Home » Race Realism » The AR Gene, Aggression and Prostate Cancer: Yet Another Hereditarian Reduction-to-Biology Fails

The AR Gene, Aggression and Prostate Cancer: Yet Another Hereditarian Reduction-to-Biology Fails

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Due to the outright failure in linking testosterone to differences in racial genetics, prostate cancer (PCa) and aggression, those who would still claim genetic or biological causation for differences in PCa incidence and aggression/crime which would then be linked to race needed to search other avenues for their long-awaited discovery and mechanism for the proposed relationships. This is where the AR (androgen receptor) gene comes in. The AR gene allows the creation of androgen receptors, and this is where androgen “dock”, if you will, allowing the physiological system to use it to carry out what it needs to. In this article, I will discuss the AR gene, CAG repeats, aggression, PCa, a just-so story and finally what may explain the differences in PCa acquisition and aggression between races, not appealing to genes.

Though, hereditarianism is concerned with the so-called biological/genetic transmission of socially-desired traits and also genetic causation of socially-undesired traits, due to the fall of the testosterone-causes-aggressive-behavior paradigm, surely some other biological mechanism could explain why blacks have higher rates of aggression, crime and PCa along with testosterone? Surely, if testosterone isn’t driving the relationship, it would somehow be implicated with it, through some other mechanism in some other kind of way? This is where the androgen receptor gene (AR gene) comes into play. So since CAG repeat length is assumed to be related to androgen receptor sensitivity, and since one report states that lower CAG repeats are associated with aggression (Simmons and Roney, 2011), this is where the hereditarian looks to next for their proposed relationships between testosterone, aggression and PCa. Simmons and Roney also, similarly to Rushton’s r/K, claim that “shorter AR-CAG repeats would have been beneficial for males inhabiting tropical regions because this genetic trait would have encouraged an androgenic response, reportedly along with higher testosterone levels” (Oubre, 2020: 293). Just-so stories all the way down.

Racial differences in AR gene and aggression/PCa

Such claims that the AR polymorphism followed racial lines and was correlated with PCa incidence began to appear in the late 1990s (eg, Giovannuci et al, 1997; Pettaway, 1999). It has been shown that the number of CAG repeats on the AR gene is related to heightened activity on the androgen receptor, and that blacks are more likely to have fewer CAG repeats on the AR gene (Sartor et al, 1997; Platz et al, 2000; Bennett et al, 2002; Gilligan et al, 2004; Ackerman et al, 2013). (But also see Gilligan et al (2004), Lange et al, (2008), and Sun and Lee (2013) for contrary evidence to these claims.) African populations have shorter CAG repeats than non-African populations on the AR gene (Samtal et al, 2022), and since carriers or short CAG repeats had a higher incidence of PCa (Weng et al, 2017; Qin et al, 2022), then this would be the next-best spot to look after the testosterone/PCa/aggression hypothesis failed so spectacularly. But since “Androgen receptor (AR) mediates the peripheral effects of testosterone” (Tirabassi et al, 2015), this has been a new haven for the hereditarian to go to and look for their relationship between aggression and biology.

Fewer CAG repeats has been linked to self-reported aggression (Mettman et al, 2014; Butovskaya et al, 2015; Fernandez-Castillo and Cormand, 2016). Though unfortunately for hereditarian theorists, they also need to look elsewhere, since the number of CAG repeats wasn’t related to aggressive behavior in men nor in women (Valenzuela et al, 2022). Vermeer (2010) found no relationship between CAG repeats and adolescent risk-taking, depression, dominance, or self-esteem. These findings are contrary to other claims, such as this from Geniole et al (2019): “Testosterone thus appears to promote human aggression through an AR-related mechanism“. Rajender et al (2008) showed that rapists and murders had fewer CAG repeats than controls (18.44 repeats, 17.59 repeats, and 21.19 repeats respectively). This is significant due to what was referenced above about testosterone modulating human aggression through an androgen receptor mechanism. Butovskaya et al (2012) also found no relationship between the AR gene and any of the aggression subscales they used.

