NotPoliticallyCorrect

Home » testosterone

Category Archives: testosterone

The ENA Theory: On Testosterone and Aggressive Behavior by Race/Ethnicity

3250 words

A commenter by the name of bbloggz alerted me to a new paper by Lee Ellis published this year titled Race/ethnicity and criminal behavior: Neurohormonal influences in which Ellis (2017) proposed his theory of ENA (evolutionary neuroandrogenic theory) and applied it to racial/ethnic differences in crime. On the face, his theory is solid and it has great explanatory power for the differences in crime rates between men and women, however, there are numerous holes in the application of the theory in regards to racial/ethnic differences in crime.

In part I, he talks about racial differences in crime. No one denies that, so on to part II.

In part II he talks about environmental causes for the racial discrepancies, that include economic racial disparities, racism and societal discrimination and subordination, a subculture of violence (I’ve been entertaining the honor culture hypothesis for a few months; Mazur (2016) drives a hard argument showing that similarly aged blacks with some college had lower levels of testosterone than blacks with less than high school education which fits the hypothesis of honor culture. Though Ellis’ ENA theory may account for this, I will address this below). However, if the environment that increases testosterone is ameliorated (i.e., honor culture environments), then there should be a subsequent decrease in testosterone and crime, although I do believe that testosterone has an extremely weak association with crime, nowhere near high enough to account for racial differences in crime, the culture of honor could explain a good amount of the crime gap between blacks and whites.

Ellis also speaks about the general stress/strain explanation, stating that blacks have higher rates of self-esteem and Asians the lowest, with that mirroring their crime rates. This could be seen as yet another case for the culture of honor in that blacks with a high self-esteem would feel the need to protect their ‘name’ or whatever the case may be and feel the need for physical altercation based on their culture.

In part III, Ellis then describes his ENA theory, which I don’t disagree with on its face as it’s a great theory with good explanatory power but there are some pretty large holes that he rightly addresses. He states that, as I have argued in the past, females selected men for higher rates of testosterone and that high rates of testosterone masculinize the brain, changing it from its ‘default feminine state’ and that the more androgens the brain is exposed to, the more likely it is for that individual to commit crime.

Strength

Ellis cites a study by Goodpaster et al (2006) in which he measured the races on the isokinetic dynamometry, pretty much a leg extension. However, one huge confound is that participants who did not return for follow-up were more likely to be black, obese and had more chronic disease (something that I have noted before in an article on racial grip strength). I really hate these study designs, but alas, it’s the best we have to go off of and there are a lot of holes in them that must be addressed. Though I applaud the researchers’ use of the DXA scan (regular readers may recall my criticisms on using calipers to assess body fat in the bench press study, which was highly flawed itself; Boyce et al, 2014) to assess body fat as it is the gold standard in the field.

Ellis (2017: 40) writes: “as brain exposure to testosterone surges at puberty, the prenatally-programmed motivation to strive for resources, status, and mating opportunities will begin to fully activate.” This is true on the face, however as I have noted the correlation between physical aggression and testosterone although positive is low at .14 (Archer, 1991; Book et al, 2001). Testosterone, as I have extensively documented, does cause social dominance and confidence which do not lead to aggression. However, when other factors are coupled with high testosterone (as noted by Mazur, 2016), high rates of crime may occur and this may explain why blacks commit crime; a mix of low IQ, high testosterone and low educational achievement making a life of crime ‘the smart way’ to live seeing as, as Ellis points out, and that intelligent individuals find legal ways to get resources while less intelligent individuals use illegal ways.

ENA theory may explain racial differences in crime

In part IV he attempts to show how his ENA theory may explain racial differences in crime—with testosterone sitting at the top of his pyramid. However, there are numerous erroneous assumptions and he does rightly point out that more research needs to be done on most of these variables and does not draw any conclusions that are not warranted based on the data he does cite. He cites one study in which testosterone levels were measured in the amniotic fluid of the fetus. The sample was 59 percent white and due to this, the researchers lumped blacks, ‘Hispanics’ and Native Americans together which showed no significant difference in prenatal testosterone levels (Martel and Roberts, 2014).

Umbilical cord and testosterone exposure

Ellis then talks about testosterone in the umbilical cord, and if the babe is exposed to higher levels of testosterone in vitro, then this should account for racial/ethnic differences in crime. However, the study he cited (Argus-Collins et al, 2012) showed no difference in testosterone in the umbilical cord while Rohrmann et al (2009) found no difference in testosterone between blacks and whites but found higher rates of SHBG (sex hormone-binding globulin) which binds to testosterone and makes it unable to leave the blood which largely makes testosterone unable to affect organ development. Thusly, if the finding of higher levels of SHBG in black babes is true, then they would be exposed to less androgenic hormones such as testosterone which, again, goes against the ENA theory.

He also cites two more studies showing that Asian babes have higher levels of umbilical cord testosterone than whites (Chinese babes were tested) (Lagiou et al, 2011; Troisi et al, 2008). This, again, goes against his theory as he rightly noted.

Circulating testosterone

Next he talks about circulating differences in testosterone between blacks and whites. He rightly notes that testosterone must be assayed in the morning within an hour after waking as that’s when levels will be highest, yet cites Ross et al (1986) where assay times were all over the place and thusly testosterone cannot be said to be higher in blacks and whites based on that study and should be discarded when talking about racial differences in testosterone due to assay time being between 10 am and 3 pm. He also cites his study on testosterone differences (Eliss and Nyborg, 1993), but, however, just as Ross et al (1986) did not have a control for WC (waist circumference) Ellis and Nyborg (1993) did not either, so just like the other study that gets cited to show that there is a racial difference in testosterone, they are pretty hugely flawed and should not be used in discussion when discussing racial differences in testosterone. Why do I not see these types of critiques for Ross et al (1986) in major papers? It troubles me…

He also seems to complain that Lopez et al (2013) controlled for physical activity (which increases testosterone) and percent body fat (which, at high levels, decreases testosterone). These variables, as I have noted, need to be controlled for. Testosterone varies and fluctuated by age; WC and BMI vary and fluctuate by age. So how does it make sense to control for one variable that has hormone levels fluctuate by age and not another? Ellis also cites studies showing that older East Asian men had higher levels of testosterone (Wu et al, 1995). Nevertheless, there is no consensus; some studies show Chinese babes have higher levels of testosterone than whites and some studies show that whites babes have higher levels of testosterone than Chinese babes. Indeed, this meta-analysis by Ethnicmuse shows that Asians have the highest levels, followed by Africans then Europeans, so this needs to be explained to save the theory that testosterone is the cause of black overrepresentation of violence (as well as what I showed that testosterone is important for vital functioning and is not the boogeyman the media makes it out to be).

Bone density and crime

Nevertheless, the next variable Ellis talks about is bone density and its relationship to crime. Some studies find that blacks are taller than whites while other show no difference. Whites are also substantially taller than Asian males. Blacks have greater bone density than the other three races, but according to Ellis, this measure has not been shown to have a relationship to crime as of yet.

Penis size, race and crime

Now on to penis size. In two articles, I have shown that there is no evidence for the assertion that blacks have larger penises than whites. However, states that penis length was associated with higher levels of testosterone in Egyptian babes. He states that self-reported penis size correlates with self-reports of violent delinquency (Ellis and Das, 2012). Ellis’ main citations for the claim that blacks have larger penises than other races comes from Nobile (1982), the Kinsey report, and Rushton and Boagert (1987) (see here for a critique of Rushton and Boagert, 1987), though he does cite a study stating that blacks had a longer penis than whites (blacks averaging 5.77 inches while whites averaged 5.53 inches). An HBDer may go “Ahah! Evidence for Rushton’s theory!”, yet they should note that the difference is not statistically significant; just because there is a small difference in one study also doesn’t mean anything for the totality of evidence on penis size and race—that there is no statistical difference!

He then cites Lynn’s (2013) paper which was based on an Internet survey and thus, self-reports are over-measured. He also cites Templer’s (2002) book Is Size Important?, which, of course, is on my list of books to read. Nevertheless, the ‘evidence’ that blacks average larger penises than whites is extremely dubious, it’s pretty conclusive that the races don’t differ in penis size. For further reading, read The Pseudoscience of Race Differences in Penis Sizeand read all of Ethnicmuses’ posts on penis size here. It’s conclusive that there is no statistical difference—if that—and any studies showing a difference are horribly flawed.

2d/4d ratio and race

Then he talks about 2d/4d ratio, which supposedly signifies higher levels of androgen exposure in vitro (Manning et al, 2008) however these results have been challenged and have not been replicated (Koehler, Simmons, and Rhodes, 2004; Yan et al, 2008, Medland et al, 2010). Even then, Ellis states that in a large analysis of 250,000 respondents, Asians had the lowest 2d/4d ratio, which if the hypothesis of in vitro hormones affecting digit length is to be believed, they have higher levels of testosterone than whites (the other samples had small ns, around 100).

Prostate-specific antigens, race, and prostate cancer

He then talks about PSA (prostate-specific antigen) rates between the races. Blacks are two times more likely to get prostate cancer, which has been blamed on testosterone. However, I’ve compiled good evidence that the difference comes down to the environment, i.e., diet. Even then, there is no evidence that testosterone causes prostate cancer as seen in two large meta-analyses (Stattin et al, 2003; Michaud, Billups, and Partin, 2015). Even then, rates of PCa (prostate cancer) are on the rise in East Asia (Kimura, 2012; Chen et al, 2015Zhu et al, 2015) which is due to the introduction of our Western diet. I will cover the increases in PCa rates in East Asia in a future article.

CAG repeats

He then reviews the evidence of CAG repeats. There is, however, no evidence that the number of CAG repeats influences sensitivity to testosterone. However, intra-racially, lower amounts of CAG repeats are associated with higher spermatozoa counts—but blacks don’t have higher levels of spermatozoa (Mendiola et al, 2011; Redmon et al, 2013). Blacks do have shorter CAG repeats, and this is consistent with the racial crime gap of blacks > whites > Asians. However, looking at the whole of the evidence, there is no good reason to assume that this has an effect on racial crime rates.

Intelligence and education

Next he talks about racial differences in intelligence and education, which have been well-established. Blacks did have higher rates of learning disabilities than whites who had higher levels of learning disabilities then Asians in a few studies, but other studies show whites and South Asians having different rates, for instance. He then talks about brain size and criminality, stating that the head size of males convicted for violent crimes did not differ from males who committed non-violent crimes (Ikaheimo et al, 2007). I won’t bore anyone with talking about what we know already: that the races differ in average brain size. However, a link between brain size and criminality—to the best of my knowledge—has yet to been discovered. IQ is implicated in crime, so I do assume that brain size is as well (no matter if the correlation is .24 or not; Pietschnig et al, 2015).

Prenatal androgen exposure

Now to wrap things up, the races don’t differ in prenatal androgen exposure, which is critical to the ENA theory; there is a small difference in the umbilical cord favoring blacks, and apparently, that predicts a high rate of crime. However, as noted, blacks have higher levels of SHBG at birth which inhibits the production of testosterone on the organs. Differences in post-pubertal testosterone are small/nonexistent and one should not talk about them when talking about differences in crime or disease acquisition such as PCa. DHT only shows a weak positive correlation with aggression—the same as testosterone (Christiansen and Winkler, 1992; however other studies show that DHT is negatively correlated with measures of physical aggression; Christiansen and Krussmann, 1987; further, DHT is not so evil after all).

Summing it all up

Blacks are not stronger than whites, indeed evidence from the races’ differing somatype, grip strength and leverages all have to do with muscular strength. Furthermore, the study that Ellis cites as ‘proof’ that blacks are stronger than whites is on one measure; an isokinetic dynamometry machine which is pretty much a leg extension. In true tests of strength, whites blow blacks away, which is seen in all major professional competitions all around the world. Blacks do have denser bones which is due to androgen production in vitro, but as of yet, there has been no research done into bone density and criminality.

The races don’t differ on penis size—and if they do it’s by tenths of an inch which is not statisitcally significant and I won’t waste my time addressing it. It seems that most HBDers will see a racial difference of .01 and say “SEE! Rushton’s Rule!” even when it’s just that, a small non-significant difference in said variable. That’s something I’ve encountered a lot in the past and it’s, frankly, a waste of time to converse about things that are not statistically significant. I’ve also rebutted the theory on 2d/4d ration as well. Finally, Asians had a similar level of androgen levels compared to blacks, with whites having the least amount. Along with a hole in the theory for racial differences in androgen causing crime, it’s yet another hole in the theory for racial differences in androgens causing racial differences in penis size and prostate cancer.

On intelligence scores, no one denies that blacks have scored about 1 SD lower than whites for 100 years, no one denies that blacks have a lower educational attainment. In regards to learning disabilities, blacks seem to have the highest rates, followed by Native Americans, than non-Hispanic whites, East Asians and the lowest rates found in South Asians. He states only one study links brain size to criminal behavior and it showed a significant inverse relationship with crime but not other types of offenses.

