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.

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.

13 comments:

Anonymous said...

Anaerobic biotransformation of estrogens seems to be consistent with estrogen getting to non-trivial levels in cold bodies of water. Presumably this would have been where population density was greatest; the higher rate of homosexuality for men born in cities is now less convincing evidence for viral transmission.

Homosexuality in the younger cohort ought to have changed since the seventies as the ratio of exclusive to faculative of at least 2:1 declined probably more than reversed.
According to Bailey 97 study of men seeking men personal adverts " On average, gay men preferred men who described themselves as masculine" . Assuming that the exclusively gay tend to be 'effeminate' their becoming more scarce should have become noticable by now.

Can it really be true that most exclusively gay men are pushing 50 years old?


(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.
While Swedish mothers were not starving there was less food about; they were less likely to be overweight Is there an association between maternal weight and the risk of testicular cancer? An epidemiologic study of Norwegian data with emphasis on WW2 "increase in TC incidence over the past decades could be at least partly attributed to the increased maternal body weight observed in most populations in the relevant time period since TC is thought to be associated with in utero conditions."
It might also be relevant that "If a mother is overweight or obese this may interfere with both the initiation and duration of breast feeding".)

Anonymous said...

Tod you said the following:

"Presumably this would have been where population density was greatest; the higher rate of homosexuality for men born in cities is now less convincing evidence for viral transmission."

I'm confused by your comment. Viral trasmissions of pathogens are easier in urban settings.


I am baffled by this statement as well: "Homosexuality in the younger cohort ought to have changed since the seventies as the ratio of exclusive to facultative of at least 2:1 declined probably more than reversed." What's your source for the ratio you state? It's been hard enough for researchers to establish the percentage of what is preferential homosexuality (3-5% is usually the range I most see stated) much less establish any figures for exclusive vs. faculative behaviors.

And this too: You state Bailey's
'97 study stating that, "On average, gay men preferred men who described themselves as masculine." Your follow-up is, "Assuming that the exclusively gay tend to be 'effeminate' their becoming more scarce should have become more noticeableby now."

IIRC, most such studies show that the male image most favored/desired by gay men is one they view as "masculine." There's no surprise there. Also, the same research shows an aversion among most gay men to viewing themselves as on the fem side (quite aside from how straights might view them.) Studies also show that gay men usually wind up with men much like themselves: the more fem they are, the more fem the partner they attract. This is pretty much how it goes in the straight world, isnt it? People who are often physically similar (attractive/average/not-so-attractive)often pair up with those who are viewed similarly. The more attractive the man/woman, usually the more attractive his/her date/mate/spouse.


I don't understand why you believe that it's the more "feminine" among gays that tend to be exclusively gay unless you are omitting the usual adolescent or very early in adulthood hetero experiences with girls/women that a very high percentage of gay boys attempt. Are you?

As a function of style and as the movement of gay pride moved into the public square (think of groups like the Village People)there came about an openness in which gay men in the cities felt free to publically embrace their masculine fantasies (the muscular construction worker, the cop, the Indian chief, etc.) Gay men seem to have discovered, along with the rest of America, that men, like women, could/should work to improve their overall appearance/health. Visits to the gym increased for much of the American population, gay men included. New emphasis on muscles, the body. If homosexuality needed no longer to be hidden, to be practiced in the deep of night in a men's public restroom, if social stigmas were relaxing enough to allow more open expression, then competition was now in play: looks mattered, to the gym they went.


What I am trying to say is that gay men, even the most feminine among them, have probably always seen the masculine (here "masculine" refers to bodily appearance) as attractive, but were not in a position to go up to a manly-appearing guy and hit on him w/out execting a fist in the face.

All that has really changed is that social changes have resulted in a lot of members of the gay community feeling free to be open and to compete for one another. How do they do this? Especially the young to whom looks are always of special importance? They primp, they try to buff those muscles, they try to attract with the body, particularly by trying to look like what they have idolized all along--the hypermasculine ideal now that they feel free to do so.

It is interesting to note that in their eyes, "masculine" seems limited to body type and size of muscles. A straight man or straight woman's idea of masculine takes into consideration a great deal more than that.

Again, another confusing statement--you ask, "Can it be that most exclusively gay men are pushing 50 years old?"

Are you suggesting that gay men younger than 50 are more bisexual in their behavior than men over 50?
If so, your source?

Anonymous said...

Another interesting concept is masculinization of female brains and behavior. There seems to be plenty of experimental evidence from other animals (esp mice etc) that high testosterone levels can masculinize female behavior.

I wonder to what extent female homosexuality is mediated by high levels of testosterone caused by CAH?

Anonymous said...

I thought that estrogen levels too high in the male body produced man boobs?

If so, shouldn't there be a lot of gay men out there who need to wear a bra? Where's Kramer and George's father with their "bro"?

Seriously, wouldn't high estrogen levels have created male mammaries that we'd have noticed by now?

Jason Malloy said...

If so, shouldn't there be a lot of gay men out there who need to wear a bra?


Gynecomastia does have an association with homosexuality.

This was first noted by Johannes Lange in his study of monozygotic twins in 'Crime as Destiny' (1931). One MZ twin was gay, the other was straight. The gay one had breasts.

