selectively alter sexual orientation for reasons that go beyond those of not harming the host too much. There are, in fact, a number of pathogens that alter the host’s behavior in order to enhance their chances of transmission. The protozoan Toxoplasma gondii causes infected rats to lose their fear of cats, thus enabling it to enter a cat body and complete its life cycle (Wikipedia – Toxoplasmosis). The parasitic worm Euhaplorchis californiensis forms cysts in the brains of infected killifish that cause the fish to swim near the surface of the water and make tight turns that show off their glinting sides, thus enabling the worm to enter a bird’s body (Zimmer, 2008).
As a child, I remember being told that a chicken is an egg’s way of making another egg. If Greg Cochran is right, a gay man is a vehicle that a pathogen has constructed for its own survival and reproduction. Everything else is human-centered delusion.
This is an interesting argument, but it has a few holes. First, some genetic conditions do reach incidences that are comparable to that of male homosexuality (about 3-5% of all men). Abnormal hemoglobin variants can reach high incidences in sub-Saharan Africans and other populations (8% in the case of Hb AS among African Americans). These variants are typically maintained through balancing selection where the heterozygote state provides some protection against malaria. Greg acknowledges that such selection exists but sees it as being confined to malaria protection. Yet balancing selection can exist for many other reasons. For example, one in 200 Hopi is albino, apparently because cultural selection offsets the environmental disadvantages of albinism (Hedrick, 2003).
Second, male homosexuality is frequently reported in small communities, including bands of Amerindian hunter-gatherers. Known as ‘berdaches’, these male homosexuals were described by early European explorers and appear to have existed in pre-contact times, as indicated by origin myths (Desy, 1978). One witness was John Tanner, a white captive who lived among the Ottawa of Ontario and then the Ojibwa of Manitoba until 1828:
Of course, neither point disproves the germ theory of male homosexuality. An infectious agent may indeed be the cause or one of several causes. If we consider the developmental pathway for heterosexual orientation, there is probably a ‘default’ sequence that leads to sexual interest in men and an ‘override’ sequence that leads to sexual interest in women. The second sequence may be disrupted for many reasons: a psychological trauma, a chemical insult, or an infectious agent in combination with a pre-existing genetic predisposition for incomplete masculinization. As one comment noted:
References
Cochran, G.M. (2005). Cause of Homosexuality: Gene or Virus? Cochran Interview. Thrasymachus Online.
Cochran, G.M. (2004?). An evolutionary look at human homosexuality. World of Greg Cochran.
Cochran, G.M., Ewald, P.W., & Cochran, K.D. (2000). Infectious causation of disease: an evolutionary perspective. Perspectives in Biology and Medicine, 43, 406-448.
Désy, P.P. (1978). L'homme-femme. (Les berdaches en Amérique du Nord), Libre — politique, anthropologie, philosophie, 78(3), 57-102.
Hedrick, P.W. (2003). Hopi Indians, “cultural” selection, and albinism. American Journal of Physical Anthropology, 121, 151-156.
Zimmer, C. (2008). The Parasite Files. Discover. Dec. 16.
Greg has never published his theory in a peer-reviewed journal, although it is briefly summarized in Cochran et al. (2000). In itself, this is no shortcoming. Most journals seem uninterested nowadays in real debate. But sometimes I wish he would at least pretend he was writing for a journal. He tends to be polemical, as if only political correctness—or sheer stupidity—could motivate his detractors.
His starting point is the same as Miller’s. Male homosexuality makes no sense as a reproductive strategy. It should die out for the same reason that the Shakers did (the Shakers were a Protestant sect dedicated to lifelong celibacy). This point might seem obvious. Or maybe not. The following is an exchange between a germ theory critic and Greg Cochran:
Critic: Is it not likely that human sexuality is in fact a bell curve, with "strict homosexual" on one end and "strict heterosexual" on the other end, and the majority of the people falling somewhere in between? (With the caveat that sexual preference and sexual practice are not necessarily the same thing).
Greg: No, it is not likely. Sheesh. That would make exactly as much sense as a bell curve of food preferences ranging from steak at the left to granite at the right, in which people in the middle liked steak and rocks equally well. Is an even split between a behavior that works and one that never does what you expect from biology? Do you expect half the geese to fly north for the winter? (source)
Since natural selection would tend to eliminate male homosexuality, it should be uncommon—like most genetic conditions that impair one’s ability to survive and reproduce.