This is a really good article and I like the theory, but it’s full of huge holes. Most of the variables described by Ellis have been shown to not vary at all or much between the races (re: penis size, testosterone, strength [whites are stronger] prostate cancer caused mainly by diet, 2d/4d ratio [no evidence of it showing a digit ratio difference], and bone density not being studied). Nevertheless, a few of his statements do await testing so I await future studies on the matter. He says that androgen exposure ‘differs by race and ethnicity’, yet the totality of evidence shows ‘not really’ so that cannot be the cause of higher amounts of crime. Ellis talks about a lot of correlates with testosterone, but they do not pass the smell test. Most of it has been rebutted. In fact, one of the central tenets of the ENA theory is that the races should differ in 2d/4d ratio due to exposure of differing levels of the hormone in vitro. Alas, the evidence to date has not shown this—it has in fact shown the opposite.

ENA theory is good in thought, but it really leaves a lot to be desired in regards to explaining racial differences in crime. More research needs to be looked into in regards to intelligence and education and its effect on crime. We can say that low IQ people are more likely to drop out of school and that is why education is related to crime. However, in Mazur (2016) shows that blacks matched for age had lower levels of testosterone if they had some college under their belt. This seems to point in the direction of the ENA theory, however then all of the above problems with the theory still need to be explained away—and they can’t! Furthermore, one of the nails in the coffin should be this: East Asian males are found to have higher levels of testosterone than white males, often enough, and East Asian males actually have the lowest rate of crime in the worle!

This seems to point in the direction of the ENA theory, however then all of the above problems with the theory still need to be explained away—and they can’t! Furthermore, one of the nails in the coffin should be this: East Asian males are found to have higher levels of testosterone than white males, often enough, and East Asian males actually have some of the lowest rate of crime in the world (Rushton, 1995)! So this is something that needs to be explained if it is to be shown that testosterone facilitates aggression and therefore, crime.

Conclusion

I’ve shown—extensively—that there is a low positive correlation between testosterone and physical aggression, why testosterone does not cause crime, and have definitively shown that, by showing how flawed the other studies are that purport to show blacks have higher testosterone levels than whites, along with citing large-scale meta-analyses, that whites and blacks either do not differ or the differences is small to explain any so-called differences in disease acquisition or crime. One final statement on the CAG repeats, they are effect by obesity, men who had shorter CAG repeats were more likely to be overweight, which would skew readings (Gustafsen, Wen, and Koppanati, 2003). So depending on the study—and in most of the studies I cite whites have a higher BMI than blacks—BMI and WC should be controlled for due to the depression of testosterone.

It’s pretty conclusive that testosterone itself does not cause crime. Most of the examples cited by Ellis have been definitively refuted, and his other claims lack evidence at the moment. Even then, his theory rests on the 2d/4d ratio and how blacks may have a lower 2d/4d ratio than whites. However, I’ve shown that there is no significant relationship between 2d/4d ratio and traits mediated by testosterone (Kohler, Simmons, and Rhodes, 2004) so that should be enough to put the theory to bed for good.

Why Testosterone Does Not Cause Crime

1800 words

Recently, I’ve written at length on racial differences in testosterone and how the correlation between testosterone and physical aggression is .14. Pitifully low to account for the cause of crime and any overall differences in racial crime (that will be touched on at length in the future). Tonight I will show, yet again, why testosterone does not cause crime by looking at what times most crimes are committed by both adults and children under the age of 18. This will definitively put the ‘testosterone causes crime’ myth to bed for good.

Before I get into the time of day that most crimes are committed, I must talk about the production of testosterone in the body. There are no ‘genes for’ testosterone (although men who had three certain alleles had a 6.5 fold higher risk of having low testosterone; Ohlsson et al, 2011, I am unaware of there being a variation by race; over 10,000 Caucasian men were studied). There is, however, an indirect control of testosterone synthesis by DNA. DNA regulates the production of testosterone by coding for enzymes that convert cholesterol to testosterone (testosterone is a cholesterol-based hormone).

There are five simple steps to the production of testosterone: 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). That’s how testosterone is produced in the body. It is indirectly controlled by DNA.

qa03401_2010

Above is a graph from the Office of Juvenile Justice and Delinquency Prevention which shows the time of day that most crimes are committed. Notice how crime goes up as the time of day goes on and since kids are at school, they’re more likely to fight. This then peaks at 3 pm when kids are getting out of school.

Now look at rates of crime for adults. At its peak of 10 pm, it’s vastly lower than that of people under the age of 18, which is important to keep in mind. You can see how at 8 am that rates of crime are low for adults and high for kids, right when they would be entering school so there would be a lot of other kids around and the chance for violence goes up. Keep the times of 8 am (kids when they enter school), 12 pm (when most kids go on lunch) and 3 pm (when most kids get out of school) along with the hours of 12 pm to 8 pm for adults (when 74 percent of crimes are committed by adults).

The OJJDP writes:

  • 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.
  • Nearly one-third (29%) of all violent crime committed by juvenile offenders occurs between 3 p.m. and 7 p.m. In comparison, 26% of all violent committed by adult offenders occurs between 8 p.m. and 12 p.m.

So since testosterone varies by day and levels are highest at 8 am and lowest at 8 pm (Brambilla et al, 2009; however testing men aged 45 years of age and older is fine before 2 pm due to a blunted circadian rhythm; Long, Nguyen, and Stevermer, 2015), then how could testosterone account for why men commit most of their crimes at night and why the crime that children commit spikes when they go to school, go to lunch and get out of school? The answer is that it doesn’t because testosterone does not cause crime. What testosterone does cause, however, are feelings of confidence and dominance, which does not—surprisingly—lead to increased aggression and assault on others (Booth et al, 2006).

What testosterone does cause, however, is social dominance and success, not physical aggression and maladjustment (Shcaal et al, 1996). The effects of environment are also more notable on testosterone than are genetics at 5 months of age (Carmaschi et al, 2010). Furthermore, aggressive behavior is first noticed in infancy and reaches its peak before school age (Tremblay et al, 2004; Cote et al, 2006). Though testosterone does seem to have an effect on aggression in preschool boys, however genetic and environmental causality has not been established (Sanchez-Martin et al, 2000).

Nevertheless, the meta-analyses I cited last week show that testosterone has an extremely low correlation of .14, so other factors must be at play. However, Sanchez-Martin et al (2000:778-779) also note that “Tremblay et al (1998) suggested that associations between testosterone titer and physical aggression are likely to be observed in contexts where such attack leads to social dominance. This may be true of the preschool boys in the present study. The data generated in the present study generally support Scerbo and Kolko (1994), who studied older children (7 to 14 years of age). They found a significant relationship between testosterone levels and aggression (as assessed by clinical staff).

It’s interesting to note that in the case of Scerbo and Kolko (1994) that after controlling for age and size, testosterone correlated with aggression when rated by staff but not parents or teachers. ‘Staff’ refers to clinic staff at a facility where the children were assessed for hyperactivity disorders. Of course, the staff would rate higher levels of aggression compared to parents of teachers—people who are around the children every day—since they would want a higher chance for diagnosis for certain drugs to ‘cure’ the hyperactivity, but I digress. Testosterone does not induce aggression in children, but it does induce social dominance and confidence which does not lead to aggression (Rowe et al, 2004; Booth et al, 2006).

There was also little difference in testosterone between socially dominant prisoners and aggressive prisoners (Ehrenkraz, Bliss, and Sheard, 1974). Furthermore, the testosterone increase leading to pubertal development in boys is not associated with increased aggression (Tremblay et al, 1998; Booth et al, 2006: 171). Indeed, increased body size is a marker for physical aggression in children, and I doubt these children have high muscle mass so, I assume, they have high levels of body fat and thusly lower levels of testosterone than they would have if they were leaner. Yet another strike against the ‘testosterone causes crime/physical aggression’ hypothesis.

Indeed, this has some implications for the honor culture hypothesis of why low-income blacks have higher levels of testosterone than similarly aged blacks with some college (Mazur, 2016). The patterns for crime as shown by the OOJDP shows that crime rises as the day progresses from the morning until its peak at 3 pm for children and then sharply declines while for adults it peaks at 10 pm.

Testosterone does increase when a challenge is issued; when one man feels his reputation is threatened, the propensity for violence is increased, but this was most notably seen in Southern men (Cohen et al, 1996). So the same would be said for this ‘culture of honor’ found in low-income black neighborhoods, the so-called ‘code of the street’ as stated by Anderson (1994: 88): “Moreover, if a person is assaulted, it is important, not only in the eyes of his opponent but in the eyes of his “running buddies,” for him to avenge himself. Otherwise, he risks being “tried” (challenged) or “moved on” by any number of others. To maintain his honor, he must show he is not someone to be “messed with” or “dissed.”

This culture of honor is found all over the world, including Brazil where homicide can be explained by the need to maintain honor and can be understood by taking into account cultural factors; biological, psychological and socioeconomic factors do not explain murder in Northeast Brazil as well as honor and culture (de Souza et al, 2015). People in honor cultures also have a higher chance of self-harm (Osterman and Brown, 2011) as well as a higher chance of committing violence in school (Brown, Osterman, and Barnes, 2009).

Testosterone does not cause crime; it does not cause aggression. Increases in testosterone before, during and after events are a physiologic process to prime the body for competition. As cited above, dominant behavior does not necessarily lead to violence in most cases, which may be surprising for some. Indeed, honor and culture may explain a nice amount of the homicide and violence rate in the South. Since testosterone is highest at 8 am and lowest at 8 pm and the rates of crime committed by adults and children are vastly different than the diurnal variance in the day, then testosterone does not cause crime and its increase is not associated with crime, but social dominance and confidence which does not lead to crime.

Hopefully—if anyone still believes testosterone to be the boogeyman its made out to be—I’ve put those misconceptions to rest. Racial differences in testosterone cannot be the cause of racial differences in crime—because there is either no statistical difference in testosterone between the races or the difference is non-existent. Testosterone is clearly a beneficial hormone—as I have extensively documented. Misunderstandings of the hormone are abound—especially in the HBD sphere—only due to literally a few paragraphs in a book (Rushton, 1997) and one study that showed blacks have higher testosterone than whites which was the cause of their higher rates of prostate cancer (Ross et al, 1986). The study is hard to find so I had to buy access to it. I will cover this in the future, but I discovered that they assayed the subjects when it was convenient for them—between the hours of 10 am and 3 pm—which is unacceptable. You cannot gauge racial differences in testosterone from a small study (n=50) and a non-representative sample (college students). For these reasons, the study should be thrown in the trash—especially when formulating evolutionary hypotheses.

Testosterone is one of the most important hormones for vital functioning. By knowing how it is processed in the body and that there are no ‘genes for’ testosterone (‘low testosterone genes’ notwithstanding) along with how testosterone has a low relationship with physical aggression one should not be scared of having high levels, on the contrary, one should be scared of having low levels. I have once again proven my case that testosterone is not related to violence in showing the diurnal variation in testosterone levels in adults, as well as the time of day that crimes are committed by both adults and children. High testosterone means high confidence and high dominance—and those two traits have a lot to do with masculinity—which do not lead to violence. 

I know why testosterone does not cause crime—because I have an understanding of the hormone, how its produced in the body and what its effects on the body are. The most important thing to note here, is that even if blacks had 15 percent higher testosterone than whites, it still wouldn’t explain higher rates of crime or disease such as prostate cancer. So those who try so hard to prove that blacks have higher levels of the hormone do so in vain, because even if they did it wouldn’t mean anything for any theories they may have. The myth of testosterone causing aggression and crime need to be put to bed for good.

Testosterone and Aggressive Behavior

1200 words

Testosterone gets a bad rep. People assume that if one has higher testosterone than average, that they will be a savage, bloodthirsty beast with an insatiable thirst for blood. This, however, is not the case. I’ve documented how testosterone is vital for male functioning, and how higher levels don’t lead to maladies such as prostate cancer. Testosterone is feared for no reason at all. The reason that people are scared of it is that of the anecdotal reports that individual A had higher testosterone when he committed crime B so, therefore, anyone who commits a crime has higher testosterone and that is the ultimate—not proximate—cause of crime. This is erroneous. There is a positive—albeit extremely low—correlation between physical aggression and violence at .14. That’s it. Furthermore, most of these claims of higher levels of testosterone causing violence is extrapolated from animal studies to humans.

Testosterone has been shown to lead to violent and aggressive behavior, largely only in animal studies (Archer, 1991; Book et al, 2001). For years, the relationship between the two variables was thought to be causal, i.e., high levels of testosterone cause violent crimes, which has been called into question over recent years. This is due to how the environment can raise testosterone levels. I have documented how these environmental factors can raise testosterone—and after these events, testosterone stays elevated.

