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Ross et al (1986) is one of the most oft-cited papers that HBDers use to attempt to show that blacks have higher levels of testosterone than whites, which then—supposedly—goes on to explain higher rates of crime, aggression, and prostate cancer. However, people 1) say this only from reading the abstract (and not reading the full paper) and 2) even if they could read the paper they would not know where the flaws were to point them out and discredit the study based on flawed methodology. I see this study getting cited every now-and-then and I’m sick of seeing it.
Ross et al (1986: 45) state that they “recently reviewed the evidence that endogenous levels of certain steroid and polypeptide hormones are causally related to a group of human cancers, including cancer of the prostate gland.” I’ve shown how even injecting a man with exogenous testosterone does not worsen his prostate cancer (Eisenberg et al, 2015; Boyle et al, 2016) and testosterone doesn’t cause prostate cancer (Stattin et al, 2003; Michaud, Billups, and Partin, 2015). So this has been falsified. Even if blacks had the testosterone levels that they claimed it still would not cause higher rates of PCa (prostate cancer) incidence.
They solicited study participants from two colleges around the Los Angeles metro area. The two universities they got their sample from were the University of Southern California and California State University of Los Angeles. They recruited individuals through postings on the school bulletin board in in the school newspaper. They got 50 blacks and 50 whites. They then write something that’s troubling to me: “A convenient time for blood collection was arranged, and students were met by a nurse epidemiologist (R. H.) at either the Student Health Center or another mutually convenient location” (Ross et al, 1986: 45). This is dumb. The students were assayed at all times between 10 am and 3 pm; testosterone levels are highest at 8 am though one study on older men shows that assaying between 8 am and 2 pm doesn’t matter (Crawford et al, 2015). However, for the purposes of discussing this paper this is irrelevant.
Table 1 from Ross et al (1986) tells us a lot about the flaws in the study—most importantly, the assay times. A majority were assayed between 10 am and 2 pm—which would depress testosterone though people assayed nearer to 10 am would have higher levels than people assayed nearer to 2 pm. Alcohol consumption only decreases testosterone while drunk, and a majority of the cohort did not consume alcohol within 12 hours of being assayed.
They come to the conclusion that the mean total testosterone level was 19 percent higher than whites whereas free testosterone was 21 percent higher. In regard to the assay collection times, Ross et al (1986: 47) write:
There was a negative correlation between time of sampling (No. of min elapsed since 0600 hr) and testosterone levels for whites (r=-O.4I) but not for blacks (r = -0.08). Adjustment for this variable caused a small reduction in geometric mean differences in levels of testosterone and free testosterone between blacks and whites. After simultaneous adjustment by analysis of covariance for time of sampling and age, weight, alcohol use, smoking, and use of prescription drugs, there
remained a 15% difference in total testosterone levels and a 13% difference in free testosterone levels between blacks and whites.
Even though they ‘adjusted for this variable’, it’s still a huge confound. Testosterone assays must be taken nearer to 8 am; the fact that people were assayed all over the place in the span of a 5 hour time period while testosterone levels decrease throughout the day is a huge red flag.
They then say that they are “uncertain why young black men have higher levels of circulating testosterone than white men“, though small sample sizes, a large range of variation in assay time, and a nonrepresentative sample is why. Other, more robust, analyses show a smaller ‘gap’, about 2.5 to 4.9 percent, favoring blacks (Richard et al, 2014). All in all, this study has huge flaws and should not be pointed to—especially today in 2017—because much larger analyses with much better methodologies have been carried out and some studies show no difference while others show a small difference favoring blacks but that still would not explain higher rates of testosterone, aggression and crime.
Ross et al (1986) is used by hereditarians such as Lynn (1990), Rushton (1997) and Hart (2007). Lynn (1990) states that these large testosterone differences discovered by Ross et al (1986) lend credence to Rushton’s r/K selection theory in which blacks have more children than whites who have more children than East Asians. Evidence for this assertion, states Lynn (1990) is the fact that blacks have higher rates of prostate cancer than whites who have higher levels of testosterone than East Asians, however this has been disproven by ethnicmuse.
Rushton (1997: 170) states that blacks had 19 percent higher levels of testosterone citing Ross et al (1986), however, Rushton didn’t cite the adjusted level which ended up being 15 percent, and, again, doesn’t mean anything to their hypothesis.
And Hart (2007) yet still repeats the same old stuff that “these differences in sexual behavior may be a consequence of the fact that blacks, on average, have higher levels of testosterone than whites“. These three researchers, clearly, are citing this study uncritically because it fits with their ‘racial hierarchy’. In fact, Rushton (1999) asked if testosterone was a ‘master switch’. In this paper, he cites Ellis and Nyborg (1992) who find that blacks had 3 percent higher levels of testosterone than whites. They gave the following values:
For the purposes of Rushton’s interpretation, writes Fish (2013), “These uncorrected figures are, of course, not consistent with their racial r- and K-continuum.” This, of course, is a big deal. Rushton cites this study as if it lends credence to his claims but it actually found the same result as Richard et al (2014). Thirty years after Ross et al (1986) we have numerous other studies showing a small gap between the races or no gap at all. We have numerous other studies showing that testosterone does not cause aggression, crime or violent behavior. However, people will still point to the abstract of Ross et al (1986) and think that they have proven that blacks have higher levels of testosterone than whites which proves how and why they have higher levels of testosterone, commit more crime and are all around more violent.
Though, as I have written about before, what Ross et al (1986) set out find the answer for (testosterone influencing higher levels of prostate cancer) can most definitely be explained by diet and lack of certain vitamins such as vitamin D, since low levels of this steroid hormone (it’s not a vitamin) cause prostate cancer (Schwartz and Hulka, 1990; Zhao and Feldman, 2001; Khan and Partin, 2004; Garland et al, 2006). Diet can explain a lot of the variation, as I have argued in the past.
In sum, Ross et al (1986) is the only study that I’ve found on racial testosterone differences that shows that extreme directionality favoring blacks over whites. This should set off some alarms in some people’s heads. People—psychologists included—need to learn about these hormones, how they’re produced in the body, and what they’re used for. Hormones don’t cause behavior, hormones influence behavior.
This fear of testosterone is largely overblown. We need testosterone for proper normal functioning. We need testosterone to be socially dominant; if you have lower levels you’ll be less socially dominant. This fear of testosterone—especially when it comes to race and it’s so-called causes—is largely pushed by Lynn, Rushton, Hart, and Ellis. I have spent a lot of time and thousands of words showing that they are wrong and testosterone is not a hormone to fear. It does not cause crime. It does not cause aggression. It does not cause prostate cancer. I’ve rebutted quite a few hereditarians on testosterone as well as testosterone and race, and if I come across more I will rebut them as well.
Testosterone and social dominance are linked, that is, when one is socially dominant then they will have higher levels of testosterone. But does this necessarily translate into violent behavior? No it does not. One longitudinal study looked at the effect of testosterone in children from kindergarten to the end of primary school (ages 6 to 13). Were high levels of testosterone associated with physical aggression and/or social dominance?
Schaal et al (1996) followed 178 boys from kindergarten to the end of primary school. To attempt to control for certain variables, they “were recruited according to the following criteria: (1) attending school in low socioeconomic areas of Montreal; (2) born from Caucasian, French-speaking parents themselves born in Canada; and (3) living with parents having medium to low educational status” (Schaal et al 1996).
They collected behavioral assessments at age 6, 10 and 13 through teacher and peer ratings. They asked questions such as “Who would you choose as a leader?” and “Who is the toughest?” To assess this, the authors made a game where they had to toss sandbags at targets to win money, with the only rules being they had to be a certain distance away from the targets. At the end of the game, the winner received 2 dollars while the others received 1 dollar. Each individual received a ‘toughness’ and ‘dominance’ score. Schaal et al (1996) write:
The crossing of both toughness and leadership scores, using the median, yielded four groups defined as follows: (1) tough-leader (n = 52); (2) toughnot leader (n = 27); (3) not tough-leader (n = 44); and (4) not tough -not leader (n = 48).
The groups did not differ on demographic or socioeconomic status, however, they showed differing ratings than they did at school in the previous year. Those rated tough by peers unfamiliar to them had also been rated more aggressive by peers who knew them than those who were rated ‘not tough’.
They assessed behavior and anxiety levels using a social behavior questionnaire. They write:
Boys were entered into the following categories according to their behavior rating scores on at least three of four assessments: (1) stable high fighter/stable high anxious (SH F-SHA; n = 20): fighting and anxiety scores at the 70th percentile or greater; (2) stable high fighter/ stable low anxious (SHF-SLA; n = 11): fighting score equaled or exceeded the 70th percentile and anxiety score was equal to or below the 50th percentile; (3) stable low fighter/stable high anxious (SLF-SHA; n = 10): equal to or less than the 50th percentile on the fighting scale and greater than the 70th percentile on the anxiety scale; and (4) stable low fighter/stable low anxious (SLFSLA; n = 25): equal to or lower than the 50th percentile on both fighting and anxiety scores.
