Among well-nourished populations of Westerners, men's high testosterone levels represent an outlier of cross‐cultural variation; probably due to intrasexual competition in reproductive contexts; it increases prostate cancer risk

From 2012... Do evolutionary life‐history trade‐offs influence prostate cancer risk? A review of population variation in testosterone levels and prostate cancer disparities. Louis Calistro Alvarado. Evolutionary Applications, December 11 2012. https://doi.org/10.1111/eva.12036

Abstract: An accumulation of evidence suggests that increased exposure to androgens is associated with prostate cancer risk. The unrestricted energy budget that is typical of Western diets represents a novel departure from the conditions in which men's steroid physiology evolved and is capable of supporting distinctly elevated testosterone levels. Although nutritional constraints likely underlie divergent patterns of testosterone secretion between Westernized and non‐Western men, considerable variability exists in men's testosterone levels and prostate cancer rates within Westernized populations. Here, I use evolutionary life history theory as a framework to examine prostate cancer risk. Life history theory posits trade-offs between investment in early reproduction and long-term survival. One corollary of life history theory is the ‘challenge hypothesis’, which predicts that males augment testosterone levels in response to intrasexual competition occurring within reproductive contexts. Understanding men's evolved steroid physiology may contribute toward understanding susceptibility to prostate cancer. Among well-nourished populations of Westerners, men's testosterone levels already represent an outlier of cross‐cultural variation. I hypothesize that Westernized men in aggressive social environments, characterized by intense male–male competition, will further augment testosterone production aggravating prostate cancer risk.



Discussion

Modern Westernized environments represent a clear deviation from the environment in which male reproductive physiology evolved. Largely removed from energetic constraint and pathogen burden, Westernized men are capable of supporting distinctly elevated testosterone at the upper limit of human variability and amplifying the incidence of hormone‐sensitive cancer. Variation in nutritional status can largely account for observed disparities in men's testosterone levels and prostate cancer between Westernized and non‐Western populations, but not within Westernized populations—the populations at highest risk of prostate cancer. By incorporating a challenge hypothesis framework, another source of lifetime variation in testosterone exposure was proposed: Aggressive social environments affect prostate cancer incidence through the responsiveness of male androgen physiology to challenges, specifically among Westerners who are able to support the energetic costs of high testosterone levels. I reviewed literature which showed that ancestry, a widely recognized risk factor for prostate cancer, is in and of itself biologically unimportant when accounting for lifestyle factors. For instance, population disparities in testosterone levels of black‐and white‐American men become attenuated and nonsignificant when comparing among college‐educated men from similar backgrounds (Mazur 1995, 2006). And in a nationally representative sample, there was no significant difference in testosterone levels of black‐and white‐American men after accounting for differences in anthropometry (age and body fat percentage) and lifestyle factors (drug use and physical activity) (Rohrmann et al. 2007). To reiterate, there is surprisingly little evidence to suggest that testosterone levels are a direct consequence of ancestry. And as discussed earlier, men of lower SES, regardless of ethnicity, demonstrate higher rates of male–male violence, higher testosterone levels, and higher prostate cancer. Using ancestry as a putative biomarker of prostate cancer risk is effective only to the extent which it tracks environmental circumstances and living conditions that influence cancer risk.

Additionally, I argued that poverty and compromised male investment lead to prioritized mating effort and increased male–male competition, culminating into chronically elevated testosterone and higher rates of prostate cancer. This general trend would be expected only if inequity in wealth distribution translated into more agonistic interactions between males at the population level. In other words, if the relationship between poverty and aggressive social environments is moderated, then there would be little expectation for lower SES to contribute to prostate cancer risk. Norwegian men, for example, deviate from the normally observed correlation between low SES and increased prostate cancer risk. This is particularly interesting because of the sizeable welfare program that is characteristic of Nordic social policy (Sachs 2006), which is associated with some of the lowest crime rates, violent or otherwise (Barclay et al. 2001). As such, Norway invests heavily in poverty reduction, boasts the lowest homicide rate within the developed world, and does not exhibit a concentration of prostate cancer among men of lower SES. Taken together, it would appear that comprehensive social programs might decouple socioeconomic differentials from male–male violence and prostate cancer risk, and may provide a surprising example of how improved social policies and poverty alleviation strategies are fundamental to the interest of public health.

And finally, the challenge hypothesis framework developed in this review may have occupational health implications, considering that men's testosterone levels vary according to occupational status (Dabbs 1992), and that some professions carry a disproportionate risk of prostate cancer (Demers et al. 1994; Zeegers et al. 2004). Dabbs (1992) and colleagues (1998) found that blue‐collar workers have higher salivary and serum testosterone than white‐collar workers. However, distinct social contexts within a profession can also give rise to differences in testosterone levels. Although lawyers as a group are white‐collar workers, trial lawyers have significantly higher salivary testosterone than nontrial lawyers, which has been attributed to the polemical nature of face‐to‐face litigation (Dabbs et al. 1998). If this pattern of elevated testosterone from agonistic interactions persists across occupations, it seems reasonable to expect that men in professions with a higher intensity of competitive interaction would exhibit a greater incidence of prostate cancer. Findings from an extensive cohort study of 58,279 Western European men (ages 55–69 years) from 20 separate occupations are consistent with this reasoning (Zeegers et al. 2004). After accounting for individual characteristics and lifestyle factors (age, diet, drug and alcohol use, education, family disease history, and physical activity), it was police officers who showed the highest relative risk for prostate cancer. Indeed, prostate cancer risk increased 67% for each 10 years of occupational duty as a policeman. The framework proposed here can explain these seemingly peculiar associations between career choice and prostate cancer risk.