Largely, animal studies are used to infer that high levels of testosterone in and of themselves lead to higher rates of aggression and therefore crime. However, two important meta-analyses show this is not necessarily the case (Archer, 1991; Book et al, 2001). Book et al, 2001 showed that two variables were important in seeing the relationship between aggression and crime—the time of day that the assay was taken and the age of the participant. This effect was seen to be largest in, not unexpectedly, males aged 13-20 (Book et al, 2001: 594). So since age confounds the relationship between aggression and testosterone in males, that is a variable that must also be controlled for (which, in the meta-analyses and other papers I cite on black and white testosterone is controlled for).

More interestingly, Book et al (2001) showed that the nature of the measure of aggression (self-reported or behavioral) did not have any effect on the relationship between testosterone and aggression. Since there is no difference between the two measures, then a pencil-and-paper test is a good enough index of measure of aggression, comparable to observing the behavior of the individual studied.

Archer (1991) also showed the same low—but positive—correlations between aggression and testosterone. Of course, as I’ve extensively documented since there is a positive relationship between the two variables does not necessarily mean that high-testosterone men commit more crime—since the outcome of certain situations can increase and decrease testosterone, no causal factors have been detangled. Book et al (2001) confirmed Archer’s (1991) finding that the correlation between violent and aggressive behavior was positive and low at .14.

Valois et al (2017) showed there was a relationship between emotional self-efficacy (ESE) and aggressive and violent behaviors in a statewide sample of high school children in South Carolina (n=3,386). Their results suggested that there was a relationship between carrying a weapon to school within the past 30 days along with being injured with a club, knife or gun in the past 12 months was significantly associated with ESE for specific race and sex groups.

Black girls who reported a low ESE reported carrying a weapon to school 30 days prior to the survey were 3.22 times more than black girls with a high ESE who did not report carrying a weapon to school within the past 30 days prior to the questionnaire. For black boys with low ESE, they were 3.07 times more likely to carry a weapon to school within the past 30 days in comparison to black boys with high ESE who did not carry a weapon to school in the past 30 days. White girls who reported low ESE had the highest chance of bringing a weapon to school in comparison to white girls with low ESE—they were 5.87 times more likely to carry a weapon to school 30 days prior to the survey. Finally, white boys with low ESE were slightly more than 2 times more likely than white boys with high ESE to carry a weapon to school 30 days prior to the survey.

Low ESE in white and black girls is associated with carrying a weapon to school, whereas low ESE for white and black boys is associated with being threatened. Further, their results suggested that carrying a weapon to school was associated with low ESE in black and white girls suggesting that low ESE is both situation-specific and specific to the female sex. The mediator between these things is low ESE—it is different for both black boys and black girls, and when it occurs different courses of action are taken, whether it’s through bringing a weapon to school or being threatened. What this tells me is that black and white boys with low ESE are more likely to be threatened because they are perceived to be more meek, while black and white girls with low ESE that get provoked at school are more likely to bring weapons. So it seems that girls bring weapons when provoked and boys fight.

The two meta-analyses reviewed above show that there is a low positive (.14) correlation between testosterone and aggression (Archer, 1991; Book et al, 2001). Thusly, high levels of testosterone on their own are not sufficient enough to explain high levels of aggression/violence. Further, there are race- and sex-specific differences when one is threatened at high school with black and white boys being more likely to report being threatened more (which implies a higher rate of physical fighting) while black and white girls when threatened brought weapons to school. These race- and sex-specific differences in the course of action taken when they are physically threatened needs to be looked into more.

I’d like to see the difference in testosterone levels for a matched sample of black and white boys from two neighboring districts with different murder rates as a proxy for the amount of violence in the area. I’d bet that the places with a higher murder rate would have children 1) report more violence and instances of bringing weapons to school and 2) report more harm from these encounters—especially if they have low ESE as seen in Valois (2017) and 3) the children in the high schools along with the residents of the area would have higher testosterone than the place with less violence. I would expect these differences to be magnified in the direction of Valois (2017) in that areas with higher murder rates would have black and white girls report bringing weapons to school when threatened whereas black and white boys would report more physical violence.

High testosterone itself is not sufficient enough to explain violence as the correlation is extremely low at .14. Testosterone levels fluctuate depending on the time of day (Brambilla et al, 2009; Long, Nguyen, and Stevermer, 2015) to the time of year (Stanton, Mullette-Gillman, and Huettel, 2011Demur, Uslu, and Arslun, 2016). How the genders/races react differently when threatened in adolescence is interesting and deserves further study.

Race, Testosterone, and Honor Culture

2300 words

Misinformation about testosterone and strength in regards to race is rampant in the HBD-o-sphere. One of the most oft-repeated phrases is that “Blacks have higher levels of testosterone than whites”, even after controlling for numerous confounds. However, the people who believe this literally only cite one singular study with 50 blacks and 50 whites. Looking at more robust data with higher ns shows a completely different story. Tonight I will, again, go through the race/testosterone conundrum (again).

Type I fibers fire first when heavy lifting. Whites have more type I fibers. Powerlifters and Olympic lifters have a greater amount type IIa fibers, with fewer type IIx fibers (like whites). This explains why blacks are hardly represented in powerlifting and strongman competitions.

Somatype, too, also plays a role. Whites are more endo than blacks who are more meso. Endomorphic individuals are stronger, on average, than mesomorphic and ectomorphic individuals.

Blacks have narrower hips and pelves. This morphological trait further explains why blacks dominate sports. Some people may attempt to pick out one variable that I speak about (fiber type, morphology, somatype, fat mass, etc) and attempt to disprove it, thinking that disproving that variable will discredit my whole argument. However, fiber typing is set by the second trimester, with no change in fiber type from age 6 to adulthood (Bell et al, 1980).

It is commonly believed that blacks have higher levels of testosterone than whites. However, this claim is literally based off of one study (Ross et al, 1986) when other studies have shown low to no difference in T levels (Richards et al, 1992; Gapstur et al, 2002; Rohrmann et al, 2007; Mazur, 2009; Lopez et al, 2013; Richard et al 2014). People who still push the “blacks-have-higher-T-card” in the face of this evidence are, clearly, ideologues who want to cushion their beliefs when presented with contradictory evidence (Nyhan and Reifler, 2010).

‘Honor Culture’ and testosterone

In all of my articles on this subject, I have stated—extensively—that testosterone is mediated by the environment. That is, certain social situations can increase testosterone. This is a viewpoint that I’ve emphatically stated. I came across a paper while back that talks about a sociological perspective (I have huge problems with social ‘science’, [more on that soon] but this study was very well done) in regards to the testosterone difference between blacks and whites.

Some people when they read this, however, may go immediately to the part of the paper that says what they want it to say without fully assessing the paper. In this section, I will explain the paper and how it confirms my assertions/arguments.

Mazur (2016) begins the paper talking about ‘honor culture‘, which is a culture where people avoid intentionally offending others while also maintaining a status for not backing down from a confrontation. This theory was proposed by Richard Nisbett in 1993 to explain why the South had higher rates of violence—particularly the Scotch-Irish.

However parsimonious the theory may sound, despite its outstanding explanatory power, it doesn’t hold while analyzing white male homicides in the South. It also doesn’t hold analyzing within-county homicide rates either, since apparently poverty better explains higher homicide rates.

But let’s assume it’s true for blacks. Let’s assume the contention to be true that there is an ‘honor culture’ that people take part in.

Young black men with no education had higher levels of testosterone than educated whites and blacks. Looking at this at face value—literally going right to the section of the paper that says that poor blacks had higher testosterone, nearly 100 ng/ml higher than the mean testosterone of whites. As Mazur (2016) notes, this contradicts his earlier 2009 study in which he found no difference in testosterone between the races.

fsoc-01-00001-g001

Note the low testosterone for both races at age 20-29—ranging from about 515 to 425—why such low testosterone levels for young men? Anyway, the cause for the higher levels is due to the type of honor culture that blacks participate in, according to Mazur (which is consistent with the data showing that testosterone rises during conflict/aggressive situations).

Mazur cites Elijah Anderson, saying that most youths have a “code of the streets” they take part in, which have to do with interpersonal communication such as “gait and verbal expressions” to deter aggressive behavior.

Testosterone is not a causal variable in regards to violent behavior. But it does rise during conflicts with others, watching a favorite sports team, asserting dominance, and even how you carry yourself (especially your posture). Since low-class blacks participate in these types of behaviors, then they would have higher levels of testosterone due to needing to “keep their status.”

When testosterone rises in these situations, it increases the response threat in mens’ brains, most notably showing increased activity in the amygdala. Further, dominant behavior and posture also increase testosterone levels. Putting this all together, since blacks with only a high school education have higher testosterone levels and are more likely to participate in honor culture compared to whites and blacks with higher educational achievement, then they would have higher testosterone levels than whites and blacks with a high school education who do not participate in honor culture.

Further, as contrary to what I have written in the past (and have since rescinded), there is no indication of higher testosterone levels in black women with low education. It seems this ‘honor culture’ effect on testosterone only holds for black men with only a high school education.

Mazur’s (2016) most significant finding was that black men aged 20-29 with only a high school education had 91 ng/ml higher testosterone than whites. Among older and/or educated men, testosterone did not vary. This indicates that since they have attained higher levels of educational success, there is no need to participate in ‘honor culture’.

This is yet further evidence for my assertion that environmental variables such as posture, dominance, and aggressive behavior raise testosterone levels.

The honor culture hypothesis is found to hold in Brazil in a comparative study of 160 inmates and non-inmates (De Souza et al, 2016). As Mazur (2016) notes, the honor culture hypothesis could explain the high murder rate for black Americans—the need to ‘keep their status’. It’s important to note that this increase in testosterone was not noticed in teenage or female blacks (because they don’t participate in honor culture).

There is a perfectly good environmental—not genetic—reason for this increase in testosterone in young blacks with only a high school education. Now that we know this, back to race and strength.

Mazur (2009) found that black men in the age range of 20-69, they averaged .39 ng/ml higher testosterone than whites, which is partly explained by lower marriage rates and low adiposity. White men are more likely to be obese than black men, since black men with more African ancestry are less likely to be obese. When controlling for BMI, blacks are found to have 2.5-4.9 percent more testosterone than whites (Gapstur et al, 2002, Rohrmann et al, 2007, Richard et al, 2014). There is little evidence for the assertion that blacks have higher levels of testosterone without environmental triggers.

Blacks between the age of 12 and 15 average lower levels of testosterone than whites. However, after the age of 15, “testosterone levels increase rapidly” with blacks having higher peak levels than whites (seen in table 2 below). After adjusting for the usual confounds (BMI, smoking, age, physical activity, and waist circumference), blacks still had higher levels of testosterone—which is attributed to higher levels of lean mass.

testosterone

As seen above in table 2 from Hu et al (2014), the difference in total testosterone between blacks and whites aged 20-39 was 6.29 ng/ml and 5.04 ng/ml respectively, with free testosterone for whites being 11.50 and 13.56 for blacks and finally bioavailable testosterone for whites and blacks aged 20-39 was 281.23 and 327.18 ng/ml respectively. These small differences in testosterone cannot account for racial disparities in violence nor prostate cancer—since there is no relationship between prostate cancer and testosterone (Stattin et al, 2003; Michaud, Billups, and Partin, 2015).

In regards to Africans, the best studies I can find comparing some African countries with the West study salivary testosterone. However, there is a direct correlation between salivary testosterone and free serum testosterone (Wang et al, 1981; Johnson, Joplin, and Burrin, 1987). Of the studies I could find, Kenyan pastoralists called the Ariaal have lower levels of testosterone than Western men (Campbell, O’Rourke, and Lipson, 2003; Campbell, Gray, and Ellison, 2006) while men in Zimbabwe had levels “much lower” compared to Western populations (Lukas, Campbell, and Ellison, 2004). Lastly, among men aged 15 to 30, salivary testosterone levels in an American sample was 335 pmol//l compared to 286 pmol/l in men from the Congo (Elisson et al, 2002). Even certain African populations don’t have higher testosterone levels than Western peoples.

Conclusion

The meme that blacks have higher rates of testosterone in comparison to whites needs to be put to rest. This is only seen in blacks who participate in ‘honor culture’, which is an environmental variable. This is in contrast to people who believe that it is genetic in nature—environmental variables can and do drive hormones. Mazur (2016) is proof of that. Mazur (2016) also shows that the honor culture hypothesis doesn’t hold for teens or black males—so they don’t have elevated levels of testosterone. Certain studies of African populations, however, do not show higher levels of testosterone than Western populations.

Looking at the complete literature—rather than a select few studies— we can see that testosterone levels between white and black Americans are not as high as is commonly stated (Richards et al, 1992; Gapstur et al, 2002; Rohrmann et al, 2007; Mazur, 2009; Lopez et al, 2013; Hu et al, 2014; Richard et al, 2014). Further, even if blacks did have higher levels of testosterone than whites—across the board (sans honor culture), it still wouldn’t explain higher rates of black violence when compared to whites, nor would it explain higher prostate cancer rates (Stattin et al, 2003; Michaud, Billups, and Partin, 2015).