Children who were noted by teachers to be more physically aggressive compared with children noted not to be physically aggressive were rated higher on “proactive aggression.” These children were also rated less popular.
They collected saliva to assay for testosterone at 8:30 am (yay), 10 am, 11 am, and 3:30 pm. There is a direct correlation between salivary testosterone levels and free testosterone levels in the body (Wang et al, 1981; Johnson, Joplin, and Burrin, 1987), and since it’s easier and way less of a biohazard to assay saliva for testosterone levels than to assay blood, it’s only logical to assay saliva since it’s easier and less of a chance for contaminated samples.
Now comes the fun part: did the socially dominant, tough leaders who were to have higher levels of testosterone more physically aggressive? To make it short: NO. The children who had LOWER testosterone were seen to be more physically aggressive. The ‘tough-not’ leaders were seen to be more aggressive; they had lower testosterone than both tough-not groups and lower than the tough leaders. Is this not ironic? This completely flys in the face of numerous theories on how and why grade-school children fight: it’s not high testosterone that causes this phenomenon, clearly.
It’s also interesting to note that those boys who were “stable high fighters” had lower testosterone levels compared to boys that were “stable low fighters” at age 13. Forty-one percent of the “stable high fighters “were in a regular classroom at the level appropriate for their age (age 13) compared with 91% of the stable low fighters” (Schaal et al 1996: 1327). The first analysis they conducted showed that, after only having met for three hours, the boys with high salivary testosterone were rated as “tough” and a “leader”. However—and this is where things get good—boys who were consistently rated as having higher levels of aggression between the ages of 6 and 12 had lower levels of testosterone at age 13.
Though, boys with high testosterone at age 13 “appear to be individuals who quickly succeed in imposing their will on peers, sometimes by aggressive behavior, but remain socially attractive over time” (Schaal et al, 1996: 1328). And, of course, boys who were rated as physically aggressive from kindergarten to age 12 (who had lower testosterone levels) were not seen as socially dominant. These children were seen as less popular and also were failing in school.
Elevated testosterone levels at age 13 were seen to be associated with social dominance when assessed after the game and three hour meet discussed above. Further, lower levels of testosterone between the ages of 6 to 12 (and assayed at 13) were associated with higher levels of aggression and more fighting. They state that higher levels of testosterone are only associated with aggression “only if the latter confers a dominant status” (Schaal et al, 1996: 1329). Higher testosterone is, of course, associated with better social well-being whereas lower levels of testosterone was associated with more violence which may be due to social isolation, stable anxiety throughout childhood or both influences influencing the aggressive behavior along with the low testosterone. High testosterone levels in adolescence is not related to antisocial disorder, but it is related to social dominance—as I have stated countless times.
Now for some comments.
I like this study. How they used behavioral questionnaires to assess children’s behavior, as well as using teacher and peer ratings to assess behavior is a great method. It’s even better that they followed them throughout their adolescent life to see any patterns that arose. I hope that there is more data on these children (I will look for any other data on this one point) because this could elucidate so many testosterone relationships with behavior. This study shows that higher testosterone levels were not associated with antisocial behavior but it was, however, associated with greater social well-being.
Clearly, we need higher-ish levels of testosterone—especially since lower levels are correlated with numerous maladies. So, it seems, that the testosterone=crime aggression myth (and in my opinion, crime) is busted. Testosterone is an extremely important hormone for proper endocrine functioning and having levels that are too low. They also state at the end of the paper that “From the perspective of the present study, it can be hypothesized that in a sample of normal adolescent males, those who dominate will tend to react to provocation and to show relatively low frustration tolerance. The results from the Olweus and colleagues’ study might then be interpreted as showing the relationship between dominance and T, rather than between antisocial behavior and T.”
So, again, testosterone is related to dominance; if you have lower testosterone you will be less socially dominant while if you have more you will be more socially dominant (this holds for adults as well). It’s interesting to note that boys perceived as dominant when around people they did not know had higher levels of testosterone than boys who were not. This shows that boys with lower levels of testosterone were seen as less popular, they were failing in school and they had higher levels of aggression. Testosterone levels in children are associated with social success and popularity, rather than antisocial behavior and violent outbursts as other studies have reported.
Testosterone=the dominance hormone—more specifically, the social dominance hormone. It does not lead to social maladjustment.
People don’t understand the relationship between testosterone, aggression, and crime. People hear the sensational media stating that testosterone causes crime, aggression, and anger. However, I have written numerous articles on this blog on the true nature of testosterone, what it’s really needed for and why we need it in high amounts. I’ve mused a lot on this hormone, which is one of my favorites to discuss due to the numerous misconceptions surrounding it.
Which way does causation run in regard to prisoners and their testosterone level?: heightened testosterone > aggression > violence or aggression > heightened testosterone > dominance > possibility (not necessarily, as I have written myself in the past) of violence.
People may use animal studies in support of their contention that testosterone causes aggressive behavior. However, for reasons I have discussed in the past, animal models only show avenues for future research and do not necessarily mean that this is the case for humans (as Mazur, 2006 point out). I don’t use animal studies. They’re good for future research, but to use them as evidence for causation in humans doesn’t make sense.
People may cite Dabbs et al showing that the more violent prisoners had higher levels of testosterone and therefore conclude that higher levels of testosterone drive the violent crime that they commit, however it is much more nuanced than that.
Does being a violent criminal raise testosterone or are violent people more likely to have high testosterone? Dabbs never untangles this; they just showed a correlation, which is small as evidenced by my other citations.
Testosterone is, as evidenced by numerous studies, related to dominance and dominance contests, however, during these dominance contests “a killing is rarely the outcome of a violent dominance contest” (Mazur, 2006: 25). Therefore, this throws a wrench in the testosterone-causes-crime hypothesis.
Some individuals may state that these dominance contests then lead to violence, however, as Mazur (2006) puts it: “Heightened testosterone is not a direct cause of male violence.”
Other animals assert dominance violently but we, necessarily, do not.
Mazur (2006) states that dominance contests rarely escalate to murder. Mazur also states that dominance contests also lead to increased T for the winners and decreased T for the losers, and these contests also don’t necessarily lead to murder/violent behavior. There is a feedback loop with high T causing behavior and behavior causing high T (Mazur, 2006) while this feedback loop may lead to “lethal effects” (Mazur and Booth, 2008).
It’s worth noting that Mazur seems to advocate for ‘testosterone-depressing drugs’. He concludes:
There are strong linkages between macro-level culture and the physiology of
individuals. We may find solutions to some of our social problems by altering these linkage.
Macro-level culture being white culture, black culture, Asian culture, etc.
The physiological differences are due to the preparation for dominance contests. So, his hypothesis goes, the culture of dominance among young black men with no education is why their T is so high. That low education was also associated with low education lends credence to the claim that this is changeable.
However, in his newer article on education, low testosterone and blacks he advocates for more sensible solutions (attempting an environmental change). I don’t know about you but I have big problems with using FDA/Big Pharma drugs to ‘reduce societal problems’, and it seems that Mazur has changed his view there. Mazur (2016) writes:
If high T does facilitate the high violence rate among young black men, there would be a troubling policy question of what, if anything, to do about it. Any notion of a medical or pharmaceutical fix, rather like prescribing Ritalin for hyperactivity, would reek of race-based chemical castration and should be regarded as outside the pale. However, social interventions might be workable and ethically acceptable.
I have railed against measures like this in the past, since proposing measures to attempt to ‘decrease crime through supposedly decreasing one of the main “causes”‘ is very Brave New World-ish, and I am highly against those measures. Social interventions are, in my view, the more sensible measures to undertake.
In regard to low education and testosterone, this same relationship was noticed by Assari, Caldwell, and Zimmerman (2014) where they note that testosterone was not associated with aggression in men, but low education was, which Mazur (2016) replicates, showing that blacks of the same age group with more education had lower levels of testosterone when compared to age-matched blacks. Mazur (2016) cites one study in support for his contention that education can decrease aggressive behavior (Carre et al, 2014)
The correlation is there, I agree. let’s take the middle value of .11 between Archer, Graham-Kevan, and Davies, 2005 at .08; and Book, Starzyk, and Quinsey, 2001 .14. So testosterone explains 3 percent of the the relationship with aggression. Not high at all.
Great evidence against the testosterone-causes-aggressive-behavior hypothesis are data on the Yanomami. About 50 percent of Yanomami men meet their deaths by other Yanomami men. So the Yanomami must have testosterone levels through the roof, right? Wrong. De Lima et al (2015) write:
We observed that Yanomamis present lower levels of testosterone (414 ng/dL) in relation to other ethnic groups (502/512 ng/dL), but still within normal limits (350-1000 ng/dL).
(Note that these values for “normal limits” changed, going into effect at the end of July.)