First we have to say what ‘common’ means, in this context. Common means common compared to the noise in the system. So 1% is very common: no disease caused by random mutations is anywhere near that common. 1 in 10,000 is surprisingly common, but there are one or two mutation-caused diseases that are in that ballpark, like Duchenne’s muscular dystrophy. Turns out that the gene involved in muscular dystrophy is maybe 20 times longer than the typical gene — there are more opportunities for typos. So 1 in 7000 boys have Duchenne’s muscular dystrophy — that’s as common as a ‘system noise’ disease gets. (Cochran 2004?)
Since male homosexuality is not rare, it cannot have a genetic cause, at least not principally. There may be a genetic predisposition (with around 30-45% heritability, according to twin studies), but this predisposition is interacting with something in the environment. And this something cannot be a recent environmental change, since male homosexuality has been around for a long time.
The only remaining cause would be some kind of infectious agent that selectively alters certain parts of the brain while leaving the rest intact. There are precedents for this sort of thing.
Do we know of diseases in which there are very specific targets—in which certain cell types are damaged or destroyed while neighboring cells are left intact? Sure. In some cases, a pathogen targets a particular cell type and has little effect on anything else. Human parvovirus (also known as fifth disease) hits erythroid precursor cells (the cells that manufacture red cells) and temporarily inhibits red cell production. In type-I diabetes, it seems likely that Coxsackie virus infections (in people with a genetic predisposition, in which HLA type plays a major role) trigger an autoimmune disease that gradually (over a year or so) destroys the islet cells which produce insulin. Other cells are not much affected. (Cochran 2004?)
Such pathogens may be more common than we think. The ones that get our attention—that make us go and see a doctor—are the ones that cause discomfort. But those ones may be a small minority of all pathogens, with most of the others flying under the radar. After all, it is in the pathogen’s own interest to be discrete and not cause too much havoc. It needs a healthy home to live in, until it can spread to another host.
Greg also argues that male homosexuality should be less common in smaller communities than in larger ones—where pathogenic transmission is likelier.
We can deduce a few things about the hypothetical agent causing homosexuality. First, it has a small, but not incredibly small, critical community size. That is the size of the clump of people required to keep the agent going. Some agents, ones in which infection results in permanent immunity, need a _large_ number of people, big enough that there are new infected people showing up by the time it circles the community. Measles for example requires almost half a million people in close proximity. An agent that causes a persistent infection can have a very small community size: I'd guess that Epstein-Barr has a CCS under 50.
Since some communities seem to have no homosexuality at all (Bushmen, some hunter-gatherer groups in Indonesia and the Philippines, pre-contact Polynesians) we can be sure that this hypothetical agent has a critical community size larger than that of Epstein-Barr. More like chickenpox, which has a CCS of about 300 people. Not that I'm saying it _is_ chickenpox, mind you. (Cochran 2005)
Finally, this pathogen may selectively alter sexual orientation for reasons that go beyond those of not harming the host too much. There are, in fact, a number of pathogens that alter the host’s behavior in order to enhance their chances of transmission. The protozoan Toxoplasma gondii causes infected rats to lose their fear of cats, thus enabling it to enter a cat body and complete its life cycle (Wikipedia – Toxoplasmosis). The parasitic worm Euhaplorchis californiensis forms cysts in the brains of infected killifish that cause the fish to swim near the surface of the water and make tight turns that show off their glinting sides, thus enabling the worm to enter a bird’s body (Zimmer, 2008).
As a child, I remember being told that a chicken is an egg’s way of making another egg. If Greg Cochran is right, a gay man is a vehicle that a pathogen has constructed for its own survival and reproduction. Everything else is human-centered delusion.
This is an interesting argument, but it has a few holes. First, some genetic conditions do reach incidences that are comparable to that of male homosexuality (about 3-5% of all men). Abnormal hemoglobin variants can reach high incidences in sub-Saharan Africans and other populations (8% in the case of Hb AS among African Americans). These variants are typically maintained through balancing selection where the heterozygote state provides some protection against malaria. Greg acknowledges that such selection exists but sees it as being confined to malaria protection. Yet balancing selection can exist for many other reasons. For example, one in 200 Hopi is albino, apparently because cultural selection offsets the environmental disadvantages of albinism (Hedrick, 2003).