Only blacks with low educational achievement have higher levels of testosterone—which, even then is not enough to explain higher rates of violence or prostate cancer acquisition. Other factors explain the higher murder rate (i.e., honor culture, which increases testosterone, the environmental trigger matters first and foremost) and violent crime that blacks commit. But attempting to explain it with 30-year-old studies (Ross et al, 1986) and studies that show that environmental factors increase testosterone (Mazur, 2016) don’t lend credence to that hypothesis.

References

Bell, R. D., Macdougall, J. D., Billeter, R., & Howald, H. (1980). Muscle fiber types and morphometric analysis of skeletal muscle in six-year-old children. Medicine & Science in Sports & Exercise,12(1). doi:10.1249/00005768-198021000-00007

Campbell, B., O’rourke, M. T., & Lipson, S. F. (2003). Salivary testosterone and body composition among Ariaal males. American Journal of Human Biology,15(5), 697-708. doi:10.1002/ajhb.10203

Campbell, B. C., Gray, P. B., & Ellison, P. T. (2006). Age-related patterns of body composition and salivary testosterone among Ariaal men of Northern Kenya. Aging Clinical and Experimental Research,18(6), 470-476. doi:10.1007/bf03324846

De Souza, Souza, B. C., Bilsky, W., & Roazzi, A. (2016). The culture of honor as the best explanation for the high rates of criminal homicide in Pernambuco: A comparative study with 160 convicts and non-convicts. Anuario de Psicología Jurídica,26(1), 114-121. doi:10.1016/j.apj.2015.03.001

Ellison, P. T., Bribiescas, R. G., Bentley, G. R., Campbell, B. C., Lipson, S. F., Panter-Brick, C., & Hill, K. (2002). Population variation in age-related decline in male salivary testosterone. Human Reproduction,17(12), 3251-3253. doi:10.1093/humrep/17.12.3251

Gapstur SM, Gann PH, Kopp P, Colangelo L, Longcope C, Liu K. Serum androgen concentrations in young men: a longitudinal analysis of associations with age, obesity, and race—the CARDIA male hormone study. Cancer Epidemiol Biomarkers Prev 2002; 11: 10417

Hu, H., Odedina, F. T., Reams, R. R., Lissaker, C. T., & Xu, X. (2014). Racial Differences in Age-Related Variations of Testosterone Levels Among US Males: Potential Implications for Prostate Cancer and Personalized Medication. Journal of Racial and Ethnic Health Disparities,2(1), 69-76. doi:10.1007/s40615-014-0049-8

Johnson, S. G., Joplin, G. F., & Burrin, J. M. (1987). Direct assay for testosterone in saliva: Relationship with a direct serum free testosterone assay. Clinica Chimica Acta,163(3), 309-318. doi:10.1016/0009-8981(87)90249-x

Lopez, D. S., Peskoe, S. B., Joshu, C. E., Dobs, A., Feinleib, M., Kanarek, N., . . . Platz, E. A. (2013). Racial/ethnic differences in serum sex steroid hormone concentrations in US adolescent males. Cancer Causes & Control,24(4), 817-826. doi:10.1007/s10552-013-0154-8

Lukas, W. D., Campbell, B. C., & Ellison, P. T. (2004). Testosterone, aging, and body composition in men from Harare, Zimbabwe. American Journal of Human Biology,16(6), 704-712. doi:10.1002/ajhb.20083

Mazur, A. (2009). The age-testosterone relationship in black, white, and Mexican-American men, and reasons for ethnic differences. The Aging Male,12(2-3), 66-76. doi:10.1080/13685530903071802

Mazur, A. (2016). Testosterone Is High among Young Black Men with Little Education. Frontiers in Sociology,1. doi:10.3389/fsoc.2016.00001

Michaud, J. E., Billups, K. L., & Partin, A. W. (2015). Testosterone and prostate cancer: an evidence-based review of pathogenesis and oncologic risk. Therapeutic Advances in Urology,7(6), 378-387. doi:10.1177/1756287215597633

Nyhan, B., & Reifler, J. (2010). When Corrections Fail: The Persistence of Political Misperceptions. Political Behavior,32(2), 303-330. doi:10.1007/s11109-010-9112-2

Richard, A., Rohrmann, S., Zhang, L., Eichholzer, M., Basaria, S., Selvin, E., . . . Platz, E. A. (2014). Racial variation in sex steroid hormone concentration in black and white men: a meta-analysis. Andrology,2(3), 428-435. doi:10.1111/j.2047-2927.2014.00206.x

Richards, R. J., Svec, F., Bao, W., Srinivasan, S. R., & Berenson, G. S. (1992). Steroid hormones during puberty: racial (black-white) differences in androstenedione and estradiol–the Bogalusa Heart Study. The Journal of Clinical Endocrinology & Metabolism,75(2), 624-631. doi:10.1210/jcem.75.2.1639961

Rohrmann, S., Nelson, W. G., Rifai, N., Brown, T. R., Dobs, A., Kanarek, N., . . . Platz, E. A. (2007). Serum Estrogen, But Not Testosterone, Levels Differ between Black and White Men in a Nationally Representative Sample of Americans. The Journal of Clinical Endocrinology & Metabolism,92(7), 2519-2525. doi:10.1210/jc.2007-0028

Ross R, Bernstein L, Judd H, Hanisch R, Pike M, Henderson B. Serum testosterone levels in healthy young black and white men. J Natl Cancer Inst. 1986 Jan;76(1):45–48

Stattin, P., Lumme, S., Tenkanen, L., Alfthan, H., Jellum, E., Hallmans, G., . . . Hakama, M. (2003). High levels of circulating testosterone are not associated with increased prostate cancer risk: A pooled prospective study. International Journal of Cancer,108(3), 418-424. doi:10.1002/ijc.11572

Wang, C., Plymate, S., Nieschlag, E., & Paulsen, C. A. (1981). Salivary Testosterone in Men: Further Evidence of a Direct Correlation with Free Serum Testosterone. The Journal of Clinical Endocrinology & Metabolism,53(5), 1021-1024. doi:10.1210/jcem-53-5-1021

Man the Athlete

5450 words

Homo nerdicus or Homo athleticus? Which name more aptly describes Man? Without many important adaptations incurred throughout our evolutionary history, modern Man as you see him wouldn’t be here today. The most important factor in this being our morphology and anatomy which evolved due to our endurance running, hunting, and scavenging. The topics I will cover today are 1) morphological differences between hominin species and chimpanzees; 2) how Man became athletic and bring up criticisms with the model; 3) the evolution of our aerobic physical ability and brain size; 4) an evolutionary basis for sports; and 5) the role of children’s playing in the evolution of human athleticism.

Morphological differences between Man and Chimp

Substantial evolution in the lineage of Man has occurred since we have split from the last common ancestor (LCA) with chimpanzees between 12.1 and 5.3 mya (Moorjani et al, 2016; Patterson et al, 2006). One of the most immediate differences that jump out at you when watching a human and chimpanzee is such stark differences in morphology, in particular, how we walk (pelvic differences) as well as our arm length relative to our torsos. Though we both evolved to be proficient at abilities that had us become evolutionarily successful in the environments we found ourselves in, one species of primate went on to become the apes the took over the world whereas the chimps continued life as the LCA did (as far as we can tell). The evolution of our athleticism is why we have a lean body with the right morphology for endurance running and associated movements. In fact, the evolution of our brain size hinged on a reduction in our fat depots (Navarette, Schaik, and Isler, 2011).

One of the largest differences you can see between the two species is how we walk. Chimps are “specially adapted for supporting weight on the dorsal aspects of middle phalanges of flexed hand digits II–V” (Tuttle, 1967). Meanwhile, humans are specifically adapted for bipedality due to the change in our pelvis over the course of our evolution (Gruss and Schmitt, 2015). Due to staying more arboreal than venturing on the ground, chimp morphology over the course of the divergence became more and more adapted to life in the trees.

Our modern gait is associated with physiologic and anatomic adaptations throughout our evolution, and are not ‘primitive retentions’ from the LCA (Schmitt, 2003). There are very crucial selective pressures that need to be looked at to see which selection pressures caused us to become athletes. Parts of Austripolithicenes still live on in us today, most notably in our lower leg/foot (Prang, 2015). Further, our ancestor, the famous Lucy had the beginnings of a modern pelvis, which was the beginning of the shift to the more energetically efficient bipedality, one thing that fully separates Man from the rest of the animal kingdom.

Of course, no conversation about human evolution would be complete without talking about Erectus. Analysis of 1.5 million-year-old footprints shows that Erectus was the first to have a humanlike weight transfer while walking, confirming “the presence of an energy-saving longitudinally arched foot in H. Erectus.” (Hatala et al, 2016). We have not yet discovered a full Homo erectus foot, but 1.5 million-year-old footprints found in Kenya show that whatever hominin made those prints had a long, striding gait with a full arch (Steudel-Numbers, 2006; Bennett et al, 2009). The same estimates from Steudel-Numbers (2006) show that Erectus nearly halved its travel costs compared to australopithecines. This is due to a longer stride which was much more Manlike than apelike due to a humanlike pelvis and gluteus maximus (Lieberman et al, 2006).

However, the most important adaptations that Erectus evolved was the ability to keep cool while walking long distances. Loss of hair loss specifically allowed individuals to be active in hot climates without overheating. Our ancestors’ hair loss facilitated sweating (Ruxton and Wilkinson, 2011b), which allowed us to become the proficient hunters—the athletes—that we would become. There is also thermoregulatory evidence that endurance running may have been possible for Homo erectus, but not any other earlier hominin (Ruxton and Wilkinson, 2011a) which was the beginnings of our selection to become athletes. The evidence reviewed in Ruxton and Wilkinson (2011a) shows that once hair loss and sweating ability reached human levels, thermoregulation was then possible under the midday sun.

Moreover, our modern gait and bipedalism is 75 percent less costly than quadrupedal/bipedal walking in chimpanzees (Sockel, Raichlen, and Pontzer, 2007), so this extra energy that was conserved with our physiologic and anatomic adaptations due to bipedalism could have gone towards other pertinent metabolic functions—like fueling a bigger brain (more energy could be used to feed more neurons).

Born to run

Before getting into how we are able to run so efficiently, I need to talk about what made it possible for us to be able to have the energy to sustain our distance running. That one thing is eating cooked food (meat). This one seemingly simple thing is the ‘prime mover’ so to speak, of our success as athletes. Eating cooked food significantly increases the amount of energy obtained during digestion. That we could extract more energy out of cooked food—no matter what type of food it was—can not be overstated. This is what gave us the energy to hunt and scavenge. We are, of course, able to hunt/scavenge while fasted, which is an extremely useful evolutionary adaptation which increases important hormones to have us search for food. The hormones released during a fasted state aid in human physiologic/metabolic functioning allowing one who is searching for food more heightened sensibilities.

We are evolutionarily adapted to be endurance runners. Endurance running is defined as the ability to run more than 5 km using aerobic metabolism (Lieberman and Bramble, 2007). Since we are poor sprinters, the idea is that our body has evolved for walking. However, numerous anatomical changes in our phenotypes in comparison to our chimp ancestors have left us some clues. In the previous section, I talked about physical changes that occurred after Man and Chimp diverged, well those evolutionary changes are why we evolved to be athletic.

Endurance running first evolved, most likely due to scavenging and hunting (Lieberman et al, 2009). Through natural selection—survival of the ‘good enough’, those who had better physiologic and anatomic adaptations could reach the animal carcass before other scavengers like vultures and hyenas could get to it. Over time, this substantially changed how we would look. Numerous physiologic changes in our lineage attest to the evolution of our endurance running. The nuchal ligament, as well as the radius of the semicircular canal is larger in Homo sapiens than in chimpanzees or australopithecines. This stabilizes our head while running—something that our ancestors could not do because they didn’t have a canal our size (Bramble and Lieberman, 2004).

Skeletal evidence that points to our evolution as athletes consists of (but not limited to):

  • The Nuchal ligament—stabilizes the head
  • Shoulder and head stabilization
  • Limb length and mass (we have legs longer than our torsos which decreases energy used)
  • Joint surface (we can absorb more shock when our feet hit the ground due to a larger surface area)
  • Plantar arch (generates spring for running but not walking)
  • Calcaneal tuber and Achilles tendon (shorter tuber length leads to a longer Achilles heel stretch, converting more kinetic energy into  elastic energy)

So people who had anatomy closer to this in our evolutionary past had more of a success of getting to that animal carcass, divvying it amongst his family/tribe, ensuring the passage of his genes to the next generation. Man had to be athletic in order to be able to run for long distances. Where this would have come in handy the most would have been the Savanna in our ancestral past. Man could now use persistence hunting—chasing animals in the heat of the day—and kill them when they tired out. The evolutionary adaptation sweating due to the loss of our fur is the only reason this is possible.