The Yanomami with an extremely high murder rate with nowhere near a modern society have T levels on the lower end of our range. So….. The Yanomami example is direct evidence against the assertion of testosterone directly causing crime, as some people assert (it is even evidence against an indirect cause). The evidence of the Yanomami having testosterone levels near our lower range is direct evidence against the testosterone/crime hypothesis. Clearly, other variables drive the high violence rate in this society that are not testosterone. More interestingly, these people have had little contact with Western societies, and their T levels are still low compared to ours despite constantly being vigilant for threats from other Yanomami.
Most dominance contests do not end violently in the first-world, there is numerous evidence to attest to this fact. So with the low correlation between testosterone and aggression (Book, Starzyk, and Quinsey, 2001; Archer, Graham-Kevan and Davies, 2005; Book and Quinsey, 2005), along with dominance contests rarely ending in murder/violent crime, then there are way more factors influencing these phenomena.
So the feedback loop goes: Testosterone rises in expectation of a challenge which then, after the dominance contest (which doesn’t always necessarily lead to violence), it affects both individuals differently depending on whether or not they won or lost that dominance contest and these values then persist over time if the dominance contests continuously end up the same.
Let’s say, for argument’s sake, that testosterone is a large cause for aggressive behavior in lower-educated blacks, what should be done about it? Mazur cites evidence that behavioral interventions seem to work to decrease violent behavior during certain circumstances (Carre et al, 2014), so that is a good way to lower violence in populations that have low education.
So heightened testosterone does lead to dominance which then facilitates a dominance contest between two individuals which does not necessarily lead to crime and aggressive, violent behavior (this outcome is rare in dominance contests among “higher primates” [Mazur’s words]) so, therefore, while testosterone does facilitate dominance contests, it rarely leads to violence in our species. Therefore, testosterone does not cause aggressive behavior and crime, but it does cause dominance which, for the most part, do not always result in violent, aggressive, murderous behavior.
I’ve shown that Mazur replicated other analyses that show that testosterone and aggressive behavior are related to lower education. Testosterone wasn’t associated with aggressive behavior in Assari, Caldwell, and Zimmerman’s (2014) study, and, as Mazur (2016) replicates, low education was. So one way to end this relationship is to educate people, as shown by Carre et al (2014), and with this education, crime will begin to fall. Heightened testosterone is not a direct cause of male violence.
(Note: I also believe that other factors such as sleep and depressed nutrition play a factor in crime, as well as racial differences in it. See Birch, 1972; Liu et al, 2003; Liu et al, 2004; Walker et al, 2007; Galler et al, 2011, 2012a, 2012b; Spratt et al, 2012; Gesch, 2013; Kuratko et al, 2013; Waber et al, 2014; Raine et al, 2015; Thompson et al, 2017 for more information, I will cover this in the future. I’m of course not daft enough to believe that no genetic differences between individuals/populations are the cause of a lot of crime between them, however, as I have laid out the case in regard to testosterone and MAOA numerous times, these two explanations for both individual differences in crime as well as racial differences in crime leave a lot to be desired. Other genetic factors, of course, influence these differences, however, I am only worried about refuting the popular notions of ‘testosterone and MAOA, the ‘warrior gene” cause crime. The relationship is a lot more nuanced as I have provided mountains of evidence for.)
Batrinos (2012) is a paper titled Testosterone and Aggressive Behavior in Man. Section 2 reviews studies on prisoners. Small ns, no controls, prison isn’t a natural environment. Similar data was reported, but it has the same problems as above. Studies of sexual offenders are contradictory, with blood T not being associated, then being associated with aggression. An investigation of veterans showed T to raise aggression, again, non-representative sample (and you also have to think of PTSD and other illnesses). Then the money quote:
It is of interest, however, that supraphysiological doses of testosterone in the order of 200 mg weekly (20), or even 600 mg weekly (21), which were administered to normal men had no effect on their aggression or anger levels.
Dominance is related to testosterone increases, and dominance can lead to aggressive behavior then to violent acts, but this is not always true. Mazur and Booth’s (1997) reciprocal model shows a feedback loop on dominance and testosterone:
Ehrenkranz et al. (1974) showed that socially dominant but unaggressive prisoners had relatively high T, not significantly different from the T levels of aggressive prisoners (who may have been dominant too). Nearly all primate studies that have been interpreted as linking T to aggression (Dixson 1980) may as easily be interpreted as liking T with dominance (Mazur 1976). Recent reviewers have questioned whether, among humans, T is related to aggressiveness per se (Archer 1991; Albert et al. 1994).
Heightened testosterone is not a direct cause of male violence.
(Much more on this paper soon.)
Small studies have shown that T increases during sports (duh because it’s competition) and that watching your favorite sports team win a game increases T (has been replicated).
Batrinos then cites a study talking about circadian rhythm and testosterone/aggression here:
Interestingly enough, Brown et al (2007) lends credence to my hypothesis that I have discussed in the past. Testosterone decreases at 8pm (most crime is comitted at 10 pm for adults) with increases in testosterone at night:
It is not surprising that T levels at 2000 h and 0800 h would be important for TS-IAB relationships because the 2000 h and 0800 h values represent the evening nadir and morning zenith.
But most crime is not comitted in the morning, for both adults and children (as seen below):
Now, anyone who has read my article on why testosterone doesn’t cause crime knows where I’m going with this:
Look at the times most crimes are committed then think about when T levels are highest (8 am).
This does seem to show a relationship with when most crimes are comitted, a sharp decrease in crime occurs as testosterone levels hit their highest in the day, which is evidence against the testosterone-causes-crime hypothesis.
In regard to the crime chart from the OJJDP, they write:
- In general, the number of violent crimes committed by adults increases hourly from 6 a.m. through the afternoon and evening hours, peaks at 10 p.m., and then drops to a low point at 6 a.m. In contrast, violent crimes by juveniles peak in the afternoon between 3 p.m. and 4 p.m., the hour at the end of the school day.
Using what I gave, what do you draw from the line graph? It’s clear that, since testosterone is highest in the morning aand at its lowest at 8 pm (when most violent crime is being comitted) that testosterone is not directly related to crime, since, as evidenced by Brown et al (2007), testosterone levels are lowest at 8 am with a sharp rise as the night/ morning progresses. Looking at their testosterone chart for the hours between 8 pm and 8 am, testosterone did increase at 8pm and into the night. However, as testosterone levels continued increasing into the night, crime does not linearly increase with the rise in testosterone (see fig. 3 in Brown et al, 2007).
Now, finally, in regards to the claim about “locally produced testosterone”, it is true that the brain can produce testosterone de novo from cholesterol; but wait! Luteinizing hormone signaling in the neurons promotes the secretion and production of steroids (Liu et al, 2007), along with the de novo production of testosterone through cholesterol (literally the only way testosterone can be produced).
Good paper, shaky claims (the prisoner claims suck, circadian rhythm claims suck). The only novel thing in this paper is saying how the brain can produce testosterone de novo from cholesterol (though luteinizing hormones are still involved, see above cite). Injecting a man with supraphysiologic doses of testosterone does not increase aggression nor anger levels. It’s definitive that testosterone does not directly cause crime, as evidenced by the low correlation between testosterone and aggression. Numerous other studies (which I have reviewed in the past), however, show that aggression precedes the testosterone increase which is only seen in certain social situations. These specific situations, by themselves, drive the production of the hormone.
Many long-time readers may know of the numerous tirades of been on in regards to the “testosterone causes crime and aggression” myth. It’s a fun subject to talk about because the intelligent human physiological system is an amazing system. However, people who are not privy to the literature on testosterone in regards to race, aggression, crime, sex differences etc are only aware of whatever they read in pop science articles. So since they never read the actual papers themselves, they get a clouded view of a subject.
In my last article, I wrote about how there are no “testosterone genes”. In previous articles on the hormone, I have proven that there is no causal link between testosterone and aggression. But when comparing the sexes, how do the results look? Do they look the same with men being more violent while women—who have substantially less testosterone than men—do not have any higher levels of aggression or crime? The most recent study I’m aware of is by Assari, Caldwell, and Zimmerman (2014) titled: Sex Differences in the Association Between Testosterone and Violent Behaviors.
To make a long story short, there was no relationship between testosterone and aggression in men, but a significant relationship between testosterone and aggression in women. This data comes from the Flint Adolescent Study, a longitudinal study conducted between the years of 1994 to 2012. In regards to testosterone collection, saliva was used which has a perfect correlation with circulating testosterone. The eligibility to be included in the testosterone assay was “provided consent for the procedure, not being pregnant, not having anything to eat, drinking nothing except water, and not using tobacco, 1 hour prior to collection” (Assari, Caldwell, and Zimmerman, 2014).