Second, male homosexuality is frequently reported in small communities, including bands of Amerindian hunter-gatherers. Known as ‘berdaches’, these male homosexuals were described by early European explorers and appear to have existed in pre-contact times, as indicated by origin myths (Desy, 1978). One witness was John Tanner, a white captive who lived among the Ottawa of Ontario and then the Ojibwa of Manitoba until 1828:
Some time in the course of this winter, there came to our lodge one of the sons of the celebrated Ojibbeway chief, called Wesh-ko-bug, (the sweet)... This man was one of those who make themselves women, and are called women by the Indians. There are several of this sort among most, if not all the Indian tribes. They are commonly called A-go-kwa, a word which is expressive of their condition. This creature, called Ozaw-wen-dib, (the yellow head), was now near fifty years old, and had lived with many husbands. I do not know whether she had seen me, or only heard of me, but she soon let me know she had come a long distance to see me, and with the hope of living with me. She often offered herself to me, but not being discouraged with one refusal, she repeated her disgusting advances until I was almost driven from the lodge. (Desy, 1978)
Of course, neither point disproves the germ theory of male homosexuality. An infectious agent may indeed be the cause or one of several causes. If we consider the developmental pathway for heterosexual orientation, there is probably a ‘default’ sequence that leads to sexual interest in men and an ‘override’ sequence that leads to sexual interest in women. The second sequence may be disrupted for many reasons: a psychological trauma, a chemical insult, or an infectious agent in combination with a pre-existing genetic predisposition for incomplete masculinization. As one comment noted:
Some of the disruptive factors implicated by empirical evidence are excess prenatal testosterone exposure (a major factor), prenatal stress, and exotic factors such as disruptive chemical agents. Infections proposed by Cochran may also disrupt development, but I do not know of any evidence that supports this assertion as of yet. (Cochran 2005)
References
Cochran, G.M. (2005). Cause of Homosexuality: Gene or Virus? Cochran Interview. Thrasymachus Online.
Cochran, G.M. (2004?). An evolutionary look at human homosexuality. World of Greg Cochran.
Cochran, G.M., Ewald, P.W., & Cochran, K.D. (2000). Infectious causation of disease: an evolutionary perspective. Perspectives in Biology and Medicine, 43, 406-448.
Désy, P.P. (1978). L'homme-femme. (Les berdaches en Amérique du Nord), Libre — politique, anthropologie, philosophie, 78(3), 57-102.
Hedrick, P.W. (2003). Hopi Indians, “cultural” selection, and albinism. American Journal of Physical Anthropology, 121, 151-156.
Zimmer, C. (2008). The Parasite Files. Discover. Dec. 16.
Thursday, February 12, 2009
Origins of male homosexuality
Male homosexuality has always puzzled evolutionary biologists. It has 30-45% heritability, so there must be some genetic predisposition (Bailey et al., 2000). But how could such a predisposition get passed down from generation to generation? It ought to die out, by its very nature.
Well, not all predispositions are fully expressed. This observation led the economist and evolutionary psychologist Ed Miller to propose that male homosexuality has survived by means of a balanced polymorphism (Miller, 2000). In the human species, the male has to invest more in his offspring, particularly if the female is less able to feed herself and her offspring through food gathering, as in non-tropical environments. To change male behavior in this direction, the fastest way, with the least genetic change, is to partially feminize the male brain. This could be done through heterozygote advantage at some gene loci: if only one allele is changed, a man would become more child-oriented while still being heterosexual; if both alleles are changed, he would also become feminized in his sexual orientation.
But heterosis effects are absent at most loci. There is usually a simple dominant/recessive mode of action. Nonetheless, a balanced polymorphism is still possible through additive effects over many loci. If a certain proportion have alleles for mental feminization, a man will take more interest in his children without becoming feminized in his object of sexual interest. There may, however, be more than one ‘right’ mix of feminization/non-feminization alleles (the number of possible permutations being a function of the number of relevant genes). Even if all men in one generation have the right mix, reshuffling of genes from their generation to the next would produce some male offspring who are too feminized and others not enough.
Of course, this situation would be gradually corrected by natural selection. The ‘right’ mixes would not be exactly equal in their adaptive value. Natural selection would tend to favor some over others and eventually there would be fixation of one mix of alleles. But this would take a long time and paternal investment varies in importance even among the relatively young populations of Homo sapiens—itself a young species.