One of the most important adaptations for endurance running is thermoregulation. All humans are adapted for long range locomotion rather than speed and to dump rather than retain heat (Lieberman, 2015). This is one of the most important adaptations we evolved that had us become successful endurance runners. We could chase down prey and wait for our prey to become exhausted/overheat and then we would move in for the kill. Of course, intelligence and sociality come into play as we needed to create hunting bands, but without our superior endurance running capabilities—that no other animal in the animal kingdom has—we would have gone down a completely different evolutionary path than the one we went down. Our genome has evolved to support endurance running (Mattson, 2012). Since there is an association between too much sitting and all-cause mortality (Biddle et al, 2016), this is yet more evidence that we evolved to be mobile, not sedentary hominins.

Further evidence that we evolved to be athletic is in our hands. When you think about our hands and how we can manipulate our environments with them—what sets us apart from every other species—then, obviously, in our evolutionary past, those who were more successful would have had a higher chance of reproducing. Aggressive clubbing and throwing are thought to be one of the earliest hominin specializations.  If true, then those who could club and throw best would have the best chance of passing their genes to the next generation, thusly selecting for more efficient hands (Young, 2003). While we may have evolved more efficient hands over time warring with other hominins, some are more prone to disk herniation.

Plomp et al (2015) propose the ‘ancestral shape hypothesis’ which is derived from studying bipedalism. They propose that those who are more prone to disk herniation preferentially affects those who have vertebrae “towards the ancestral end of the range of shape variation within H. sapiens and therefore are less well adapted for bipedalism” (Plomp et al, 2015). One of the most amazing things they discovered was that humans with signs of intervertebral disc herniation are “indistinguishable from those of chimpanzees.” Of course, due to this, we should then look towards evolutionary biology in regards to a lot of human ailments (which I have also argued here on dietary evolutionary mismatches as well as on obesity).

Of course there are some naysayers arguing that endurance running didn’t drive our evolution. He wrongly states that it’s about what drove the evolution of our bipedalism; however, what the endurance running hypothesis argues is that there are certain physiologic and anatomic changes that only could have occurred from endurance running. Better endurance runners got selected for over time, leading to novel adaptations that stayed in the gene pool and got selected for. One thing is a larger gluteus maximus. A humanlike pelvis is found in the fossil record as far back as 1.9 mya in Erectus (Lieberman et al, 2006). Furthermore, longer toes had a larger mechanical cost, and were thusly selected against, which also helped in the evolution of our endurance running (Rolian et al, 2009). All in all, there are too many adaptations that our bodies have that can only be explained by adapting to endurance running. Just because we may have gotten to the weaker animals sometimes doesn’t falsify the hypothesis; Man still needed to sweat and persist in the hot mid-day temperatures chasing prey.

Brain size and aerobic physical capacity

When speaking about the increase in our brain size/neuronal count, fire/cooking, the social brain hypothesis, and other theories are brought up first. Erectus had a lot of humanlike qualities, including the ability to control/use fire (Berna et al, 2012), and the appearance of our modern gait/stride which first appeared in Erectus (Steudel-Numbers, 2006; Bennet et al, 2009). This huge change also occurred around the time our lineage began cooking meat/using fire. Without the increased energy from cooking, we wouldn’t be able to hunt for too long. However, we do have very important specific adaptations during a fasted state—the release of hormones such as catecholamines (adrenaline and noradrenaline) which have as react faster to predators/possible prey. Though, a plant-based diet wouldn’t cut it in regards to our daily energy requirements to feed our huge brain with a huge neuronal count (Fonseca-Azevedo and Herculano-Houzel, 2012). Cooked meat is the only way we’d be able to have enough energy required to hunt game.

What kind of an effect did it have on our cranial capacity/evolution?

Four groups of mice selectively bred for high amounts of “voluntary wheel-running”, ran 3 times further than the controls which increased Vo2 max in the mice. Those mice had higher levels of BDNF (Brain Derived Neurotrophic Factor) several days after the experiment concluded as well as also showing greater cell creation in the hippocampus when allowed to run compared to the controls. In two lines of selected mice, the hormone VEGF (Vascular Endothelial Growth Factor) which was correlated with higher muscle capillary density compared to controls. This shows that the evolution of endurance running in mice leads to important hormonal changes which then affected brain growth (Raichlen and Polk, 2012).

The amount of oxygen our brains use increased by 600 percent compared to 350 percent for our brain size over the course of our evolutionary history. This is important. What would cause an increase in oxygen consumption to the brain? Endurance running. There was further selection in our skeleton for endurance running in our morphology such as the semicircular canal radii. The first humanlike semicircular canal radii were found in Erectus (Spoor, Wood, and Zonneveid, 1994). This meant that we had the ability for running and other agile behaviors which were then selected for. There is also little to no activation of the gluteus medius while walking (Lee et al, 2014), implying that it evolved for more efficient endurance running.

Controlling for body mass in humans, extinct hominins and great apes, Raichlen and Polk (2012) found significant positive correlations with encephalization quotient and hindlimb length (0.93), anterior and posterior radii (0.77 and 0.66 respectively), which support the idea that human athletic ability is tied to neurobiological evolution. A man that was a better athlete compared to another would have a better chance to pass on his genes, as physical fitness is a good predictor of biological fitness. Putting this all together, selection improved our aerobic capacity over our evolutionary history by specifically altering signaling systems responsible for metabolism and oxygen intake (BDNF, VEGF, and IGF-1 (insulin-like growth factor 1), responsible for the regulation of growth hormone), which are important for blood flow, increased muscle capillary density, and a larger brain.

Putting this all together, selection improved our aerobic capacity over our evolutionary history by specifically altering signaling systems responsible for metabolism and oxygen intake (BDNF, VEGF, IGF-1). More evidence is needed to corroborate Raichlen and Polk’s (2012) hypothesis. However, with what we know about aerobic capacity and the hormones that drive it and brain size, we can make inferences based on the available data and say, with confidence, that part of our brain evolution was driven by our increased aerobic capacity/morphology, with the catalyst being endurance running. Though with our increased proclivity for athleticism and endurance running, when we became ‘us’, this just shifted the competition and athletic competition—which, hundreds of thousands/millions of years ago would mean life or death, mate or no mate, food or no food.

Clearly, without the evolution of our bipedalism/athleticism we wouldn’t have evolved the brains we have and thus we would be something completely different today.

Sport and evolutionary history

We crowd into arenas to watch people compete against each other in athletic competition. Why? What are the evolutionary reasons behind this? One view is that sport (and along with it playing) was a way for men to get practice hunting game, with playing also affecting children’s ability to assess the strength of others (Lombardo, 2012).

In an evolutionary context, sports developed as a way for men to further develop skills in order to better provide for his family, as well as assessing other men’s physical strength so he can adapt his fighting to how his opponent fights in a possible future situation. Men would then be selected for these advantageous traits. You see people crowd into arenas to watch their favorite sports teams. We are ‘wired’ to like these types of competitions, which then leads to more competition. Since we evolved to be athletes, then it would stand to reason that we would like to watch others be athletic (and hit each other as hard as they can), as a type of modern-day gladiator games.

Better hunters have better reproductive success (Smith, 2004). Further, hunter-gatherer men with lower-pitched voices have more children, while men with higher-pitched voices had higher child mortality rate (Apicella, Feinberg, and Marlowe, 2007). This signals that the H-G men with more children have higher testosterone than others, which then attracts more women to them. Champion athletes, hunters, and warriors all obtain high reproductive success. Women are sexually attracted to certain traits, which events of human athleticism show. However, men follow sports more closely than women (Lombardo, 2012), and for good reason.

Men may watch sports more than women since, in an evolutionary context, they may learn more about potential allies and who to steer clear from because they would get physically dominated. Further, men could watch the actions of others at play and mimic their actions in an attempt to gain higher status with women. Another reason is a man’s character: you can see a man’s character during sports competition and by watching one’s actions closely during, for instance, playing, you can better ascertain their motivations during life or death situations. Men may also derive thrills from watching “idealized men” perform athletic activities. These are consistent with Lombardo’s (2012) male lek hypothesis, “where male physical prowess and the behaviors important in conflict and cooperation are displayed by athletes and evaluated primarily by male, not female, spectators.”

Testosterone changes based on whether one’s favorite sports team wins or loses (Bernhardt et al, 1998). This is important. Testosterone does change under stressful/group situations. Testosterone is also argued to have a role in the search for, and maintenance of social status (Eisenegger, Haushofer, and Fehr, 2011). Testosterone responses to competition in men are also related to facial masculinity (Pound, Penton-Voak, and Surrin, 2009). Male’s physical strength is also signaled through facial characteristics of dominance and masculinity, considered attractive to women (Fink, Neave, and Seydel, 2007). Since testosterone fuels both competition, protectiveness and confidence (Eisenegger et al, 2016), a woman would be attracted to a man’s athleticism/strength, which would then be correlated with his facial structure further signaling biological fitness to possible mates. Testosterone doesn’t cause prostate cancer, as is commonly stated (Stattin et al, 2003; Michaud, Billups, and Partin, 2015). Testosterone is a beneficial hormone; you should be worried way more about low T than high T. Further, young men interacting with similar young men increases testosterone while interacting with dissimilar men decreases testosterone (DeSoto et al, 2009). This lends credence to the hypothesis that testosterone raises in response to male-male competition.

Since testosterone is correlated with the above traits, and since athletes have higher testosterone than non-athletes (Wood and Stanton, 2011) then certain types of males would be left in the dust. Athleticism can be looked at as a way to expend excess energy. Those with more excess energy would be more sexually attractive to women and mating opportunities would increase. This is why it’s ridiculous to believe that we evolved to be the ‘nerds’ of the animal kingdom when so much of our evolutionary success has hinged on our athleticism and superior endurance running and other athletic capabilities.

Playing

Child’s play is how children feel out the world in a ‘setting’ in which there are no real-world consequences so they can get a feel for how the world really is. Human babes are born helpless, yet with large heads. Natural selection has lead to large brains to care for children, causing earlier childbirths and making children more helpless, which selected for higher intelligence causing a feedback loop (Piantadosi and Kidd, 2016). They show that across the primate genera, the helplessness of an infant is an extremely strong predictor of adult intelligence.

Indeed, a lot of the crucial shaping of our intelligence and motor capabilities are developed in our infancy and early childhood, which we have over chimpanzees. Blaisdell (2015) defines play as: “an activity that is purposeless in that it tends to be detached from the outcome, is imperfect from the goal-directed form of the activity, and that tends to occur when the individual is in a non-stressed state.” Playing is just a carefree activity that children do to get a feel for the world around them. During this time, skills are honed that, in our ancestral past, allowed us to survive and prosper during times of need (persistence hunting, scavenging, etc).

Anthropological evidence also suggests that the existence of extended childhood in humans adapted to establish the skills and knowledge needed to be a proficient hunter-gatherer. Since there are no real-world outcomes to playing (other than increased/decreased pride), a child can get some physical experience without suffering the real life repercussions of failing. Studies of hunter-gatherers show that play fosters the skills needed to be proficient in tool-making and tool-use, food provisioning, shelter, and predator defense. Play time also hones athletic ability and the brain-body connection so one can be prepared for a stressful situation. In fact, children’s fascination with ‘why’ questions make them ‘little philosophers’, which is an evolutionary adaptation to prepare for possible future outcomes.

Think of play fighting. While play fighting, the outcome has no important real life applications (well, the loser’s pride is hit) and what is occurring is the honing of skills that are useful to survival. During our ancestral evolution, play fighting between brothers could have honed the skills needed during a life our death situation when another band of humans was encountered. As you begin to associate certain movements with certain events, you then become better prepared subconsciously for when novel situations occur. The advantage of an extended childhood with large amounts of play time allow the brain and body to make certain connections between things and when these situations arise during a life or death situation, the brain-body will already have the muscle memory to handle the situation.

Conclusion

Studying our evolution since the divergence between Man and chimp, we can see the types of adaptations that we have incurred over our evolutionary history that have lead to us being specifically adapted for long-term endurance running. The ability to sweat, which, as far as we know began with Erectus, was paramount in our history for thermoregulation. Looking at the evolution of our pelvis, toes, gluteal muscles, heads, shoulders, brains, etc all will point to how they are adapted to a bipedal ape that is born to run—born to be an athlete. Without our athleticism, our intelligence wouldn’t be possible. We have a brain-body connection, our brain isn’t the only thing that drives our body, the two work in concert giving each other information, reacting to familiar and novel stimuli. That’s for another time though.