The adolescent who contributed saliva gave a whole slew of demographic factors including SES, demographics, psychological factors, family relations, religion, social relations, behavior, and health. They were aged 14 to 17 years of age. They collected data during face-to-face interviews,
Age and SES were used as control variables in their multivariate analysis. For violent behaviors, the authors write:
Youths were asked how often they had engaged in the following behaviors; ‘had a fight in school’, ‘taken part in a rumble where a group of your friends were against another group’, injured someone badly enough to need bandages or a doctor’, ‘hit a teacher or supervisor at work (work supervisor)’, used a knife or gun or other object (like a club) to get something romantic a person’, ‘carried a knife or razor’, or ‘carried a gun’. All items used a Likert response, ranging from 1 (0 times) to 5 (4 or more times). Responses to each item were averages to calculate the behavior during the last year. Total score was calculated as the average of all items. Higher scores indicated more violent behaviors (a = 0.79). This measure has shown high reliability and validity and it has been used previously in several published reports.
This is a great questionnaire. The only thing I can think of that’s missing is fighting/arguing with parents.
In regards to testosterone assaying, they were assayed after 11 am to “control for changes due to diurnal rhythm” (Assari, Caldwell, and Zimmerman, 2014). I’m iffy on that since testosterone levels are highest at 8 am but whatever. This analysis is robust. Saliva was not taken if the subject had smoked or ingested something other than water or if a subject was pregnant. Assays should be taken as close to 8 am, as that’s when levels are highest. However one study does argue to extend the range to 8 am to 2 pm (Crawford et al, 2015) while other studies show that this only should be the case for older males (Long, Nguyen, and Stevermer, 2015). Even then assays were done at the higher end of the range as stated by Crawford et al (2015), so differences shouldn’t be too much.
86.4 percent of the sample was black whereas 13.4 percent were white. 41.2 percent of the subjects had some college education whereas 58.2 percent of the subjects lived with a partner or relative. 21.4 percent of the subjects were unemployed.
The mean age was 20.5 for both men and women, however, which will be a surprise to some, testosterone did not predict aggressive behavior in men but did in women. Testosterone and aggressive behavior were positively correlated, whereas there was a negative correlation between education and testosterone and aggressive behavior. Though education was associated with aggressive behavior in men but not women. So sex and education was associated with aggressive behavior (the sex link being women more privy to aggressive behavior while men are more privy to aggressive behavior due to lack of education). Females who had high levels of education had lower levels of aggressive behavior. Again: testosterone wasn’t associated with violent behavior in men, but it was in women. This is a very important point to note.
This was a community sample, so, of course, there were different results when compared to a laboratory setting, which is not surprising. Laboratory settings are obviously unnatural settings whereas the environment you live in every day obviously is more realistic.
This study does contradict others, in that it shows that there is no association between testosterone and aggression in men. However, still other research shows that testosterone is not linked to aggression or impulsivity, but to sensation-seeking, sexual experience or sociality (Daitzman and Zuckerman, 1980; Zuckerman, 1984). Clearly, testosterone is a beneficial hormone and due to the low correlation of testosterone with aggression (between .08 and .14; Book, Starzyk, and Quinsey, 2001; Archer, Graham-Kevan and Davies, 2005; Book and Quinsey, 2005). This paper, yet again, buttresses my arguments in regards to testosterone and aggressive behavior.
In regards to the contrast in the literature the authors describe, they write:
One of the many factors that may explain the inconsistency in these findings is the community versus clinical setting, which has been shown to be a determinant of these associations. Literature has previously shown that many of the findings that can be found in clinical samples may not be easily replicated in a community setting (36).
This is like the (in)famous, unreplicable stereotype threat (see Stroessner and Good). It can only be replicated in a lab, not in an actual educational setting. And it also seems that this is the case for testosterone and aggressive behavior.
Just because women have lower testosterone and are less likely to engage in aggressive behavior, that doesn’t mean that a relationship does not exist between females. “It is also plausible to attribute sex differences in the above studies to differential variations in the amount of testosterone among men and women” (Assari, Caldwell, and Zimmerman, 2014). This view supports the case that testosterone is linked to aggression in females, even though their range of testosterone is significantly lower than men’s, while it may also be easier to assay women for testosterone due to less diurnal variation in comparison to men (Book, Starzyk, and Quinsey, 2001).
Assari, Caldwell, and Zimmerman, (2014) also write (which, again, buttresses my arguments):
Age may explain some of the conflicting results across the studies. A meta-analysis of community and selected samples suggested that there might be only low to modest association between testosterone and aggression, with mean weighted correlations ranging from 0.08 to 0.14, in males. Overall, these meta-analyses suggest that the testosterone-aggression association is equally strong in 12 to 21-year-olds, as it is in 22 to 35-year-olds, but that it may be less strong in age groups younger than 12, than in those who are older.
So, testosterone may be associated with aggressive behavior and violence in women but not in men. In men, the significant moderator was education. It’s interesting to note that Mazur (2016) noted that young black males with little education had higher levels of testosterone than age-matched samples of other blacks. This, along with the evidence provided here, may be a clue that if the social environment changes, then so will higher levels of testosterone (as I have argued here).
They, perhaps taking too large of a leap here, argue that “aggressive behaviors may be more social and less biologically based among men” (Assari, Caldwell, and Zimmerman, 2014). Obviously social factors are easier to change than biological ones (in theory), so, they argue, preventative measures may be easier for men than women. More studies need to be done on the complex interactions between sex, testosterone, aggression, biology and the social environment which then shapes the aggressive behaviors of those who live there.
Testosterone and aggression studies are interesting. However, you must know a good amount of the literature to be able to ascertain good studies from the bad, what researchers should and should not have controlled for, time of assay, etc because these variables (some not in the author’s hands, however) can and do lead to false readings if certain variables are not controlled for. All in all, the literature is clearly points to, though other studies contest this at times, the fact that testosterone does not cause aggressive behavior in men. The myth needs to die; the data is piling up for this point of view and those who believe that testosterone causes aggressive behavior and crime (which I have shown it does not, at least for men) will soon be left in the dust as we get a better understanding of this pivotal hormone.
(In case anyone was going to use this as evidence that black women have higher levels of testosterone than white women, don’t do it because it’s not true. You’ll only embarrass yourself like this guy did. Read the comments and see him say that you don’t need scientific measurements, you only need to ‘observe it’ and through ‘observation’ we can deduce that black women have higher levels of testosterone than white women. This is not true. Quoting Mazur, 2016:
The pattern [high testosterone] is not seen among teenage boys or among females.
There is no indication of inordinately high T among young black women with low education.
Whoever still pushes that myth is an idealogue; I have retracted my article ‘Black Women and Testosterone‘, but idealogues just gloss over it and read what they think will bolster their views when I have provided the evidence to the contrary. It pisses me off that people selectively read things then cite my article because they think it will confirm their pre-conceived notions. Well too bad, things don’t work like that.)
Testosterone has a similar heritability to IQ (between .4 and .6; Harris, Vernon, and Boomsma, 1998; Travison et al, 2014). To most, this would imply a significant effect of genes on the production of testosterone and therefore we should find a lot of SNPs that affect the production of testosterone. However, testosterone production is much more complicated than that. In this article, I will talk about testosterone production and discuss two studies which purport to show a few SNPs associated with testosterone. Now, this doesn’t mean that the SNPs cause high/low testosterone, just that they were associated. I will then speak briefly on the ‘IQ SNPs’ and compare it to ‘testosterone SNPs’.
Complex traits are ‘controlled’ by many genes and environmental factors (Garland Jr., Zhao, and Saltzman, 2016). Testosterone is a complex trait, so along with the heritability of testosterone being .4 to .6, there must be many genes of small effect that influence testosterone, just like they supposedly do for IQ. This is obviously wrong for testosterone, which I will explain below.
Back in 2011 it was reported that genetic markers were discovered ‘for’ testosterone, estrogen, and SHGB production, while showing that genetic variants in the SHGB locus, located on the X chromosome, were associated with substantial testosterone variation and increased the risk of low testosterone (important to keep in mind) (Ohlsson et al, 2011). The study was done since low testosterone is linked to numerous maladies. Low testosterone is related to cardiovascular risk (Maggio and Basaria, 2009), insulin sensitivity (Pitteloud et al, 2005; Grossman et al, 2008), metabolic syndrome (Salam, Kshetrimayum, and Keisam, 2012; Tsuijimora et al, 2013), heart attack (Daka et al, 2015), elevated risk of dementia in older men (Carcaillon et al, 2014), muscle loss (Yuki et al, 2013), and stroke and ischemic attack (Yeap et al, 2009). So this is a very important study to understand the genetic determinants of low serum testosterone.
Ohlsson et al (2011) conducted a meta-analysis of GWASs, using a sample of 14,429 ‘Caucasian’ men. To be brief, they discovered two SNPs associated with testosterone by performing a GWAS of serum testosterone concentrations on 2 million SNPs on over 8,000 ‘Caucasians’. The strongest associated SNP discovered was rs12150660 was associated with low testosterone in this analysis, as well as in a study of Han Chinese, but it is rare along with rs5934505 being associated with an increased risk of low testosterone(Chen et al, 2016). Chen et al (2016) also caution that their results need replication (but I will show that it is meaningless due to how testosterone is produced in the body).