So this is Miller’s theory: male homosexuality is the tail end of a balanced polymorphism due to selection for men who invest more in rearing their children and provisioning their families. Santtila et al. (2009) tried to test this theory, which they describe as follows:
This isn’t quite what Miller had in mind. Yes, a heterosexual carrier would be less likely to harm his partner and children, but a more critical factor would be his willingness to provide for them. Nor is it necessary to assume that such men are preferred as mates. Their greater reproductive success would come from the higher survival rate of their children. We’re talking natural selection here, not sexual selection.
This misunderstanding affected Santilla et al.’s experimental design. Heterosexual men with homosexual brothers were questioned on a wide range of behaviors: psychopathy, sexual aggression, sexual coercion, sexual activity, and number of children. No questions were asked about interest in children or willingness to care for them. Number of children might inversely correlate with paternal investment (some could die through neglect or insufficient care), but only if there are enough of them. Nowadays, family size is too small for this factor to be significant. Indeed, the heterosexual subjects had each fathered less than one child on average.
No significant differences were found between the heterosexual ‘carriers’ and a control heterosexual group. But it’s not clear to me that a difference should be expected, given the experimental design.
References
Bailey, J.M., M.P. Dunne, & N.G. Martin. (2000). Genetic and environmental influences on sexual orientation and its correlates in an Australian twin sample. Journal of Personality and Social Psychology, 78, 524-536.
Miller, E.M. (2000). Homosexuality, birth order and evolution: Toward an equilibrium reproductive economics of homosexuality. Archives of Sexual Behavior, 29, 1-34.
Santtila, P., A-L. Högbacka, P. Jern, A. Johansson, M. Varjonen, K. Witting, B. von der Pahlen, N. K. Sandnabba. (2009). Testing Miller’s theory of alleles preventing androgenization as an evolutionary explanation for the genetic predisposition for male homosexuality. Evolution and Human Behavior, 30, 58-65.
Well, not all predispositions are fully expressed. This observation led the economist and evolutionary psychologist Ed Miller to propose that male homosexuality has survived by means of a balanced polymorphism (Miller, 2000). In the human species, the male has to invest more in his offspring, particularly if the female is less able to feed herself and her offspring through food gathering, as in non-tropical environments. To change male behavior in this direction, the fastest way, with the least genetic change, is to partially feminize the male brain. This could be done through heterozygote advantage at some gene loci: if only one allele is changed, a man would become more child-oriented while still being heterosexual; if both alleles are changed, he would also become feminized in his sexual orientation.
But heterosis effects are absent at most loci. There is usually a simple dominant/recessive mode of action. Nonetheless, a balanced polymorphism is still possible through additive effects over many loci. If a certain proportion have alleles for mental feminization, a man will take more interest in his children without becoming feminized in his object of sexual interest. There may, however, be more than one ‘right’ mix of feminization/non-feminization alleles (the number of possible permutations being a function of the number of relevant genes). Even if all men in one generation have the right mix, reshuffling of genes from their generation to the next would produce some male offspring who are too feminized and others not enough.
Of course, this situation would be gradually corrected by natural selection. The ‘right’ mixes would not be exactly equal in their adaptive value. Natural selection would tend to favor some over others and eventually there would be fixation of one mix of alleles. But this would take a long time and paternal investment varies in importance even among the relatively young populations of Homo sapiens—itself a young species.
So this is Miller’s theory: male homosexuality is the tail end of a balanced polymorphism due to selection for men who invest more in rearing their children and provisioning their families. Santtila et al. (2009) tried to test this theory, which they describe as follows:
Miller (2000) speculates that if a typical man inherits only a few of the alleles partially preventing androgenization, he would express more kindness, sensitivity, tendermindedness, and empathy. Only occasionally would a sufficient number of these alleles come together to produce homosexuality. Heterosexual carriers of these alleles would be better fathers and more attractive mates as men with such traits are less likely to harm their partner or children (Miller, 2000). These traits in men would help them to attract women and, thus, lead to greater reproductive success, ensuring the survival of the alleles in the gene pool. A heterosexual man without any of these alleles would exhibit traits such as ruthlessness, selfishness, insensitivity, and cruelty, making them unattractive to women.
This isn’t quite what Miller had in mind. Yes, a heterosexual carrier would be less likely to harm his partner and children, but a more critical factor would be his willingness to provide for them. Nor is it necessary to assume that such men are preferred as mates. Their greater reproductive success would come from the higher survival rate of their children. We’re talking natural selection here, not sexual selection.