We didn’t evolve to be Homo nerdicus, we evolved to be Homo athleticus. This can be seen with how exercise has such a huge impact on cognition. We can further see the relationship between our athletic ability and our cognition/brain size. Without the way our evolution happened, Man—along with everything else you see around you—would not be here today. In a survival situation—one in which society completely breaks down—one who has better control over his body and motor functions/capabilities will outlast those who do not. Ultimate and conscious control over our bodies, reacting to stimuli in the environment is fostered in our infancy during our play time with others. Playing allows an individual to get experience in a simulated event, getting important muscle memory to react to future situations. The brain itself, of course, is being molded during playing as well. This just attests to the large part that playing has on cognition, survival skills and athletic ability over our evolutionary history.

Aerobic capacity throughout our evolutionary history beginning with Erectus was paramount for what we have become today. Without the evolution of certain muscles like our gluteus maximus along with certain appendages that gave us the ability to trek/run long distances, we would have lost a very important variable in our brain evolution. Aerobic activity increases blood flow to the brain and so the more successful endurance runners/hunters would increase their biological fitness (as seen in Smith, 2004) and thusly those who were more athletically successful would have more children, increasing selection for important traits for endurance running/athleticism throughout our evolutionary history.

We still play sports today since we love competition. Testosterone fuels the need for competition and sports is the best way to engage in competition in the modern day. Women are much more attracted to men with higher levels of testosterone which in turn means a more masculinized face which signals dominance and testosterone levels during competition. Women are attracted to men with higher levels of testosterone and a more masculinized face. This just so happens to mirror athletes, who have both of these traits. However, being in top physical condition is not enough; an athlete must also have a strong mental background if, for instance, they wish to break world records (Lippi, Favaloro, and Guidi, 2008).

The evolution of human playing ties this together. These sports competitions that we have made hearken back to our evolutionary past and show who would have fared best in the past. When we play, we are feeling our competition and who we can possibly make allies with/watch out for due to their actions during playing. One would also see who he would likely need to avoid and form an alliance with as to not get on his bad side and prevent a loss of status in his band. This is what it really comes down to—loss of status. Higher-status men do have higher levels of testosterone, and by one losing to a more capable person, they show that they aren’t fit to lead and they fall in the social hierarchy.

To fully understand human evolution and how we became ‘us’ we need to understand the evolution of our morphology and how it pertains to things such as our cognition and overall brain size and what advantages/disadvantages it afforded us. Whatever the case may be, it’s clear that we have evolved to be athletic and any change in that makeup will lead to a decrease in quality of life.

Homo athleticus, not Homo nerdicus, best describes Man.

References

Apicella, C. L., Feinberg, D. R., & Marlowe, F. W. (2007). Voice pitch predicts reproductive success in male hunter-gatherers. Biology Letters,3(6), 682-684. doi:10.1098/rsbl.2007.0410

Biddle, S. J., Bennie, J. A., Bauman, A. E., Chau, J. Y., Dunstan, D., Owen, N., . . . Uffelen, J. G. (2016). Too much sitting and all-cause mortality: is there a causal link? BMC Public Health,16(1). doi:10.1186/s12889-016-3307-3

Bennett, M. R., Harris, J. W., Richmond, B. G., Braun, D. R., Mbua, E., Kiura, P., . . . Gonzalez, S. (2009). Early Hominin Foot Morphology Based on 1.5-Million-Year-Old Footprints from Ileret, Kenya. Science,323(5918), 1197-1201. doi:10.1126/science.1168132

Berna, F., Goldberg, P., Horwitz, L. K., Brink, J., Holt, S., Bamford, M., & Chazan, M. (2012). Microstratigraphic evidence of in situ fire in the Acheulean strata of Wonderwerk Cave, Northern Cape province, South AfricaProceedings of the National Academy of Sciences,109(20). doi:10.1073/pnas.1117620109

Bernhardt, P. C., Jr, J. M., Fielden, J. A., & Lutter, C. D. (1998). Testosterone changes during vicarious experiences of winning and losing among fans at sporting events. Physiology & Behavior,65(1), 59-62. doi:10.1016/s0031-9384(98)00147-4

Blaisdell, A. P. (2015). Play as the Foundation of Human Intelligence: The Illuminating Role of Human Brain Evolution and Development and Implications for Education and Child Development. Journal of Evolution and Health,1(1). doi:10.15310/2334-3591.1016

Bramble, D. M., & Lieberman, D. E. (2004). Endurance running and the evolution of Homo. Nature,432(7015), 345-352. doi:10.1038/nature03052

Desoto, M. C., Hitlan, R. T., Deol, R. S., & Mcadams, D. (2010). Testosterone Fluctuations in Young Men: The Difference between Interacting with like and Not-Like others. Evolutionary Psychology,8(2), 147470491000800. doi:10.1177/147470491000800203

Eisenegger, C., Haushofer, J., & Fehr, E. (2011). The role of testosterone in social interaction. Trends in Cognitive Sciences,15(6), 263-271. doi:10.1016/j.tics.2011.04.008

Eisenegger, C., Kumsta, R., Naef, M., Gromoll, J., & Heinrichs, M. (2016). Testosterone and androgen receptor gene polymorphism are associated with confidence and competitiveness in men. Hormones and Behavior. doi:10.1016/j.yhbeh.2016.09.011

Fink, B., Neave, N., & Seydel, H. (2006). Male facial appearance signals physical strength to women. American Journal of Human Biology,19(1), 82-87. doi:10.1002/ajhb.20583

Fonseca-Azevedo, K., & Herculano-Houzel, S. (2012). Metabolic constraint imposes tradeoff between body size and number of brain neurons in human evolution. Proceedings of the National Academy of Sciences,109(45), 18571-18576. doi:10.1073/pnas.1206390109

Gruss, L. T., & Schmitt, D. (2015). The evolution of the human pelvis: changing adaptations to bipedalism, obstetrics and thermoregulation. Philosophical Transactions of the Royal Society B: Biological Sciences,370(1663), 20140063-20140063. doi:10.1098/rstb.2014.0063

Hatala, K. G., Roach, N. T., Ostrofsky, K. R., Wunderlich, R. E., Dingwall, H. L., Villmoare, B. A., . . . Richmond, B. G. (2016). Footprints reveal direct evidence of group behavior and locomotion in Homo erectus. Scientific Reports,6, 28766. doi:10.1038/srep28766

Lee, S., Lee, S., & Jung, J. (2014). Muscle Activity of the Gluteus Medius at Different Gait Speeds. Journal of Physical Therapy Science,26(12), 1915-1917. doi:10.1589/jpts.26.1915

Lieberman, D. E., Raichlen, D. A., Pontzer, H., Bramble, D. M., & Cutright-Smith, E. (2006). The human gluteus maximus and its role in running. Journal of Experimental Biology,209(11), 2143-2155. doi:10.1242/jeb.02255

Lieberman, D. E., & Bramble, D. M. (2007). The Evolution of Marathon Running. Sports Medicine,37(4), 288-290. doi:10.2165/00007256-200737040-00004

Lieberman, D. E., Bramble, D. M., Raichlen, D. A., & Shea, J. J. (2009). Brains, Brawn, and the Evolution of Human Endurance Running Capabilities. Vertebrate Paleobiology and Paleoanthropology The First Humans – Origin and Early Evolution of the Genus Homo, 77-92. doi:10.1007/978-1-4020-9980-9_8

Lieberman, D. E. (2015). Human Locomotion and Heat Loss: An Evolutionary Perspective. Comprehensive Physiology, 99-117. doi:10.1002/cphy.c140011

Lippi, G., Favaloro, E. J., & Guidi, G. C. (2008). The genetic basis of human athletic performance. Why are psychological components so often overlooked? The Journal of Physiology,586(12), 3017-3017. doi:10.1113/jphysiol.2008.155887

Lombardo, M. P. (2012). On the Evolution of Sport. Evolutionary Psychology.

Mattson, M. P. (2012). Evolutionary aspects of human exercise—Born to run purposefully. Ageing Research Reviews,11(3), 347-352. doi:10.1016/j.arr.2012.01.007

Michaud, J. E., Billups, K. L., & Partin, A. W. (2015). Testosterone and prostate cancer: an evidence-based review of pathogenesis and oncologic risk. Therapeutic Advances in Urology,7(6), 378-387. doi:10.1177/1756287215597633

Moffit, D. M., & Swanik, C. B. (2011). The Association between Athleticism, Prenatal Testosterone, and Finger Length. Journal of Strength and Conditioning Research,25(4), 1085-1088. doi:10.1519/jsc.0b013e3181d4d409

Moorjani, P., Amorim, C. E., Arndt, P. F., & Przeworski, M. (2016). Variation in the molecular clock of primates. doi:10.1101/036434

Navarrete, A., Schaik, C. P., & Isler, K. (2011). Energetics and the evolution of human brain size. Nature,480(7375), 91-93. doi:10.1038/nature10629

Patterson, N., Richter, D. J., Gnerre, S., Lander, E. S., & Reich, D. (2006). Genetic evidence for complex speciation of humans and chimpanzees. Nature,441(7097), 1103-1108. doi:10.1038/nature04789

Piantadosi, S. T., & Kidd, C. (2016). Extraordinary intelligence and the care of infants. Proceedings of the National Academy of Sciences,113(25), 6874-6879. doi:10.1073/pnas.1506752113

Pound, N., Penton-Voak, I. S., & Surridge, A. K. (2009). Testosterone responses to competition in men are related to facial masculinity. Proceedings of the Royal Society B: Biological Sciences,276(1654), 153-159. doi:10.1098/rspb.2008.0990

Plomp, K. A., Viðarsdóttir, U. S., Weston, D. A., Dobney, K., & Collard, M. (2015). The ancestral shape hypothesis: an evolutionary explanation for the occurrence of intervertebral disc herniation in humans. BMC Evolutionary Biology,15(1). doi:10.1186/s12862-015-0336-y

Prang, T. C. (2015). Rearfoot posture of Australopithecus sediba and the evolution of the hominin longitudinal arch. Scientific Reports,5, 17677. doi:10.1038/srep17677

Raichlen, D. A., & Polk, J. D. (2012). Linking brains and brawn: exercise and the evolution of human neurobiology. Proceedings of the Royal Society B: Biological Sciences,280(1750), 20122250-20122250. doi:10.1098/rspb.2012.2250

Rolian, C., Lieberman, D. E., Hamill, J., Scott, J. W., & Werbel, W. (2009). Walking, running and the evolution of short toes in humans. Journal of Experimental Biology,212(5), 713-721. doi:10.1242/jeb.019885

Ruxton, G. D., & Wilkinson, D. M. (2011). Avoidance of overheating and selection for both hair loss and bipedality in hominins. Proceedings of the National Academy of Sciences,108(52), 20965-20969. doi:10.1073/pnas.1113915108

Ruxton, G. D., & Wilkinson, D. M. (2011). Thermoregulation and endurance running in extinct hominins: Wheeler’s models revisited. Journal of Human Evolution,61(2), 169-175. doi:10.1016/j.jhevol.2011.02.012

Schmitt, D. (2003). Insights into the evolution of human bipedalism from experimental studies of humans and other primates. Journal of Experimental Biology,206(9), 1437-1448. doi:10.1242/jeb.00279

Schulkin, J. (2016). Evolutionary Basis of Human Running and Its Impact on Neural Function. Frontiers in Systems Neuroscience,10. doi:10.3389/fnsys.2016.00059

Smith, E. A. (2004). Why do good hunters have higher reproductive success? Human Nature,15(4), 343-364. doi:10.1007/s12110-004-1013-9

Sockol, M. D., Raichlen, D. A., & Pontzer, H. (2007). Chimpanzee locomotor energetics and the origin of human bipedalismProceedings of the National Academy of Sciences,104(30), 12265-12269. doi:10.1073/pnas.0703267104

Spoor, F., Wood, B., & Zonneveld, F. (1994). Implications of early hominid labyrinthine morphology for evolution of human bipedal locomotion. Nature,369(6482), 645-648. doi:10.1038/369645a0

Stattin, P., Lumme, S., Tenkanen, L., Alfthan, H., Jellum, E., Hallmans, G., . . . Hakama, M. (2003). High levels of circulating testosterone are not associated with increased prostate cancer risk: A pooled prospective study. International Journal of Cancer,108(3), 418-424. doi:10.1002/ijc.11572

Steudel-Numbers, K. L. (2006). Energetics in Homo erectus and other early hominins: The consequences of increased lower-limb length. Journal of Human Evolution,51(5), 445-453. doi:10.1016/j.jhevol.2006.05.001

Tuttle, R. H. (1967). Knuckle-walking and the evolution of hominoid hands. American Journal of Physical Anthropology,26(2), 171-206. doi:10.1002/ajpa.1330260207

Wood, R. I., & Stanton, S. J. (2012). Testosterone and sport: Current perspectives. Hormones and Behavior,61(1), 147-155. doi:10.1016/j.yhbeh.2011.09.010

Young, R. W. (2003). Evolution of the human hand: the role of throwing and clubbing. Journal of Anatomy,202(1), 165-174. doi:10.1046/j.1469-7580.2003.00144.x

Testosterone and Society

1050 words

In my last post on testosterone, I showed how the alarmism against having high testosterone is blown out of proportion. The hormone testosterone was extremely important in our evolutionary history, with skull changes that are affected by testosterone changing, indicating that it’s a cause of the rise of civilization. By looking at the skulls and skeletons of our hominin ancestors, we can infer how high the testosterone was due to changes in their skeletons over time. It seems that a decrease in testosterone was partly responsible for the advent of civilization, but too low of a dip is causing problems in the West.