Ohlsson et al (2011) also found the same associations with the same two SNPs, along with rs6258 which affect how testosterone binds to SHGB. Ohlsson et al (2011) also validated their results: “To validate the independence of these two SNPs, conditional meta-analysis of the discovery cohorts including both rs12150660 and rs6258 in an additive genetic linear model adjusted for covariates was calculated.” Both SNPs were independently associated with low serum testosterone in men (less than 300ng/dl which is in the lower range of the new testosterone guidelines that just went into effect back in July). Men who had 3 or more of these SNPs were 6.5 times more likely to have lower testosterone.
Ohlsson et al (2011) conclude that they discovered genetic variants in the SHGB locus and X chromosome that significantly affect serum testosterone production in males (noting that it’s only on ‘Caucasians’ so this cannot be extrapolated to other races). It’s worth noting that, as can be seen, these SNPs are not really associated with variation in the normal range, but near the lower end of the normal range in which people would then need to seek medical help for a possible condition they may have.
In infant males, no SNPs were significantly associated with salivary testosterone levels, and the same was seen for infant females. Individual variation in salivary testosterone levels during mini-puberty (Kurtoglu and Bastug, 2014) were explained by environmental factors, not SNPs (Xia et al, 2014). They also replicated Carmaschi et al (2010) who also showed that environmental factors influence testosterone more than genetic factors in infancy. There is a direct correlation between salivary testosterone levels and free serum testosterone (Wang et al, 1981; Johnson, Joplin, and Burin, 1987), so free serum testosterone was indirectly tested.
This is interesting because, as I’ve noted here numerous times, testosterone is indirectly controlled by DNA, and it can be raised or lowered due to numerous environmental variables (Mazur and Booth, 1998; Mazur, 2016), such as marriage (Gray et al, 2002; Burnham et al, 2003; Gray, 2011; Pollet, Cobey, and van der Meij, 2013; Farrelly et al, 2015; Holmboe et al, 2017), having children (Gray et al, 2002; Gray et al, 2006; Gettler et al, 2011); to obesity (Palmer et al, 2012; Mazur et al, 2013; Fui, Dupuis, and Grossman, 2014; Jayaraman, Lent-Schochet, and Pike, 2014; Saxbe et al, 2017) smoking is not clearly related to testosterone (Zhao et al, 2016), and high-carb diets decrease testosterone (Silva, 2014). Though, most testosterone decline can be ameliorated with environmental interventions (Shi et al, 2013), it’s not a foregone conclusion that testosterone will sharply decrease around age 25-30.
Studies on ‘testosterone genes’ only show associations, not causes, genes don’t directly cause testosterone production, it is indirectly controlled by DNA, as I will explain below. These studies on the numerous environmental variables that decrease testosterone is proof enough of the huge effects of environment on testosterone production and synthesis.
How testosterone is produced in the body
There are five simple steps to testosterone production: 1) DNA codes for mRNA; 2) mRNA codes for the synthesis of an enzyme in the cytoplasm; 3) luteinizing hormone stimulates the production of another messenger in the cell when testosterone is needed; 4) this second messenger activates the enzyme; 5) the enzyme then converts cholesterol to testosterone (Leydig cells produce testosterone in the presence of luteinizing hormone) (Saladin, 2010: 137). Testosterone is a steroid and so there are no ‘genes for’ testosterone.
Cells in the testes enzymatically convert cholesterol into the steroid hormone testosterone. Quoting Saladin (2010: 137):
But to make it [testosterone], a cell of the testis takes in cholesterol and enzymatically converts it to testosterone. This can occur only if the genes for the enzymes are active. Yet a further implication of this is that genes may greatly affect such complex outcomes as behavior, since testosterone strongly influences such behaviors as aggression and sex drive. [RR: Most may know that I strongly disagree with the fact that testosterone *causes* aggression, see Archer, Graham-Kevan and Davies, 2005.] In short, DNA codes only for RNA and protein synthesis, yet it indirectly controls the synthesis of a much wider range of substances concerned with all aspects of anatomy, physiology, and behavior.
Genes only code for RNA and protein synthesis, and thusly, genes do not *cause* testosterone production. This is a misconception most people have; if it’s a human trait, then it must be controlled by genes, ultimately, not proximately as can be seen, and is already known in biology. Genes, on their own, are not causes but passive templates (Noble, 2008; Noble, 2011; Krimsky, 2013; Noble, 2013; Also read Exploring Genetic Causation in Biology). This is something that people need to understand; genes on their own do nothing until they are activated by the system.
What does this have to do with ‘IQ genes’?
My logic here is very simple: 1) Testosterone has the same heritability range as IQ. 2) One would assume—like is done with IQ—that since testosterone is a complex trait that it must be controlled by ‘many genes of small effect’. 3) Therefore, since I showed that there are no ‘genes for’ testosterone and only ‘associations’ (which could most probably be mediated by environmental interventions) with low testosterone, may the same hold true for ‘IQ genes/SNPS’? These testosterone SNPs I talked about from Ohlsson et al (2011) were associated with low testosterone. These ‘IQ SNP’ studies (Davies et al, 2017; Hill et al, 2017; Savage et al, 2017) are the same—except we have an actual idea of how testosterone is produced in the body, we know that DNA is indirectly controlling its production, and, most importantly, there is/are no ‘gene[s] for’ testosterone.
Testosterone has the same heritability range as IQ, is a complex trait like IQ, but, unlike how IQ is purported to be, it [testosterone] is not controlled by genes; only indirectly. My reasoning for using this example is simple: something has a moderate to high heritability, and so most would assume that ‘numerous genes of small effect’ would have an influence on testosterone production. This, as I have shown, is false. It’s also important to note that Ohlsson et al (2011) showed associated SNPs in regards to low testosterone—not testosterone levels in the normal range. Of course, only when physiological values are outside of the normal range will we notice any difference between men, and only then will we find—however small—genetic differences between men with normal and low levels of testosterone (I wouldn’t be surprised if lifestyle factors explained the lower testosterone, but we’ll never know that in regards to this study).
Testosterone production is a real, measurable physiologic process, as is the hormone itself; which is not unlike the so-called physiologic process that ‘g’ is supposed to be, which does not mimic any known physiologic process in the body, which is covered with unscientific metaphors like ‘power’ and ‘energy’ and so on. This example, in my opinion, is important for this debate. Sure, Ohlsson et al (2011) found a few SNPs associated with low testosterone. That’s besides the point. They are only associated with low testosterone; they do not cause low testosterone. So, I assert, these so-called associated SNPs do not cause differences in IQ test scores; just because they’re ‘associated’ doesn’t mean they ’cause’ the differences in the trait in question. (See Noble, 2008; Noble, 2011; Krimsky, 2013; Noble, 2013.) The testosterone analogy that I made here buttresses my point due to the similarities (it is a complex trait with high heritability) with IQ.
Back in July I wrote about how there is controversy on whether or not MtF transgenders should compete with ‘bio women’ and whether or not their anthropometry or hormones gave them an advantage over biological women (I am aware that T levels decrease once they go on HRT, just a lot of them still have T ranges in near the low end of the new numbers for men). Well I am reading The Sports Gene by Jerry Epstein and he brings up two (anecdotal) examples of MtF transgenders who take HRT and see a decrease in performance due to decreased T:
No scientist can claim to know the precise impact of testosterone on any individual athlete. But a 2012 study that spent three months following female athletes from a range of sports—including track and field and swimming—showed that elite-level competitors had testosterone levels that consistently remained more than twice as high as those of the nonelites. And there are powerful anecdotes as well.
Joanna Harper, fifty-five, is a medical physicist who was born a male and later transitioned to living as a woman. Harper also happens to be a nationally accomplished age-group runner, and when she started hormone therapy in August 2004 to suppress her body testosterone and physically transition to female [Note from RR: I, of course, do not agree with the use of ‘her’ and that ‘she’ ‘physically transition[ed] to female’] like any good scientist, she took data. Harper figured she would slow down gradually, but was surprised to find herself getting slower and weaker by the end of the first month. “I felt the same when I ran,” she says. “I just couldn’t go as fast.” In 2012, Harper won the U.S. national cross-country title for the fifty-five-to-fifty-nine age group, but age and gender-graded performance standards indicate that Harper is precisely as competitive now as a female as she was as a male. That is, as a female, Harper is just as good relative to women as she was relative to men before her transition, but she’s far slower than her former, higher-testosterone self.
In 2003, as a man, Harper ran Portland’s Helvetia Half-Marathon in 1:23:11. In 2005, as a woman, she ran the same race in 1:34:01. Harper’s male time was about fifty seconds faster than her female time. She has compiled data from five other runners who have transitioned from male to female, and all show the same pattern of precipitous speed decline. One runner competed in the same 5K for fifteen years straight, eight times as a man and then seven times as a woman following testosterone suppression therapy; always faster than nineteen minutes as a man, and always slower than twenty minutes as a woman. (Epstein, 2013: 78) [Keep in mind that I have the nook version so the physical copy may have this on a different page.