Later, John Money found that 8 of 41 youths (20%) with idiopathic adolescent gynecomastia were homosexual, and reported having gender atypical behavior long before puberty. (a control group with gynecomastia due to prenatal hyper-masculization, had 1 homosexual out of 33, which is normal.)

Anonymous said...

Tod,

Thanks for the reference!! I was looking for a study on the fate of estrogen in cold bodies of water.

In theory, there should be less exclusive male homosexuality in age cohorts that follow the 1970s shift to secondary treatment of wastewater, i.e., people under 35 years old. In practice, this would be difficult to prove. There is still disagreement over the percentage of exclusive male homosexuality. The best estimates fall in the 3-5% range, but there are still people who cite the 'one-in-ten' figure.

Dear all,

There may be a correlation between exclusive male homosexuality and other indices of estrogenization (e.g., breast development, higher-pitched voice, testicular cancer, low sperm count, etc.) On the other hand, early estrogen exposure may be interacting with a genetic predisposition that itself varies within the male population.

In my opinion, this genetic predisposition has been identified by Ed Miller, i.e., weakened heterosexuality as a result of selection for men who invest more in their children and are more monogamous. But I don't think this evolutionary change, in itself, led to the level of 3-5% male homosexuality we now have. I'm pretty convinced that this level is a recent phenomenon and is not simply due to gays 'coming out of the closet'.

Anonymous said...

Peter,

If you've a hypothesis that in the late 19th century and into the 20th century a higher number of men were "exclusively" homosexual than had been so in previous centuries, in order to argue that point effectively, you need reliable estimates of the percentage who were "exclusively" homosexual previous to that. I don't see that you have such data. No one does.

Admittedly, if you did have such data, I'd still ask you to clarify what you mean by "exclusive homosexuality." Exclusive in practice? Or in thoughts?

After all, Bailey, on whose research you've relied to make another point, argues against the existence of true bi-sexuality. At least he claims he has not been able to find it. Yes, he says, there are those who engage in sex with both men and women, but he's not found those for whom both men and women cause anything resembling equal physical arousal.

Doesn't research suggest that many gay men performed with women, particularly when young and struggling to fit in and be heterosexual, but that they did so with less enthusiasm and with less excitation than when they performed with men? And, in such relationships with women, doesn't research show that such men admit to having to fantasize about men in order to perform with women?

Isn't it likely that these are the gays of yesteryears? Isn't it likely that today such men are increasingly likely to be in the openly gay community where they can be "exclusively" gay?

I guess we disagree on this, but I do think your findings about estrogen in the drinking and bathing water to be quite interesting.

Anonymous said...

Decay of endocrine-disrupting chemicals in aerobic and anoxic groundwater
Hypoxia or oxygen depletion conditions seems to be the most important factor.

Anonymous said...

Isn't it much easier to assume that Testicular cancer is caused by a common STD? Kids don't get it, and old people might have less susceptability or increased immunity.

Anonymous said...

"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."

How does this waste system of the late 19th C. in North America and northern Europe compare to how waste was deposited in southern Europe, say Italy and Greece or in Central and South America during the same time frame?

Anonymous said...

I live in a university setting in a liberal area of the country. That is, there are a lot of openly gay men in this community as a whole and on this large college campus.

I can't see evidence that these guys are more masculine than those of other generations.

It does seem they are pretty interested in their bodies but in all other ways they still seem much more feminine in mannerisms and in the kinds of things they are interested in than the average straight guy.

Anonymous said...

Change in urban gay communities
seems consistent with "...less exclusive male homosexuality in age cohorts that follow the 1970s shift to secondary treatment of wastewater, i.e., people under 35 years ". The study: Are gay communities dying or just in transition?

Anonymous said...

Anon (1),

Prior to the late 19th century, there are frequent references to male homosexuality, but it is usually of the facultative sort, i.e., older heterosexual men who seek sex with boys or servile men. Exclusive male homosexuality is mentioned only rarely.

Then, sometime in the late 19th century, this situation reversed. A number of authors have commented on this shift, including Foucault. You seem to suggest that this shift is an artefact of a change in public attitudes, i.e., people became more accepting of exclusive male homosexuality, so more of it 'came out of the closet'. This argument is plausible for the late 20th century. Is it plausible for the late 19th century?

Anon (2),

If testicular cancer were due to an STD, there wouldn't be a birth cohort effect. The birth cohort effect points to a prenatal or neonatal causation.

Anon (3),

Modern sewer systems were introduced to Western Europe, the United States, and Canada in the late 19th century. They're more recent elsewhere in the world. In any case, the temperature of water bodies is also a factor. Decomposition of the estrogen molecule in lake water seems to reflect three factors: 1) temperature; 2) presence of organic matter (and nitrifying bacteria); and 3) level of oxygen. For these reasons, estrogen retention seems to be optimal at northern latitudes in cold, clear bodies of water with low oxygen levels.

Anon (4),

It would be difficult to prove this point either way. For one thing, modern gay culture tends to overcompensate by adopting cultural markers of masculinity. For another thing, I would not expect to see a strong correlation between effeminacy and exclusive male homosexuality. It's possible for a man to have a weak heterosexual orientation and still score relatively high on other indices of masculinity.


Tod,

Thanks!!