Testosterone on its own is very important for male fertility, and confidence with there being no evidence showing causation in regards to prostate cancer. There are, however, large increases and dips and testosterone throughout evolutionary history. This can be inferred from looking at the skeletal remains of our ancestors.

One such study was completed by Cieri et al (2014). Cieri et al found that there was substantial feminization of Homo sapiens facial anatomy. Most notably there were reductions in average brow projection and the shortening of the upper facial skeleton. If you have knowledge of testosterone and its effects on the body, this is not surprising. Relaxing either testosterone or androgen sensitivity will cause softer, more feminized facial features over time. They argue that changes in craniofacial morphology reflects reduction in circulating levels of testosterone, “or reduced androgen receptor densities”, which, they argue “reflect the evolution of enhanced social tolerance since the Middle Pleistocene.”

The reduction in human craniomorphology coincides with larger populations from the Agricultural Revolution, which meant greater social tolerance and reduced aggression towards the group. Due to this, people were more altruistic to each other. Men that were more altruistic and had more pro-social behaviors, for instance, would be able to trade with other men in the band, which became sort of a fallback when they couldn’t forage any food. Over time, those men who could cooperate better (and had more feminized craniomorphology due to less circulating testosterone/androgen receptors).

Due to the selection of more pro-social behaviors, humans started becoming less aggressive and facial features became more feminized (due to less circulating testosterone/androgen receptors). Testosterone itself is correlated with aggressive behavior (Olweus et al, 1988) so with the selection against testosterone due to people who were more altruistic makes sense in this evolutionary context.

Cieri et al argue a good case—that the beginnings of behavioral modernity was due to selection against aggressive behavior, shifted towards pro-sociality. The fact that this began to occur around the Agricultural Revolution is no coincidence, in my opinion.

However, there seems to be a level of testosterone that a civilization needs to remain standing. Testosterone levels have reduced in the past two decades. Men are becoming more feminized, partly due to the environments we have constructed for ourselves. It’s in part due to the foods we eat/what we eat out of that is causing the drop. For instance, imagine being in an environment that destroys human testosterone levels. For instance, let’s say that a lot of the food we eat is made with/stored in a lot of BPA-containing storage. Over time, this would cause differing gene expression. People who are eating these testosterone-lowering foods will have children and, theoretically, pass on the genetically expressed genes to their children, in an epigenetic transference. Since those genes would then be advantageous in the environments we have constructed for ourselves, they would then get selected for. Once enough people get the gene in the population then it will reach fixation. That gene will then get selected in that population. If that gene is one that lowers testosterone, you will then begin to have a more feminized population (like we are seeing now, with men having lower levels of testosterone now than we did twenty years ago).

As I argued in my previous article on testosterone, what Rushton described in his 1988 paper was the Graeco-Roman elite did not breed due to having less circulating testosterone. As I have covered, low testosterone is correlated with having fewer children. As Rushton hypothesized, the elite did not breed while the lower classes did. We can look at it today and look at the ‘elite’ as upper-middle/upper class and look at the lower class, as, well the lower class. We do see the testosterone/class relationship today, with higher classes having lower levels of testosterone, vice versa for lower classes (Dabbs and Morris, 1990).

When looking at testosterone changes over time, fertility rates need to be looked at. Testosterone is down across the board all over the Western hemisphere, and it just so happens that the West is in a fertility crisis (with Europe having the lowest fertility in the world). Not surprisingly, testosterone is taking a dip in the West which is then having a negative effect on testosterone levels. This is due, partly, to the anti-testosterone environments that we have unknowingly (?) constructed for ourselves. To mediate these problems, we need to construct environments that keep testosterone levels raised as to side-step all of the horrible health problems associated with low testosterone, especially later in life.

So, since testosterone is the dominance/confidence/stress hormone, it’s clear that most men don’t put themselves into situations where the hormone would be heightened by the body. Testosterone levels do change throughout the day and depending on events that occur. If you’re around a lot of rowdy people, your testosterone will raise in response to the action around you. Testosterone rises significantly when in large groups and others around are committing violence and being destructive. This is natural, though. When this occurs, you’ll be at the ready for anything that happens, there will be no surprises. It’s a stress hormone, in that it rises mostly in stressful situations.

For society to form, there needed to be somewhat of a testosterone reduction throughout our evolutionary history. This allowed us to trade with each other and so, altruistic behaviors then were selected for. However, too much of a testosterone reduction within single populations leads to lower fertility, and, eventually, the fall of societies due to lower fertility rates. The key here is that we need to construct environments that encourage higher levels of testosterone. If something is not done, then Western society will fall sooner, rather then later (all things eventually come to an end; nothing lasts forever).

The Testosterone and Fertility Conundrum: A Western Perspective

2750 words

Some people are scared of testosterone. This is no surprise, since a super-majority of people have no background in the human sciences. I’m sure plenty men know what it’s like to have low testosterone, just like some men know what it’s like to have higher T levels than average. What is the optimum level of testosterone? Why are some people scared of this hormone?

Rushton (1997) posited that r/K Selection Theory could be used to classify the races of Man on a spectrum, going from r-selection (having many children but showing little to no parental care) to K-selection (having fewer children but showing a lot of parental care). He stated that the traits of the races were also on the r/K spectrum, with the races having stark differences in morphology. Rushton’s application of r/K theory to humans isn’t completely wrong, though I do have some problems with some of his claims, such as his claims that the races differ in average penis size. He contends that testosterone is the cause for higher crime rates for black Americans and higher rates of prostate cancer in black Americans compared to white Americans.

However, in 2014, Richard et al showed that when controlling for age, blacks had 2.5 to 4.9 percent more testosterone than whites, on average. This cannot explain racial differences in prostate cancer. However, some people may emphatically claim that the races differ in average testosterone, with blacks having 13 percent higher free testosterone than whites on average. The citation that gets used the most to prove that blacks supposedly have higher testosterone than whites is Ross et al (1986), which is based on a sample of 100 people (50 black, 50 white). He claims that it’s when T levels are higher, so it’s a ‘better study’ even though the sample leaves a lot to be desired. A much more robust study showed that the difference was negligible, and not enough to account for the differential prostate cancer rates between the races.

Rohrmann et al (2007) show that there are no differences in circulating testosterone between blacks and whites in a nationally representative sample of American men. Mexicans had the highest levels. There were, however, B-W differences in estradiol production. They couldn’t confirm the other studies that stated that blacks had higher testosterone, possibly due to variations in age or using non-representative samples (that’s the culprit). Their nationally representative sample showed there was no difference in testosterone between blacks is whites, while the meta-analysis showed by Richard et al (2014) showed the difference was negligible at 2.5 to 4.9 percent higher rate of testosterone which doesn’t explain why blacks have a higher rate of acquiring prostate cancer.

The much more likely culprit for blacks having higher rates of prostate cancer, as I have written about before, are environmental factors. The two main factors are receiving less sunlight and diet. There is no evidence that higher levels of testosterone lead to prostate cancer (Michaud, Billups, and Partin, 2015). Contrary to those who say that higher levels of T cause prostate cancer, there is growing evidence that lower levels of T lead to prostate cancer (Park et al, 2015). Put simply, there is no evidence for testosterone’s supposed impact on the prostate (Stattin et al, 2013).

Differences in androgen/androgen receptors have been explained as a cause for racial differences in prostate cancer (Pettaway, 1999), however, these results haven’t been consistent (Stattin et al, 2003) and these differences in circulating androgen may possibly be explained by differences in obesity between the two populations (Gapstur et al, 2002; also see my posts on obesity and race).

Due to the ‘testosterone scare’, some people may believe that having low T is a ‘good thing’, something that’s preferred over being a high T savage. However, testosterone and the androgen receptor gene polymorphism are both associated with competitiveness and confidence in men (Eisenegger et al, 2016) and a reduced risk of cardiovascular disease in elderly men (Ohlsson et al, 2011). Obviously, lower testosterone is related to less overall confidence. People who have the thought in their head that testosterone is a ‘bad hormone’ will believe the negativity about it in the media and popular headlines.

Testosterone alone does not cause violence, but it does cause men to be socially dominant. Testosterone has been shown to increase in the aggressive phases of sports games and when shown artificial humans made to invoke physiologic responses, leading some researchers to argue that testosterone should be classified as a stress hormone. Testosterone does change based on watching one’s favorite soccer team winning or losing in a sample of 21 men (Bernhardt et al, 1998), lending some credence to the claim that testosterone is and should be classified as a stress hormone. Also of interest is that men who administered high levels of testosterone did not report higher levels of aggression (Batrinos, 2012).

I’ve heard some people literally say that having low testosterone is ‘a good thing’. People say this out of ignorance. There are a whole slew of problems associated with low testosterone, including but not limited to: insulin resistance in diabetic men (Grossmann et al, 2008); metabolic syndrome (Tsuijimura et al, 2013); muscle loss (Yuki et al, 2013); stroke and transient ischemic attack (a mini-stroke; Yeap et al, 2009); associated with elevated risk for dementia in older men (Carcaillon et al, 2014); myocardial infarction (heart attack) in diabetic men (Daka et al, 2015) etc. So it seems that the fear of testosterone from those in the anti-testosterone camp are largely blown out of proportion.

Testosterone is also a ‘food’ for the brain, with low levels being related to mental illness, sexual dysfunction, lower quality of life and cognitive impairment (Moffat et al, 2011) in both sexes (Ciocca et al, 2016). Noticed in both men in women with testosterone deficits were: cognitive impairment (reduction of working memory, episodic memory, processing speed, visual-spatial functioning and executive performance); a decrease in sexual activity; anxiety, schizophrenia, depression and stress; and alterations in cortical thickness in the brain. The fact that testosterone is so heavily important to the body’s central functioning is extremely clear. This is why it’s laughable that some people would be happy and brag about having low testosterone.

I recently came across a book called The Testosterone Hypothesis: How Hormones Regulate the Life Cycles of Civilization. Barzilai’s main premise is that the rise and fall of the West is mediated by the hormone testosterone, and due to lower testosterone levels this is one large reason for what is currently occurring in the West. The book has an extremely interesting premise. Barzilai’s hypothesis does line up with the declining levels of testosterone in America (Travison et al, 2007) though other research shows no decline in American testosterone levels from the years 88-91 to 99-04 (Nyante et al, 2007). Moreover, men who had higher level of n-6 in their blood then n-3 were far more likely to be infertile (Safarinejad et al, 2010) a marker of low testosterone (Sharpe, 2012). The ratio of n-6 to n-3 from the years 1935 to 1939 were 8.4 to 1, whereas from the years 1935 to 1985, the ratio increased to about 10 percent (Raper et al, 1992). The ratio of n-6 to n-3, on top of lowering sperm count (which is correlated with testosterone) also has negative effects on male and female cognitive ability (Lassek and Gaulin, 2011).

Barzilai’s research also corroborates Rushton’s (1986) theory of why there are lower birthrates for Europeans around the world. Rushton stated that this cycle has been noticed throughout history, with empires rising and falling due to differential birthrates between the ruling class and the ruled. Rushton also hypothesized that the cultures and gene pools associated with the Graeco-Roman empire were “evolutionary dead ends” (Rushton, 1986: 148). Knowing what we now know about the relationship between cognitive ability, testosterone, and fertility, we now have a plausible hypothesis for Rushton’s hypothesis and one of the (many) reasons why the Graeco-Roman empire collapsed. Rushton further hypothesized that the cause for lower fertility in European populations “may be partly mediated by a psychological process in which the desire to be in control of both oneself and one’s environment is taken to an extreme.” Of course there’s a good chance that this psychological process is mediated/influenced by testosterone.

Europe is the continent with the lowest fertility (ESHRE Capri Workshop Group, 2010). Testosterone has declined in Europe as a whole (Rivas et al, 2014), and this is a strong cause for the lower birthrates in Europe (along with genetic reasons) and in Finland (Perheentupa et al, 2013). The introduction of Westernized diets lowers testosterone, so this is no surprise that a reduction is seen in countries that begin to consume a Western diet. Another probable cause for lower testosterone/fertility in Europe at the moment is the large number of European men that died in WWI and WWII. Those that were more willing to fight died, meaning there was less of a chance he spread his genes. So, over time, this lead to the current cucking of Europe that we are now witnessing.