Yes this is anecdotal evidence that testosterone gave an advantage while ‘male’ and then when they ‘transitioned’ to ‘female’ it showed that they became weaker, but still at the top level of women’s performance. Knowing this—how this man had an advantage ‘as a man’ and kept the same relative advantage when he ‘transitioned to a woman’ is a large clue that testosterone does infer an inherent advantage to athletes who have more of the hormone surging through their body.
Testosterone is known to affect skeletal muscle growth, but the mechanisms by which testosterone affects muscle growth are not known (Bhasin, Woodhouse, and Storer, 2001). Also, women with very high androgen levels—whether it’s due to endogenous or exogenous testosterone—have a 2.5 to 5 percent advantage over women who have androgen levels in the normal range (Berman, 2017). So the difference in performance—between women at least—with high and low levels of testosterone is not too great, though that 2.5 to 5 percent advantage most likely would come into play at the very end of the race.
Also recall that I previously wrote that, per the IOC guidelines, a ‘MtF’ needs to ‘declare herself’ a woman for at least four years while taking HRT for 1-2 years to be able to compete with ‘the gender they think they are’. Well, the testosterone levels that the IOC states is ‘OK’ for ‘MtFs’ is still in the low range of the new testosterone guidelines for men! Testosterone most definitely does give an advantage in sports. Think of sports as a modern day test of survival. Basically, those good at sports—such as football and basketball for instance—would have been better able to form hunting parties in our evolutionary past. So while forming these parties, testosterone rose since testosterone raises while men are in groups as well as preparing for competition (Booth et al, 1989). So since our modern body plans sprang up around 2 mya with the appearance of Homo erectus in the fossil record, we can logically infer that cooperation and testosterone—among other things—were needed to be successful hunters.
So if you look at most sports as just a way for men to have a competitive spirit and simulate fighting/hunting with other men, then it makes it clear that testosterone does infer an advantage in sports. For instance, there is a clear relationship between testosterone and explosive jumping (Cardinale and Stone, 2006). These relationships are very clear, have large effects yet bodies like the IOC disregard these findings, allowing MtFs to compete with real women, even when the data and verbal argumentation against letting them compete are logically sound.
Studies do state, of course, that the relationship between high testosterone and athletic performance hasn’t been proven, they also haven’t been refuted either (Sudai, 2017). In fact, all you need to look at is traits that are influenced by testosterone—height, size of limbs, fat mass, shoulder width/size (the most androgen receptors lie in the shoulders and traps muscles, so to tell if someone is juicing, they will have low levels of body fat but ‘3-D delts’ and large traps) etc. So just by looking at a few simple traits and then comparing anatomy with females who have high testosterone compared to women who do not have high levels of testosterone, we can draw the logical conclusion that testosterone does increase sports performance for both men and women, and we have both anecdotal and experimental evidence for the assertion.
In sum, the anecdotal evidence from Epstein’s book is a good start. However, we will need more than anecdotal evidence to prove that testosterone truly does give individuals an advantage if they do have higher testosterone levels than their competition. As larger studies get done, these effects will begin to get teased out. I am certain that testosterone will be found to give a huge advantage in terms of sports, and since sports are a way for us to compete with each other, impress women, gauge other males’ fighting skills, and began as a way to hone skills used to hunt and fight (Lombardo, 2012). Sports began as a way for us to develop the skills needed to survive and hunt, among other things, and so, to hunt, you need to have high levels of testosterone to give that ‘boost’. So if sports began as a way to gauge potential rivals and allies, and as a way to hone/improve fighting skills, then we can logically state that testosterone does give an advantage in sports competition.
I came across this video on YouTube last night by a geneticist/science writer Steve Jones. He is also the Emeritus Professor of genetics at University College London. This makes what he says in the video I will speak about below very troubling—especially to a man of his caliber with the knowledge he has—views he has on the hormone.
In the very beginning of the video titled Testosterone and Crime: What Can Genes Tell Us About Behavior?, Jones says “But in fact, there are genes—there is a gene—for crime, which causes nearly all the crime, and is widely used and we understand a great deal about it. It’s a chemical gene it produces a particular chemical, which we understand in detail is the chemical testosterone. Testosterone—we all have it but some of us have rather more than others—testosterone is of course a gene that is made—switched on by the Y chromosome and makes males male. Women have a small amount but only a small amount and as they get older … Now testosterone is a dangerous, dangerous thing to have. I don’t recommend it, those of you who have it, don’t get it. And if you’ve got some, don’t get any more.” What bullshit! This guy is a literal genetics Ph.D. saying this; this is proof that knowledge/educational attainment does not stop you from saying dumb, untrue things.
“I don’t know that this character does it, but certainly plenty of bodybuilders inject steroids—testosterone—into themselves. They damage themselves severely. Their life expectancy goes down strikingly. They die for all those male reasons. They die from violence, they die from suicide, they die from car accidents, they die from heart disease, all those things are true of males. … But even if you look at males and females in general, there is kind of a depressing picture for half of the room, I’m not sure which half.” Jones then talks about how men die at a much higher rate than women for a slew of reasons. This is his logic: Men have higher testosterone than women. Testosterone is shown to cause violence, aggression, heart disease, risk-taking, etc. Men have way more testosterone than women. Therefore testosterone is the reason why men die more than women and commit more violence than women. This is horrible logic—coming from a geneticist no less!
“Men actually—less expectedly perhaps—are much less good at dealing with parasites and infectious disease than women are. And that’s because testosterone—the male hormone—suppresses the immune system. Now the immune system fights off the parasites and we don’t do nearly as well.” There is actually some empirical data for his argument here. Back in 2013, it was shown that testosterone, gene expression, and the immune system were linked. They discovered that higher levels of testosterone prevented Module 52 genes from turning on. So higher levels of testosterone result in more Module 52 expression. Testosterone also does exert immune-suppressing effects, “increasing the severity of malaria, leishmaniasis, amebiasis, and tuberculosis, while at the same time supporting the clearance of toxoplasmosis (Bernin & Lotter, 2014; Nhamoyebonde & Leslie, 2014)” (Giefing-Kroll et al, 2015). The suppressive effects of testosterone on the immune system and how down-regulates “the systemic immune response by cell type specific effects in the context of immunological disorders.” (Trigunaite, Dimo, and Jorgensen, 2015).
The effects of testosterone replacement therapy (TRT) on the immune system have not been looked into, but it has a positive effect on elderly men (Osterberg, Bernie, and Ramasamy, 2014). However, Braude, Tang-Martinez, and Taylor (1999) challenge the wisdom that testosterone is an immuno-depressor. This is Jones’ only claim that is not outright wrong; there is data out there for both positions (of course I think that Braude, Tang-Martinez and Taylor, 1999 drive a solid argument against the testosterone-causes-immuno-suppression hypothesis).
The Jones says one of the dumbest things I’ve ever heard “And men, of course, are murdered much more than women. And who murders them—of course—other men. … Men murder at a much higher rate than women. … And that effect is striking—that effect is true worldwide—all over the world men, testosterone, murder at 10 times the rate of women. … So it’s a universal, it’s a biological universal, it’s clearly due to testosterone. There’s no question. The evidence is absolutely clear. So it’s a genetic phenomenon, it’s a gene for crime.” Should I be nice here and assume that whatever ‘gene’ he’s proposing that ’causes’ testosterone production actually causes the crime? Or should I take what he said at face value—that testosterone is a literal gene that causes crime? I think I’ll go with the second one.
“It’s certainly genetic, it’s also environmental. And you can’t disentangle it. You can change part of it—the environment—you can’t change the other part—the genes. And I always find it kind of odd that the public is so interested in the bit you can’t change—the genes—and is so uninterested in the bit you can—the environment.” This is wrong. Not all of it, but most of it. I don’t think that people are more interested in genes and toss aside environment—especially for testosterone. Because, as I documented yesterday, hereditarians assume that since testosterone has a heritability of around .6 then it must be mostly genetic in nature. This is wrong. As Jones said, the environment effects testosterone production too (though he didn’t go into the mechanisms).
The Left goes to the environment side—change the environment, change hormone production (this is true)—whereas the Right goes to the genes side—can’t change genes and environment is a product of genes so nothing can be done. (Oversimplified, don’t crucify me.) Both are wrong. Strong genetic determinism (gene G almost always leads to the development of trait T. (G increases the probability of T and the probability of T, given G, is 95% or greater) doesn’t make sense because a large majority of traits are moderately or weakly determined by genetics (Resnick and Vorhaus, 2006).
