Testosterone is a fascinating hormone—the most well-known hormone to the lay public. What isn’t well-known to the lay public is how the hormone is produced and the reasons why it gets elevated. I’ve covered racial differences in testosterone in regards to crime, penis size and Rushton’s overall misuse of r/K selection theory. In this article, I will talk about what raises and decreases testosterone, as well as speak about racial differences in testosterone again since it’s such a fun topic to cover.
JP Rushton writes, in his 1995 article titled Race and Crime: An International Dilemma:
One study, published in the 1993 issue of Criminology by Alan Booth and D. Wayne Osgood, showed clear evidence of a testosterone-crime link based on an analysis of 4,462 U.S. military personnel. Other studies have linked testosterone to an aggressive and impulsive personality, to a lack of empathy, and to sexual behavior.
Booth and Osgood (1993: 93) do state that “This pattern of results supports the conclusions that (I) testosterone is one of a larger constellation of factors contributing to a general latent propensity toward deviance and (2) the influence of testosterone on adult deviance is closely tied to social factors.” However, as I have extensively documented, the correlation between testosterone and aggression is extremely low (Archer, 1991; Book et al (2001); Archer, Graham-Kevan and Davies, 2005), and therefore cannot be the cause of crime.
Another reason why testosterone is not the cause of aggression/deviant behavior is due to what times most crimes are committed at. Therefore, testosterone cannot possibly be the cause of crime. I’ve also shown that, contrary to popular belief, blacks don’t have higher levels testosterone than whites, along with the fact that testosterone does not cause prostate cancer, that even if blacks did have these supposed higher levels of the hormone, that it would NOT explain higher rates of crime.
Wu et al (1995) show that Asian Americans had the highest testosterone levels, African Americans were intermediate and European Americans were last, after adjustments for BMI and age were made. Though, I’ve shown in larger samples that, if there is any difference at all (and a lot of studies show no difference), it is a small advantage favoring blacks. We then are faced with the conclusion that this would not explain disease prevalence nor higher rates of crime or aggression.
Testosterone, contrary to Rushton’s (1999) assertion, is not a ‘master switch’. Rushton, of course, cites Ross et al (1986) which I’ve tirelessly rebutted. Assay times were all over the place (between 10 am and 3 pm) with testosterone levels being highest at 8 am. The most important physiological variable in Rushton’s model is testosterone, and without his highly selected studies, his narrative falls apart. Testosterone doesn’t cause crime, aggression, nor prostate cancer.
The most important take away is this: Rushton’s r/K theory hinges on 1) blacks having higher levels of testosterone than whites and 2) that these higher levels of testosterone then influence higher levels of aggression which lead to crime and then prostate cancer. Even then, Sridhar et al (2010) meta-analyzed 17 articles which talk about racial differences in prostate cancer survival rates. They state in their conclusion that “there are no differences between African American and Whites in survival from prostate cancer.” Zagars et al (1998) show that there were no significant racial differences in serum testosterone. Furthermore, when matched for major prognostic factors “the outcome for clinically local–regional prostate cancer does not depend on race (6,7,14–19). Moreover there appear to be no racial differences in the response of advanced prostate cancer to androgen ablation (29,47). Our study provides further evidence that racial differences in disease outcome are absent for clinically localized prostate cancer” (Zagars et al, 1998: 521). So it seems that these two studies also provide further support that Rushton et al were wrong in regards to prostate cancer mortality as well.
Rushton (1997 185) writes:
In any case, socialization cannot account for the early onset of the traits, the speed of dental and other maturational variables, the size of the brain, the number of gametes produced, the physiological differences in testosterone, nor the evidence on cross-cultural consistency.
There are no racial differences in testosterone and if there were, social factors would explain the difference between the races. However, as I’ve noted in the past, testosterone levels are high in young black males with low educational attainment (Mazur, 2016). The higher levels of testosterone in blacks compared to whites (which, if you look at figure 1 the levels are not high at all) is accounted for by honor culture, a social variable. Furthermore, the effects of the environment are also more notable on testosterone than are genetics at 5 months of age (Carmaschi et al, 2010). Environmental factors greatly influence testosterone (Booth et al, 2006), so Rushton stating that “socialization cannot account for the early onset” of “physiological differences in testosterone” is clearly wrong since environmental influences can be seen in infants as well as adults. Testosterone is strongly mediated by the environment; this is not up for debate.
Testosterone is one of many important hormones in the body; the races do not differ in the variable. So, therefore, all of Rushton’s ‘r/K predictions’, which literally hinge on testosterone (Lynn, 1990) fall apart without this ‘master switch’ (Rushton, 1999) driving all of these behaviors. Any theories of crime that include testosterone as a main driver in crime need to be rethunk; numerous studies attest to the fact that testosterone does not cause crime. Racial differences in testosterone only appear in small studies and the studies that do show these differences get touted around all the while, all of the better, larger analyses don’t get talked about because it goes against a certain narrative.
Finally, there is no inevitability of a testosterone decrease in older men. So-called “age-related declines” in the hormone are largely explained by smoking, obesity, chronic disease, marital status, and depression (Shi et al, 2013), and even becoming a father explains lower levels of testosterone (Gray, Yang, and Pope, 2006). On top of that, marriage also reduces testosterone, with men who went from unmarried to married showing a sharp decline in testosterone over a ten-year period (Holmboe et al, 2017). This corroborates numerous other studies showing that marriage lowers testosterone levels in men (Mazur and Michalek, 1998; Nansunga et al, 2014) But some of this decrease may be lessened by frequent sexual intercourse (Gettler et al, 2013). So if you live a healthy lifestyle, the testosterone decrease that plagues most men won’t occur to you. The decreases are due to lifestyle changes; not explicitly tied to age.
People are afraid of higher levels of testosterone at a young age and equally as terrified of lowering testosterone levels at an old age. However, I’ve exhasutively shown that testosterone is not the boogeyman, nor the ‘master switch’ (Rushton, 1999) it’s made out to be. There are no ‘genes for’ testosterone; its production is indirect through DNA. Thusly, if you keep an active lifestyle, don’t become obese, and don’t become depressed, you can bypass the so-called testosterone decrease. Fear mongering on both sides of the ‘testosterone curve’ are seriously blown out of proportion. Testosterone doesn’t cause crime, aggression, nor prostate cancer (even then, large meta-analyses show no difference in PCa mortality between blacks and whites).
The fear of the hormone testosterone is due to ignornace of what it does in the body and how it is produced in the body. If people were to understand the hormone, they would not fear it.