Human populations vary in their incidence of polygyny. In general, the more it costs a man to provide for a second wife, the less the population will be polygynous. This cost is highest among arctic hunter-gatherers, where women depend on meat from men to feed themselves and their children. It is lower among tropical hunter-gatherers, where women need less male provisioning because they can gather fruits, vegetables, and tubers. Finally, the cost becomes negative among tropical agricultural peoples, where a woman is able to raise enough food through year-round farming to feed herself and her children, with little assistance from a male provider.
In the last group of societies, men best serve their reproductive fitness by having as many wives as possible. Result: a relative shortage of wives and intense male-male competition for the few women available. Highly polygynous societies usually deal with this problem by raising the age of marriage for men, typically by ten years past the age of puberty. Such a constraint may be imposed formally or informally. Often, a man may not marry until he has proven himself as a warrior or has attained a certain standing within the community.
This social rule has the effect of concentrating male sexual competition among young adults. Over time, the resulting selection pressure may have led to the higher levels of blood testosterone that we see in tropical agricultural peoples of sub-Saharan Africa and Papua-New Guinea, where 20 to 50% of all marriages are polygynous (see previous post). In particular, it may explain why this hormonal advantage seems to be limited to young men. Testosterone levels are higher in black boys than in white boys as early as 5 to 9 years of age (Abdelrahaman et al., 2005). In black males, these levels peak during adolescence and early adulthood (Ross et al., 1986; Winters et al., 2001). The black-white difference then shrinks after 24 years of age and is gone by the early 30s (Gapstur et al., 2002). It actually seems to reverse in later years (Nyborg, 1994, p. 111-113).
Broadly speaking, lifetime exposure to testosterone correlates with the incidence of prostate cancer. The highest incidences in the world are among African American men (Brawley and Kramer, 1996). It was once thought that lower incidences prevail in other populations of black African descent (i.e., West Indians and sub-Saharan Africans), but this difference has since been shown to reflect underreporting (Glover et al., 1998; Ogunbiyi and Shittu, 1999; Osegbe, 1997). Conversely, the lowest incidences are among East Asians (Ross et al., 1992).
Testosterone has a wide range of physiological, morphological, and behavioral effects that in one way or another improve male reproductive success, particularly under conditions of intense sexual competition. These effects may be achieved not only by raising the concentration of testosterone in the bloodstream, but also by making androgen receptors more effective or by converting testosterone into the physiologically more active DHT (5α-dihydrotestosterone). Because such changes multiply the actual impact of testosterone on the human organism, we may underestimate this impact by looking only at blood testosterone levels. For instance, East Asians have the lowest incidences of prostrate cancer, yet their blood testosterone levels are intermediate between those of white and black Americans. They do, however, have less 5α-reductase than either white or black Americans, this being the enzyme that converts testosterone into DHT (Ross et al., 1992).
There is other evidence that human populations vary not only in blood testosterone levels, but also in testosterone/DHT conversion and in androgen receptor activity. It has been shown that androgen receptors seem to be more numerous and more receptive in African-American subjects (Kittles et al., 2001). Now, another study has looked at the other extreme of human variation. Giwercman et al. (2007) have found that Inuit Greenlanders have very low levels of prostate cancer because they have fewer alleles of the sort that increase androgen receptor activity or facilitate testosterone to DHT conversion.
The difference was striking, even in comparison with Swedish subjects—whose incidence of prostrate cancer falls within the world average. The authors concluded:
Our results suggest that Greenlanders are genetically predisposed to a lower activity in testosterone to 5α-dihydrotestosterone turnover and to lower AR activity, which, at least partly, could explain their low incidence of prostate cancer.
Abdelrahaman, E., Raghavan, S., Baker, L., Weinrich, M., and Winters, S.J. (2005). Racial difference in circulating sex hormone-binding globulin levels in prepubertal boys. Metabolism, 54, 91-96.
Brawley, O.W. and Kramer B.S. (1996). Epidemiology of prostate cancer. In Volgelsang, N.J., Scardino, P.T., Shipley, W.U., and Coffey, D.S. (eds). Comprehensive textbook of genitourinary oncology. Baltimore: Williams and Wilkins,
Gapstur, S.M., Gann, P.H., Kopp, P., Colangelo, L., Longcope, C., and Liu, K. (2002). Serum androgen concentrations in young men: A longitudinal analysis of associations with age, obesity, and race. The CARDIA male hormone study. Cancer Epidemiology, Biomarkers & Prevention, 11, 1041-1047.
Giwercman, C., A. Giwercman, H.S. Pedersen, G. Toft, K. Lundin, J-P. Bonde, and Y.L. Giwercman. (2007). Polymorphisms in genes regulating androgen activity among prostate cancer low-risk Inuit men and high-risk Scandinavians. International Journal of Andrology, 31, 25-30.
Glover, F., Coffey, D., et al. (1998). The epidemiology of prostate cancer in Jamaica. Journal of Urology, 159, 1984-1987.
Kittles, R.A., Young, D., Weinrich, S., Hudson, J., Argyropoulos, G., Ukoli, F., Adams-Campbell, L., and Dunston, G.M. (2001). Extent of linkage disequilibrium between the androgen receptor gene CAG and GGC repeats in human populations: implications for prostate cancer risk. Human Genetics, 109, 253-261.
Nyborg, H. (1994). Hormones, Sex, and Society. The Science of Physiology. Westport (Conn.): Praeger.
Ogunbiyi, J. and Shittu, O. (1999). Increased incidence of prostate cancer in Nigerians. Journal of the National Medical Association, 3, 159-164.Osegbe, D. (1997). Prostate cancer in Nigerians: facts and non-facts. Journal of Urology, 157, 1340.
Ross, R.K., Bernstein, L., Lobo, R.A., Shimizu, H., Stanczyk, F.Z., Pike, M.C., and Henderson, B.E. (1992). 5-apha-reductase activity and risk of prostate cancer among Japanese and US white and black males. Lancet, 339, 887-889.
Ross, R., Bernstein, L., Judd, H., Hanisch, R., Pike, M., and Henderson, B. (1986). Serum testosterone levels in healthy young black and white men. Journal of the National Cancer Institute, 76, 45-48.
Winters, S.J., Brufsky, A., Weissfeld, J., Trump, D.L., Dyky, M.A., and Hadeed, V. (2001). Testosterone, sex hormone-binding globulin, and body composition in young adult African American and Caucasian men. Metabolism, 50, 1242-1247.