In sum, Jones is clueless about testosterone. He only really said one thing that is not outright wrong (but it is questionable). It doesn’t cause crime, it doesn’t cause men to murder more. The press has gotten all of these views into people’s heads because they want to demonize men—and the hormone that is largely responsible for male-ness. It’s incredible that this guy is both a geneticist, science writer and professor of genetics and still calls testosterone a ‘gene’ saying that it is responsible for ‘most of the crime’ committed. Anyone who has been reading this blog for the past year or so since I have began revising many of my main views knows how wrong this is. People really need to get a clue on testosterone and stop spreading bullshit. I know that I’ll have to keep correcting misconceptions on testosterone for a good long time (like with r/K theory) but I enjoy writing about both things so it’s not too big a deal. I just wish people would actually educated themselves on basic physiology so that the trainwreck of a video that Jones made does not get made.
No, Black Women Do Not Have Higher Testosterone than White Women (And More On Hereditarian Claims on Racial Testosterone Differences)
It has been over a year since I wrote the article Black Women and Testosterone, and I really regret it. Yes, I did believe that black women had higher levels of testosterone than white women due to one flimsy study and another article on pregnant black women. I then wised up to the truth about testosterone and aggression/crime/race/sex and revised the articles (like I have done with r/K selection theory). However, after I revised my views on the supposed differences in testosterone between black men/white men and black women/white women, people still cite the article, disregarding the disclaimer at the top of the article. I quoted Mazur (2016), who writes (emphasis mine):
The pattern [high testosterone] is not seen among teenage boys or among females.
There is no indication of inordinately high T among young black women with low education.
Honor cultures are cast as male affairs, but with T data in hand for both sexes, it is worth exploring whether or not a similar pattern exists among women. Mean T was calculated as a function of age for the four combinations of race and education used in Table 1 but now for women. All plots show T declining with age, from about 35 ng/dL in the 20–29 age group to about 20 ng/dL among women 60 years and older. The four plots essentially overlap without discernible differences among them. Given the high skew of T among adult females, both raw and ln-transformed values were analyzed with similar results. There is no indication of inordinately high T among young black women with low education.
In the present study, at least, the sexes differ because the very high T seen among young black men with low education does not occur among young black women with low education.
This is very clear… Mazur (2016) analyzed the NHANES 2011-2012 data and this is what he found. I understand that most HBD bloggers do believe this, well, like a lot of their strong assertions (which I have rebutted myself), they’re wrong. They don’t get it. They do not understand the hormone.
The reason why I’m finally writing this (which is long overdue) is that I saw a referral from this website today: https://www.minds.com/RedPillTV who writes about the aforementioned black women and testosterone article:
It is known that blacks have the highest levels of testosterone out of the major races of humanity. However, what’s not known is that black women have higher rates than white women. The same evolutionary factors that make it possible for black men to have high testosterone make it possible for women as well.
…..No. It seems that people just scroll on by the disclaimer at the top that is bolded and italicized and just go to the (now defunct) article and attempt to prove their assertion that black women have higher testosterone than white women with an article that I have stated myself I no longer believe and have provided the rationale/data for the position. This shows that people have their own biases and no matter what the author writes about their views that have changed due to good arguments/data, they will still attempt to use the article to prove their assertion.
I’ve written at length that testosterone does not cause 1) aggression, 2) crime and 3) prostate cancer. People are scared of testosterone mostly due to the media fervor of any story that may have a hint of ‘toxic masculinity’. They (most alt-righters) are scared of it because of Lynn/Rushton/Templer/Kanazawa bullshit on the hormone. Richard Lynn doesn’t know what he’s talking about on testosterone. No, Europeans did not need lower levels of aggression in the cold; Africans didn’t need higher levels of aggression (relative to Europeans) to survive in the tropics. The theory that supposed differential testosterone differences between the races are “the physiological basis in males of the racial differences in sexual drive which form the core of the different r/K reproduction strategies documented by J.P. Rushton” (Lynn, 1990: 1203). The races, on average, do not differ in testosterone as I have extensively documented. So hereditarians like Lynn and others need to look for other reasons to explain blacks’ higher rate of sexual activity.
Rushton’s views on the testosterone and supposed r/K continuum have been summarily rebutted by me. These psychologists’ views on the hormone (that they don’t understand the production of nor do they understand the true reality of the differences between the races) are why people are afraid of testosterone. No, testosterone is not some ‘master switch’ as Rushton (1999) asserts. Rushton asserts that racial differences in temperament are mediated by the hormone testosterone. He further dives into this assertion stating “Testosterone level correlates with temperament, self-concept, aggression, altruism, crime, and sexuality, in women as well as in men (Harris, Rushton, Hampson, & Jackson, 1996). It may ‘correlate’ with aggression and crime, but as I have documented, they do not cause either.
The aggression/testosterone correlation is only .08 (Archer, Graham-Kevan, and Davies, 2005). Furthermore, the diurnal variation in testosterone does not directly correlate to when testosterone levels are highest in the day (at 8 am and drop thereafter), with adults peaking in crime at 10 pm and kids at 3 pm, with rises at 8 pm and 12 pm (not surprisingly, kids go in to school around 8 am, go to recess at 12 and leave at 3).
If you’ve read as much Rushton as I have, you’ll notice that he begins to sound like a broken record when talking about certain things. One of the most telling is Rushton’s repeated assertions that blacks average 3-19 percent higher testosterone than whites. The 3 percent number comes from Ellis and Nyborg (1992) and the 19 percent number comes from Ross et al (1986) (which Rushton should know that after adjustments for confounding, it decreased to 13 percent). These are the only studies that hereditarians ever cite for these claims that blacks average higher testosterone than whites. That seems a bit fishy to me. Cite a 30-year-old study along with a 25-year-old study (with such huge variation from Rushton and those who cite him for this matter—3-19 percent!!) as ‘proof’ that blacks average such higher levels of testosterone in comparison to whites.
Ross et al (1986) is one of the most important studies to rebut for this hereditarian claim that testosterone causes all of these maladies in black American populations. Ross et al (1986) propose that higher levels of the hormone lead to the higher rates of prostate cancer in black American populations. However, meta-analyses do not show this (Zagars et al, 1998; Sridhar et al, 2010).
Rushton et al’s assertions—largely—lie on this supposed testosterone difference between the races and how it supposedly leads to higher rates of crime, prostate cancer, aggression, and violence. However, the truth of the matter is, this is all just hereditarian bullshit. Larger analyses—as I have extensively documented—do not show this trend. And even accepting the claim that blacks have, say, 19 percent higher levels of testosterone than whites, it still would not explain the supposed prostate cancer rates between the races (Stattin et al, 2003; Michaud, Billups, and Partin, 2015). Even if blacks had 19 percent higher testosterone than whites, it would not explain higher levels of crime nor aggression due to such a hilariously low correlation of .08 (Archer, Graham-Kevan, and Davies, 2005).
Finally, I have a few words for Michael Hart and his (albeit sparse) claims on testosterone in his 2007 book Understanding Human History.
Hart (2007) writes:
(Many of these differences in sexual behavior may be a consequence of the fact that
blacks, on average, have higher levels of testosterone than whites.7) (pg. 127)
And….. footnote number 7 is…. surprisingly (not): 7) Ross, R., et al. (1986). Not going to waste my time on this one, again. I’ve pointed out numerous flaws in the study. (I will eventually review the whole thing.)
It seems unlikely, though, that the higher testosterone level in blacks — which is largely genetic in origin — has no effect on their sexual behavior (pg. 128; emphasis mine)
This is bullshit. People see the moderately high heritability of testosterone (.60; Harris, Vernon, and Boomsma, 1998) and jump right to the “It’s genetics!!!” canard without even understanding its production in the body (it is a cholesterol-based hormone which is indirectly controlled by DNA, there are no ‘genes for’ testosterone). Here are the steps: 1) DNA codes for mRNA; 2) mRNA codes for the synthesis of an enzyme in the cytoplasm; 3) luteinizing hormone stimulates the production of another messenger in the cell when testosterone is needed; 4) this second messenger activates the enzyme; 5) the enzyme then converts cholesterol to testosterone
I have documented numerous lines of evidence showing that testosterone is extremely sensitive to environmental factors (Mazur and Booth, 1998; Mazur, 2016), and due to the homeodynamic physiology we have acquired due to ever-changing environments (Richardson, 2017), this allows our hormones to up- or down-regulate depending on what occurs in the environment. The quote from Hart is bullshit; he doesn’t know what he’s talking about.
For females in Siberia, the disadvantages of failing to find a man who would
provide for her and her children during their childhood were much greater than they were in tropical climates, and females who were not careful to do so were much less likely to pass on their genes. Furthermore, because females in harsh climates were so demanding on this point, males who seemed unlikely to provide the needed assistance found it hard to find mates. In other words, there was a marked sexual selection against such males. Such selection could result, for example, in the peoples living in northerly climates gradually evolving lower levels of testosterone than the peoples living in subSaharan Africa. (pg. 131)
This is a bullshit just-so story. Africans in Africa have lower levels of testosterone than Western men (Campbell, O’Rourke, and Lipson, 2003; Lucas and Campbell, and Ellison, 2004; Campbell, Gray, and Ellison, 2006).