Since shorter CAG repeats on the AR gene were also related to the severity of PCa incidence (Giovannuci et al, 1997), then what explains the 2 times higher incidence of PCa in blacks compared to whites and 3 to 4 times higher incidence in Asians (Hinata and Fujisawa, 2022; Yamoah et al, 2022) should be related to AR gene and CAG repeats. (Though shorter CGN repeats don’t increase PCa risk in whites and blacks; Li et al, 2017.) However, when blacks and whites had similar preventative care, differences almost entirely vanished (Dess et al, 2019; Yamoah et al, 2022). Lewis and Cropp (2020) have a good review of PCa incidence in blacks. Thus, external—not internal—factors influenced mortality rates, and even though there may be some biological factors that cause either a higher incidence of PCa or survival once it metastatizes, that doesn’t preclude the possibility of inequities on healthcare which cause this relationship (Reddick, 2018). But how can we explain this in an evolutionary context, either recently or in the deep past? Don’t worry, the just-so storytellers have us covered.

Just-so stories and androgen receptors

Urological surgeon William Aiken (2011), publishing in the prestigious journal Medical Hypotheses “speculated” that slaves thsg survived the Middle Passage were more sensitive to androgens, which would then protect them from the conditions they found themselves in on the slave ships during the Passage. This, he surmised, is why African descendants are way disproportionately represented in sprinting records and why, then, blacks have a higher incidence of PCa than whites. Aiken (2011: 1122) explains the “reasoning” behind his hypothesis:

This hypothesis emerged from an exploration of the possible interplay between historical events and biological mechanisms resulting in the similarity in the disproportionate racial and geographic distributions in seemingly unrelated phenomena such as sprinting ability and prostate cancer. The hypothesis is equally a synthesis of the interpretations of observations of a disparate nature such as the high incidence and mortality rates of prostate cancer amongst men of African descent in the Americas while West Africans residing in urban West African centre’s have a lower prostate cancer incidence and mortality [2], the 3-fold greater prostate cancer incidence in Afro-Trinidadians compared to Indo Asian-Trinidadians despite exposure to largely similar environmental conditions [5], the improvement in athletic sprinting performance observed when athletes take anabolic steroids [3], the observation that both sprinting ability and prostate cancer are related to specific hand patterns which in turn are related to antenatal exposure to high testosterone levels [6,7], the observation that prostate cancer is androgen-dependent and undergoes involution when testosterone is inhibited or withdrawn [4], the observation that West Africans born in West Africa are under-represented amongst the elite sprinters [1] despite their relatively large populations and despite West Africa being the region of origin of the ancestors of today’s elite sprinters and finally the observation that prostate cancer is related to androgen receptor responsiveness which in turn is related to its CAG-repeat length [8].

One of Aiken’s predictions is that black Americans and Caribbean blacks should have lower shorter CAG repeats than the populations of descent in Africa. Unfortunately for him, West Africans seem to have shorter CAG repeats than descendants of the Middle Passage (Kittles et al, 2001). Not least, neither of the two predictions he proposed to explain the relationship are risky or novel. By risky prediction I mean a hypothesis that would disprove the overarching hypothesis should the relationship not hold under scrutiny. By novel fact I mean a predicted fact that’s not used in the construction of the hypothesis. Quite clearly, Aiken’s hypothesis doesn’t meet this criteria, and so it is a just-so story.

But such fantastical, selection-type stories have been in the media relatively recently. Like Oprah’s and Dr. Oz’s assertions that blacks that survived the Middle Passage did so in virtue of their ability to retain salt during the voyage which then, today, leads to higher incidences of hypertension. This is known as the slavery hypertension hypothesis (Lujan and DiCarlo, 2018) and is, of course, also a just-so story. Just like the just-so story cited above, those Africans who took the voyage across the sea had some kind of advantage which explained why they survived and, consequently, explained relationships between maladies in their descendants. These types of stories—no matter how well-crafted—are nothing more than stories that explain what they purport to explain with no novel evidence that would raise the probability of the hypothesis being true.