This misunderstanding affected Santilla et al.’s experimental design. Heterosexual men with homosexual brothers were questioned on a wide range of behaviors: psychopathy, sexual aggression, sexual coercion, sexual activity, and number of children. No questions were asked about interest in children or willingness to care for them. Number of children might inversely correlate with paternal investment (some could die through neglect or insufficient care), but only if there are enough of them. Nowadays, family size is too small for this factor to be significant. Indeed, the heterosexual subjects had each fathered less than one child on average.
No significant differences were found between the heterosexual ‘carriers’ and a control heterosexual group. But it’s not clear to me that a difference should be expected, given the experimental design.
References
Bailey, J.M., M.P. Dunne, & N.G. Martin. (2000). Genetic and environmental influences on sexual orientation and its correlates in an Australian twin sample. Journal of Personality and Social Psychology, 78, 524-536.
Miller, E.M. (2000). Homosexuality, birth order and evolution: Toward an equilibrium reproductive economics of homosexuality. Archives of Sexual Behavior, 29, 1-34.
Santtila, P., A-L. Högbacka, P. Jern, A. Johansson, M. Varjonen, K. Witting, B. von der Pahlen, N. K. Sandnabba. (2009). Testing Miller’s theory of alleles preventing androgenization as an evolutionary explanation for the genetic predisposition for male homosexuality. Evolution and Human Behavior, 30, 58-65.
Labels:
balanced polymorphism,
Ed Miller,
homosexuality
Thursday, February 5, 2009
Bernard Arcand R.I.P.
The anthropologist Bernard Arcand passed away last Friday at the age of 63. He was one of my favorite professors at Laval, probably because he was among the least ideological ones. He avidly read the works of different Marxist writers but never considered himself to be one. In fact, he often criticized the unconscious Marxism that had seeped into much of anthropology, particularly the tendency to classify different populations by their mode of subsistence, notably hunter-gatherers versus agriculturalists. He would point out to us the artificiality of this distinction, and how there was just as much difference within these two categories as between them. In comparison to most agriculturalists, some hunter-gatherers were actually more sedentary, others more densely populated, and others still less egalitarian.
According to Bernard, this unconscious Marxism reflected an economic determinism that was equally popular on the left and the right.
Bernard was also a man of letters who wrote not only academic articles but also readable essays for the public at large, such as Abolissons l'hiver and an essay on pornography called Le jaguar et le tamanoir. His analysis was striking in its originality. To be sure, his works suffered from one shortcoming: very few of them have been translated into English.
He will be missed.
Reference
Arcand, B. (1988). Il n’y a jamais eu de société de chasseurs-cueilleurs. Anthropologie et Sociétés, 12, 39-58.
The Calusa of southern Florida formed a society divided into classes, lived in villages that could hold over 2,000 people, built temples, and kept an army that ensured the payment of tribute needed for a hierarchical system of local chiefdoms. This social complexity and these unequal social relations were supported by a hunting and gathering economy. (Arcand, 1988, p. 43)
According to Bernard, this unconscious Marxism reflected an economic determinism that was equally popular on the left and the right.
… an emergent industrial ideology ... succeeded, mainly in the 19th century, in postulating that the economy has an autonomous status and should be seen as the ultimate determinant of society and culture. The argument is already well known and need not be repeated. Industrial capitalism and its socialist critics affirmed the crucial determining role of the development of productive forces, which would ensure rising productivity and be a key condition for progress and happiness. Despite the radical contrast between their political programs and goals, capitalism and socialism wanted to take over the same producing machine. More humbly placed, the anthropology of hunter-gatherers could not easily claim that everyone was wrong and that this was all just secondary. So it went on pretending that the mode of subsistence was what mattered. (Arcand, 1988, p. 52)
Bernard was also a man of letters who wrote not only academic articles but also readable essays for the public at large, such as Abolissons l'hiver and an essay on pornography called Le jaguar et le tamanoir. His analysis was striking in its originality. To be sure, his works suffered from one shortcoming: very few of them have been translated into English.
He will be missed.
Reference
Arcand, B. (1988). Il n’y a jamais eu de société de chasseurs-cueilleurs. Anthropologie et Sociétés, 12, 39-58.
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