Note also that a difference in testosterone level frequently affects not
only the sexual behavior of a young male, but also his aggressiveness.
No it does not (Archer, Graham-Kevan, and Davies, 2005).
Thankfully, that’s all he wrote about testosterone. There is so much bullshit out there. Though, people who like and seek out the truth will learn that there are no racial differences and that testosterone does not cause crime/aggression/prostate cancer and that it’s just hereditarian bullshit.
The evidence I have amassed and the arguments I have given point to a few things: 1) the races do not differ in testosterone/there is a small negligible difference; 2) testosterone does not cause crime; 3) testosterone does not cause aggression; 4) black women do not have higher levels of testosterone than white women; 5) high levels of testosterone do not cause prostate cancer; and 6) even allowing a 19 percent black/white difference will not have hereditarian claims hold true.
So for anyone who comes across my old articles on testosterone and sex/race, do a bit more reading of my newer material here to see my new viewpoints/arguments. DO NOT cite these articles as proof for your claims of higher levels of black men/women. DO cite the old articles ALONG WITH the new ones to show how and why my views changed along with the studies I have cited that changed my view. (Actually understanding the production of testosterone in the body was a huge factor too, which I talk about in Why Testosterone Does Not Cause Crime.)
According to a new article published at The Guardian, testosterone does affect human cognition and decision-making. The article, titled, Now we men can blame our hormones: testosterone is trouble, by Phil Daoust, is yet more media sensationalism against testosterone. Daoust’s article is full of assumptions and conclusions that do not follow from an article he cites on testosterone and cognitive reflection and decision making.
The cited article, Single dose testosterone administration impairs cognitive reflection in men, states that endogenous testosterone (testosterone produced in the body) is correlated with physical aggression. However, I’ve shown that this is not true. They conclude overall the exogenous testosterone is related to an increase in irrational thinking and decision-making. Nothing wrong with concluding that from the data. However, Daoust’s interpretation and conclusions he draws from this study are wrong, mostly due to the same old tales and misconceptions about testosterone.
This is the largest study of the effect of exogenous testosterone and decision-making and cognition. The authors show that men administered a gel that was rubbed into the upper body that is used for TRT (testosterone replacement therapy) showed “incorrect intuitive answers were more common, and correct answers were less common in the T group, for each of the three CRT questions analyzed separately” (Nave et al, 2017: 8). However, what The Guardian article does not state is that this relationship could be mediated by more than testosterone, such as motivation and arithmetic skills.
Nevertheless, those who rubbed themselves with the testosterone gel answered 20 percent fewer questions correctly. This was attributed to the fact that they were more likely to be anxious and not think about the answer. One of the authors also states that either testosterone inhibits the action of mentally checking your work or it increases the intuitive feeling that you’re definitely right (since those who rubbed themselves with T gel gave more intuitive answers, implying that the testosterone made them go to their first thought in their head). I have no problems with the paper—other than the fact that gel has an inconsistent absorption rate and has high rates of aromatization. The study has a good design and I hope it gets explored more. I do have a problem with Dauost’s interpretation of it, however.
A host of studies have already shown a correlation between elevated testosterone levels and aggression – and now they’re being linked to dumb overconfidence.
The ‘host of studies‘ that ‘have already shown a correlation between elevated testosterone levels and aggression‘ don’t say what you think they do. This is another case of the testosterone sensationalism of the media—talking about a hormone they don’t really know anything about.
That won’t help with the marketing – though it may explain Donald Trump and his half-cocked willy-waggling. Perhaps it’s not the president’s brain that’s running things, but the Leydig cells in his testicles.
Nice shot. This isn’t how it works, though. You can’t generalize a study done on college-aged males to a 71-year-old man.
Women aren’t entirely off the hook – their bodies also produce testosterone, though in smaller quantities, and the Caltech study notes that “it remains to be tested whether the effect is generalisable to females” – but for now at least they now have another way to fight the scourge of mansplaining: “You’re talking out of your nuts.”
Another paragraph showing no understanding, even bringing up the term ‘mansplaining’—whatever that means. This article is, clearly, demonizing high T men, and is a great example of the media bias on testosterone studies that I have brought up in the past.
Better still, with the evils of testosterone firmly established, the world may learn to appreciate older men. Around the age of 30, no longer “young, dumb and full of cum”, we typically find our testosterone levels declining, so that with every day that passes we become less aggressive, more rational and generally nicer.
“The evils of testosterone firmly established“, nice job at hiding your bias. Yes the cited article (Nave et al 2017) does bring up how testosterone is linked to aggression. But, for the millionth time, the correlation between testosterone and aggressive behavior is only .08 (Archer, Graham-Kevan, and Davies, 2005).
Even then, most of the reduction of this ‘evil hormone’ is due to lifestyle changes. It just so happens that around the ages 25-30—when most men notice a decrease in testosterone levels—that men begin to change their lifestyle habits, which involve marriage which decreases testosterone levels (Gray et al, 2002; Burnham et al, 2003; Gray, 2011; Pollet, Cobey, and van der Meij, 2013; Farrelly et al, 2015; Holmboe et al, 2017), having children (Gray et al, 2002; Gray et al, 2006; Gettler et al, 2011) to obesity (Palmer et al, 2012; Mazur et al, 2013; Fui, Dupuis, and Grossman, 2014; Jayaraman, Lent-Schochet, and Pike, 2014; Saxbe et al, 2017) smoking is not clearly related to testosterone (Zhao et al, 2016), and high-carb diets decrease testosterone (Silva, 2014).
So the so-called age-related decline in testosterone is not really age-related at all—it has to do with environmental and social factors which then decreases testosterone (Shi et al, 2013). Why should a man be ‘happy’ that his testosterone levels are decreasing due—largely—to his lifestyle? Low testosterone is related to cardiovascular risk (Maggio and Basaria, 2009), insulin sensitivity (Pitteloud et al, 2005; Grossman et al, 2008), metabolic syndrome (Salam, Kshetrimayum, and Keisam, 2012; Tsuijimora et al, 2013), heart attack (Daka et al, 2015), elevated risk of dementia in older men (Carcaillon et al, 2014), muscle loss (Yuki et al, 2013), and stroke and ischemic attack (Yeap et al, 2009).
So it seems that, contrary to Phil Daoust’s (the author of The Guardian article on testosterone) claims that low testosterone is associated with less aggressive behavior, more rationality and being nicer, in general, are wrong. Low testosterone is associated with numerous maladies, and the Daoust is trying to make low testosterone out to be ‘a good thing’, while demonizing men with higher levels of testosterone with cherry-picked studies and not large meta-analyses like I have cited that show that testosterone has an extremely low correlation with aggressive behavior.
As I have covered in the past, testosterone levels in the West are declining, along with semen count and quality. These things are due, largely in part, to social and environmental factors such as obesity, low activity, and an overall change in lifestyle. One (albeit anecdotal) reason I could conjure up has to do with dominance. Testosterone is the dominance hormone and so if testosterone levels are declining, then that means men must not be showing dominance as much. I would place part of the blame here on feminism and articles like the one reviewed here as part of the problem. So contra the author’s assertion, lower levels of testosterone into old age are not good, since that signifies a change in lifestyle—many of which are in the control of the male in question (I, of course, would not advise anyone to not have children or get married).
Nave et al (2017) lead the way for further research into this phenomenon. If higher doses of exogenous testosterone do indeed inhibit cognitive reflection, then, as the authors note, “The possibility that this widely prescribed treatment has unknown deleterious influences on specific aspects of decision-making should be investigated further and taken into account by users, physicians, and policy makers” (Nave et al, 2017: 11). This is perhaps one of the most important sentences in the whole article. This is about the application of testosterone-infused gel and decision-making. They’re talking about the implications of administering the gel to men and how it affects decision-making and cognitive reflection. This study is NOT generalizable for 1) endogenous testosterone and 2) non-college students. If the author understood the paper and science, he wouldn’t make those assumptions about Trump’s Leydig cells in his testicles “running the show”.
Because of the testosterone fear, good studies like Nave at al (2017) get used for an agenda by people who don’t understand the hormone. People the the Right and Left both have horrible misconceptions about the hormone, and some cannot interpret studies correctly and draw the correct conclusions from them. Testosterone—endogenous or exogenous—does not cause aggression (Batrinos, 2012). This is an established fact. The testosterone decrease between the ages of 25-30 is avoidable if you don’t change to bad habits that decrease testosterone. All in all, the testosterone scare is ridiculous. People are scared of it because they don’t understand it.
Daoust didn’t understand the article he cited and drew false conclusions from his misinterpretations. I would be interested to see how men would fare on a cognitive reflection test after, say, their favorite team scored during a game, and not after being given supraphysiological doses of testosterone gel. Drawing conclusions like Daoust did, however, is wrong and will mislead numerous more people under the guise of science.