Aggression is related to crime, in that it is surmised that more aggressive individuals would then commit more crimes. I’ve noted the failure of hereditarian explanations over the years, so what do I think best explains the relationship between aggression and crime and, ultimately, criminal activity? Well, since crime is an action, it is therefore irreducible. I would propose a kind of situationism in explaining this.

Situational action theory (SAT) (eg Wilkstrom, 2010, 2019) is a cousin of situationism, and is a kind of moral action theory, placing the agent in situations (environments) which then would lead to criminal action as a discourse to take. “The core principle of SAT is that crime is ultimately the outcome of certain ‘kinds of people’ being exposed to certain ‘kinds of situations’” (Messner, 2012). For instance, a good example of this would be for black Americans. Mazur’s (2016) honor culture hypothesis states that blacks who are constantly vigilant for threats to their status and self have higher rates of testosterone in virtue of the fact that aggression increases testosterone.

So this would then be an example of the kind of relationship that SAT would look for. So SAT and the honor culture hypothesis are interactionist in that they recognize the interaction between the agent and the environment (situations) the agent finds themselves in. Violence is merely situational action (Wikstrom and Treiber, 2009), so to explain a violent crime, we need to know the status of the agent and the environment that the crime occurred in, along with the victim and motivating factors for the action in question. The fact of the matter is, actions are irreducible and what is irreducible isn’t physical, so physical (biological) explanations won’t work here. Further, the longer that people stay in criminogenic environments, the more likely they are to commit crime, due to the situations they find themselves in. Thus, a kind of analytic criminology should be employed to discover how and why crimes occur (Wikstrom and Kroneberg, 2022). Considerations in biology should not be looked at when talking about actions and their causes.

Prostate cancer

I have discussed this in the past: What best explains the incidences in PCa between races is diet. For instance, blacks have lower rates of vitamin D than other races (Guiterrez et al, 2022; Thamattoor, 2021). People with lower levels of vitamin D are more likely to acquire PCa, and those with the lowest levels of vitamin D were more likely to have aggressive PCa (Xie et al, 2017). Since consuming high IUs of vitamin D seems to stave off PCa (Khan and Parton, 2004; Naier-Shalliker et al, 2021), and since there seems to be a dose-response relationship between vitamin D consumption and PCa mortality (Song et al, 2018) along wkth vitamin D seeming to reverse low-grade PCa (Samson, 2015), it stands to reason that the higher incidences of PCa in blacks in comparison to whites are due to socio-environmental dietary factors. We don’t need any assumed biological/genetic factors in order to explain the relationship when we know the etiology of PCa.


Due to the old, 1980s and 1990s explanations from hereditarians on the etiology of PCa and aggression with its link to race and testosterone, researchers had to look to other avenues in order to find the “biological etiology” between the relationships. They then pivoted to the AR gene and CAG repeats to explain the relationship between PCa and testosterone when the original testosterone-causes-PCa-and-aggression claim was refuted (Tricker et al, 1996; Book, Starzyk, and Quinsey, 2001; O’Connor et, 2002; Stattin et al, 2004; Archer, Graham-Kevan, and Davies, 2005Book and Quinsey, 2005; Michaud, Billups, and Partin, 2015; Boyle et al, 2016).

But as can be seen, again, the relationships between the proposed explanations in order to continue pushing their biological/genetic theories of PCa and aggression linked with testosterone and race also fails. Rushton’s r/K theory, for instance, implicated testosterone as a “master switch” (Rushton, 1999). Attempted reductions to biology were also seen in (the now-retracted) Rushton and Templer (2012) (see responses here and here). Reductions to biology quite clearly fail, but that doesn’t deter the hereditarian from pushing the racist theory that genes and biology explain the poor outcomes of blacks.


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