I don't necessarily agree that it's "unlikely that population differences in reproductive endocrine function are the result of genetic polymorphisms". What is clear, however, is that (1) the role of genetics (if any) in population differences in sex hormone levels is far from being fully ascertained, and (2) the differences that exist do not consistently line up with Rushton's assumptions/predictions.
Richard Bribiescas [1]:
Medical literature focuses primarily on the physiology of individuals from industrial nations. this is especailly true in endocrinology since hormone measurements have typically involved costly tests that require careful treatment of perishable samples. However, recent advances in sample storage techniques and the advent of robust and more sensitive assays have resulted in significant growth in our knowledge of reproductive hormone physiology in nonwestern populations who are more representative of humans around the globe (Ellison 1994).
The earliest endocrinological studies of male reproductive function consistently suggested that interpopulation variation may be related to ecological factors. In the 1940s, Africans were reported to exhibit what was then called "estrinization," that is, elevated levels of estrogens (Davies 1949). Other researchers echoed these results, suggesting that indigenous Africans had higher levels of estrogens than did Europeans (Bersohn and Oelofse 1957). However, no explanatory mechanism was ever found.
With the advent of salivary steroid assays, data from remote populations grew steadily (Figure 5.1). The ability to store salivary samples at ambient temperatures without refrigeration as well as the reflection of only free bioactive steroid in circulation makes this methodology ideal for biological anthropologists (Ellison 1988; Lipson and Ellison 1989). In addition to finding significantly lower progesterone levels in Lese women (Ellison et al. 1989b), researchers note that Efe and Lese men exhibit significantly lower salivary testosterone levels compared to Boston men (Bently et al. 1993; Ellison et al. 1989a). other African populations such as the !Kung (Christiansen 1991b) and Namibians (Christiansen 1991a) presented salivary testosterone levels significantly lower than western samples. Interestingly, Turkana males of Kenya exhibit testosterone levels that are not different from those of western populations despite their extreme leanness (Campbell et al. 1995).
Other nonwestern populations also exhibited significant variation. Urinary testosterone levels were shown to differ between Bolivian men living at high altitude and men at sea level (Guerra-Garcia et al. 1969). Moreover, undernourished Indian men exhibited blunted testosterone response to hCG stimulation, suggesting that developmental processes underlie adult Leydig cell insensitivity (Smith et al. 1975). Among New World populations presenting lower salivary testosterone levels compared with those of American males are the Ache of Paraguay (Bribiescas 1996, 1997) and the Aymara of Bolivia (Beall et al. 1992), although there is no evidence to suggest that low salivary testosterone levels among these populations are indicative of subfecundity (Galard at al. 1987). The Gainj of New Guinea manifest high FSH levels in otherwise healthy mean, a reflection of possible Sertoli cell insensitivity. The investigators suggest that this may indicate male subfecundity, although sperm couns were not available (Campbell 1994).
Salivary testosterone measurements of healthy urban men in Venezuela, Poland, Zimbabwe, and Japan have shown that the distinction between American and non-American populations is even more profound than previously suspected. Salivary testosterone levels from these urban populations, with the exception of Polish men, were lower than those for Americans. Moreover, modest age-related declines in salivary testosterone were noted relative to Americans (Campbell et al. 2000; Ellison et al. 1998).
It is unlikely that population differences in reproductive endocrine function are the result of genetic polymorphisms. With the exception of extremely rare gonadotropin transcription mutations that may be inherent to specific communities (Tapanainen et al. 1997), and perhaps testosterone hormone binding globulin (TeBG) (Larrea et al. 1995), there is little evidence to suggest that genetic population differences in gonadotropin production or transcription underlie population variation (Jameson 1996). Genetic differences in receptor affinities area possibility, but evidence is lacking. Most likely, chronic dietary intake and activity patterns during development are at the core of population variation. For example, poor urban youths in Kenya revealed significantly lower FSH levels in urinary gonadotropins compared with economically privileged Kenyan adolescents (Kulin et al. 1984).
Sperm count. Sperm counts have been reported to vary between populations (Fisch et al. 1996), although the differences do not suggest any differences in fecundability (Cooper et al. 1991). Longitudinal studies of nonwestern populations are few; however, available evidence does not indicate any significant temporal changes in sperm counts or semen quality (Seo et al. 2000; Tortolero et al. 1999).
Prostate cancer risk. Steroid-sensitive cancers vary significantly across populations (Rose et al. 1986). Although caution is merited when attempting to examine the etiology of disease by race owing to the ambiguous and often misleading nature of this classification (Lewontin 1972), certain communities do exhibit differential rates of prostate disease. African-American males have a twofold higher risk of contracting prostate cancer compared with non-African-American males and present significantly higher androgen levels (Ross et al. 1986). Given the central role of androgens in promoting prostate carcinomas (Henderson et al. 1982), differences in community steroid levels are noteworthy, although the relationship between individual lifetime androgen levels and prostate cancer risk remains unclear (Carter et al. 1995).
Environmental factors such as diet and activity patters warrant close attention because of their impact on the neuroendocrine system (Key 1995). Nigerian males exhibit less aggressive bouts of prostate cancer as well as lower androgen levels than do urban African-American males, suggesting that lifestyle differences before and after adolescence, such as diet, stress, and activity, may influence population risk (Jackson et al. 1977; Sminzu et al. 1991).
Data from nonwestern populations as well as ethnic differences in prostate cancer risk imply that population variation in testosterone levels reflects hormonal release in American populations rather than hormonal suppression among nonwestern populations. Ethnic differences in cancer risk and androgen levels also underscore the importance of developing an increased awareness of population variation in neuroendocrine function as well as the central role of environmental factors such as diet, activity, and stress. As suggested in reference to female reproductive endocrine function (Ellison 1994), clinical research on American male population must be viewed as representative of the extreme range of human variability and not the common or "healthiest" representation of Homo sapiens.
[1] pp. 116-119. "Reproductive Physiology of the Human Male: An Evolutionary and Life History Perspective". In
Reproductive Ecology and Human Evolution. Evolutionary foundations of human behavior. New York: Aldine de Gruyter, 2001.