Testosterone is also hypothesized to have driven evolution (Howard, 2001). Testosterone is such an important part of human evolution and development, so much so that if we had a lower level of the hormone all throughout our evolution that we would be a different species today. Testosterone is needed for sexual functioning, good mental and brain health, fertility, cognitive ability, muscle mass retention in both young and old men, etc. Testosterone is one of the most important hormones for both men and women, and low levels for both sexes are detrimental to a high quality of life. The current data on testosterone and prostate cancer shows that higher levels of testosterone don’t contribute to prostate cancer. Testosterone, then, also isn’t a cause for the racial gap in prostate cancer because other environmental factors better explain it. If people really are happy about having lower testosterone, then I hope they have fun living a life with a low sex drive, lower cognition in old age, lower muscle mass and a higher chance of stroke and metabolic syndrome.

One of the most interesting things about testosterone is the possibility that it explains why civilizations rise and fall. There is anecdotal evidence from Rushton, as well as his theorizing that the higher classes in Rome didn’t breed which led to their downfall. We now know that lower fertility rates for men are associated with lower testosterone, so along with Barzilai’s thesis of testosterone causing the rise and fall of civilizations, Rushton’s theorizing of the cause of lower European fertility and the cause of the fall of the Graeco-Roman empire.

Testosterone is an extremely important hormone, one that drives human evolution and society formation since it’s associated with dominance and confidence. Low testosterone is looked at as ‘good’ because those with higher intelligence have lower levels of the hormone (indicated by lower confidence and having sex at a later age). I showed that the higher IQ East Asian men have a problem finding dates and being looked at as sexually attractive (even though they rated themselves as average). Along with lower East Asian fertility, specifically in Japan, does it seem to you like the high IQ people are more desired if they are having problems keeping their birthrates up? The fact of the matter is, lower levels of testosterone are correlated with lower levels of fertility. If men don’t have as much testosterone pumping through their veins, they will be less likely to have sex and thusly reproduce.

References

Batrinos, M. L. (2012). Testosterone and aggressive behavior in man. International Journal of Endocrinology & Metabolism,10(3), 563-568. doi:10.5812/ijem.3661

Bernhardt, P. C., Jr, J. M., Fielden, J. A., & Lutter, C. D. (1998). Testosterone changes during vicarious experiences of winning and losing among fans at sporting events. Physiology & Behavior,65(1), 59-62. doi:10.1016/s0031-9384(98)00147-4

Carcaillon, L., Brailly-Tabard, S., Ancelin, M., Tzourio, C., Foubert-Samier, A., Dartigues, J., . . . Scarabin, P. (2014). Low testosterone and the risk of dementia in elderly men: Impact of age and education. Alzheimer’s & Dementia,10(5). doi:10.1016/j.jalz.2013.06.006

Ciocca G, Limoncin E, Gravina GL, et al. Is testosterone a food for brain? Sex Med Rev 2016;4:15-25.

Daka, B., Langer, R. D., Larsson, C. A., Rosén, T., Jansson, P. A., Råstam, L., & Lindblad, U. (2015). Low concentrations of serum testosterone predict acute myocardial infarction in men with type 2 diabetes mellitus. BMC Endocrine Disorders,15(1). doi:10.1186/s12902-015-0034-1

ESHRE Capri Workshop Group. Europe the continent with the lowest fertilityHum Reprod Update 2010; 16: 590–602.

Eisenegger, C., Kumsta, R., Naef, M., Gromoll, J., & Heinrichs, M. (2016). Testosterone and androgen receptor gene polymorphism are associated with confidence and competitiveness in men. Hormones and Behavior. doi:10.1016/j.yhbeh.2016.09.011

Gapstur SM, Gann PH, Kopp P, Colangelo L, Longcope C, Liu K. Serum androgen concentrations in young men: a longitudinal analysis of associations with age, obesity, and race—the CARDIA male hormone study. Cancer Epidemiol Biomarkers Prev 2002; 11: 10417

Grossmann, M., Thomas, M. C., Panagiotopoulos, S., Sharpe, K., Macisaac, R. J., Clarke, S., . . . Jerums, G. (2008). Low Testosterone Levels Are Common and Associated with Insulin Resistance in Men with Diabetes. The Journal of Clinical Endocrinology & Metabolism,93(5), 1834-1840. doi:10.1210/jc.2007-2177

Howard JM (2001): Androgens in human evolution. A new explanation of human evolution.

Lassek, W. D., & Gaulin, S. J. (2011). Sex Differences in the Relationship of Dietary Fatty Acids to Cognitive Measures in American Children. Frontiers in Evolutionary Neuroscience,3. doi:10.3389/fnevo.2011.00005

Michaud, J. E., Billups, K. L., & Partin, A. W. (2015). Testosterone and prostate cancer: an evidence-based review of pathogenesis and oncologic risk. Therapeutic Advances in Urology,7(6), 378-387. doi:10.1177/1756287215597633

Moffat, S. D., Zonderman, A. B., Metter, E. J., Blackman, M. R., Harman, S. M., & Resnick, S. M. (2002). Longitudinal Assessment of Serum Free Testosterone Concentration Predicts Memory Performance and Cognitive Status in Elderly Men. The Journal of Clinical Endocrinology & Metabolism,87(11), 5001-5007. doi:10.1210/jc.2002-020419

Nyante, S. J., Graubard, B. I., Li, Y., Mcquillan, G. M., Platz, E. A., Rohrmann, S., . . . Mcglynn, K. A. (2011). Trends in sex hormone concentrations in US males: 1988-1991 to 1999-2004. International Journal of Andrology,35(3), 456-466. doi:10.1111/j.1365-2605.2011.01230.x

Ohlsson C, Barrett-Connor E, Bhasin S, et al. High serum testosterone is associated with reduced risk of cardiovascular events in elderly men: the MrOS (Osteoporotic Fractures in Men) study in Sweden. J Am Coll Cardiol. 2011; 58(16):1674-1681.

Park, J., Cho, S. Y., Jeong, S., Lee, S. B., Son, H., & Jeong, H. (2015). Low testosterone level is an independent risk factor for high-grade prostate cancer detection at biopsy. BJU International,118(2), 230-235. doi:10.1111/bju.13206

Perheentupa, A., Makinen, J., Laatikainen, T., Vierula, M., Skakkebaek, N. E., Andersson, A., & Toppari, J. (2012). A cohort effect on serum testosterone levels in Finnish men. European Journal of Endocrinology,168(2), 227-233. doi:10.1530/eje-12-0288

Pettaway CA. Racial differences in the androgen/androgen receptor pathway in prostate cancer. J Natl Med Assoc 1999, 91: 653:650

Raper, N. R., Cronin, F. J., & Exler, J. (1992). Omega-3 fatty acid content of the US food supply. Journal of the American College of Nutrition,11(3), 304-308. doi:10.1080/07315724.1992.10718231

Richard, A., Rohrmann, S., Zhang, L., Eichholzer, M., Basaria, S., Selvin, E., . . . Platz, E. A. (2014). Racial variation in sex steroid hormone concentration in black and white men: a meta-analysis. Andrology,2(3), 428-435. doi:10.1111/j.2047-2927.2014.00206.x

Rivas AM, Mulkey Z, Lado-Abeal J, Yarbrough S. Diagnosing and managing low serum testosteroneProc (Bayl Univ Med Cent) 2014;27:321-324

Rohrmann, S., Nelson, W. G., Rifai, N., Brown, T. R., Dobs, A., Kanarek, N., . . . Platz, E. A. (2007). Serum Estrogen, But Not Testosterone, Levels Differ between Black and White Men in a Nationally Representative Sample of Americans. The Journal of Clinical Endocrinology & Metabolism,92(7), 2519-2525. doi:10.1210/jc.2007-0028

Ross R, Bernstein L, Judd H, Hanisch R, Pike M, Henderson B. Serum testosterone levels in healthy young black and white men. J Natl Cancer Inst. 1986 Jan;76(1):45–48

Rushton, J. P. (1986). Gene-Culture Coevolution and Genetic Similarity Theory: Implications for Ideology, Ethnic Nepotism, and Geopolitics. Politics and the Life Sciences,4(02), 144-148. doi:10.1017/s0730938400004706

Rushton J P (1997). Race, Evolution, and Behavior. A Life History Perspective (Transaction, New Brunswick, London).

Safarinejad, M. R., Hosseini, S. Y., Dadkhah, F., & Asgari, M. A. (2010). Relationship of omega-3 and omega-6 fatty acids with semen characteristics, and anti-oxidant status of seminal plasma: A comparison between fertile and infertile men. Clinical Nutrition,29(1), 100-105. doi:10.1016/j.clnu.2009.07.008

Sharpe, R. M. (2012). Sperm counts and fertility in men: a rocky road ahead. EMBO reports,13(5), 398-403. doi:10.1038/embor.2012.50

Stattin, P., Lumme, S., Tenkanen, L., Alfthan, H., Jellum, E., Hallmans, G., . . . Hakama, M. (2003). High levels of circulating testosterone are not associated with increased prostate cancer risk: A pooled prospective study. International Journal of Cancer,108(3), 418-424. doi:10.1002/ijc.11572

Travison, T. G., Araujo, A. B., O’Donnell, A. B., Kupelian, V., & Mckinlay, J. B. (2007). A Population-Level Decline in Serum Testosterone Levels in American Men. The Journal of Clinical Endocrinology & Metabolism,92(1), 196-202. doi:10.1210/jc.2006-1375

Tsujimura, A., Miyagawa, Y., Takezawa, K., Okuda, H., Fukuhara, S., Kiuchi, H., . . . Nonomura, N. (2013). Is Low Testosterone Concentration a Risk Factor for Metabolic Syndrome in Healthy Middle-aged Men? Urology,82(4), 814-819. doi:10.1016/j.urology.2013.06.023

Yeap, B. B., Hyde, Z., Almeida, O. P., Norman, P. E., Chubb, S. A., Jamrozik, K., . . . Hankey, G. J. (2009). Lower Testosterone Levels Predict Incident Stroke and Transient Ischemic Attack in Older Men. Endocrine Reviews,30(4), 411-411. doi:10.1210/edrv.30.4.9994

Yuki, A., Otsuka, R., Kozakai, R., Kitamura, I., Okura, T., Ando, F., & Shimokata, H. (2013). Relationship between Low Free Testosterone Levels and Loss of Muscle Mass. Scientific Reports,3. doi:10.1038/srep01818

Are There Race Differences in Penis Size? Part II

1000 words

I haven’t completely discredited the notion that Rushton and Lynn may be correct on this variable, but I’m highly skeptical. Hormonal data doesn’t show it. Hormones like IGF-1 and androgen don’t show the differences between races that would lead you to believe that Rushton’s Rule applies here.

PP is at it again, citing the same studies, not providing primary sources, and not addressing what I say to him about hormones in regards to penis size. Hormones affect the body in different ways, and different races have different levels of hormones. This is what I will discuss today.

Insulin-like growth factor 1 (IGF-1) is a hormone that, as it’s name implies, is structurally similar to the hormone insulin. IGF-1 is “partly responsible for systemic GH activities although it possesses a wide number of own properties (anabolic, antioxidant, anti-inflammatory and cytoprotective actions).” Laron and Klinger (1998) showed that children with Laron syndrome who stopped receiving IGF-1 injections showed reductions in penile and testicular size and they returned to pretreatment serum levels. This shows the effects of IGF-1 on sexual organ size.

Knowing this about IGF-1, for Rushton’s theory to be plausible, Blacks would have higher levels, Asians the lowest, and whites in the middle, skewing towards Asians. Platz et al (1999) investigated whether there were racial differences in circulating IGF-1 and insulin-like growth factor-binding protein 3 (IGFBP-3). IGFBP-3 binds IGF-1 and 2, with a dysregulation of IGFBP-3 correlating with cancer. IGFBP-3 is the main transporter of IGF-1 and 2 in the blood stream. The researchers tested men whose self-described ancestry (we know that self-describer ancestry is a great proxy for race, having a 99.86 percent success rate) African American (63) a random sample of Asians and Caucasians (75 respectively) aged 45 to 78 years old. Caucasians had the highest levels of IGF-1 (224 ng/ml), Asians (208 ng/ml), and African Americans (205 ng/ml). The IGF-1:IGFBP-3 ratio was greatest in Caucasians and lowest in Asians. This study was carried out to see if IGF-1 had an effect on prostate cancer. The 13 percent difference in IGFBP-3 between blacks and whites may account for the higher levels of prostate cancer, as IGFBP-3 can control IGF-1 bioavailabilty.

PP also cites Ross et al (1986) showing that blacks have “19 percent higher testosterone”, attempting to use this as evidence for the theory in favor of an inverse relationship between brain size and penis size. He seems to think that total testosterone matters, when what matters is free testosterone.It’s also 15 percent circulating testosterone, 13 percent free testosterone in that one study.  Free testosterone is biologically active, and is able to exert its effect by passing through a cell and activating its receptor. Speaking of free testosterone, in this meta-analysis of 23 studies on black-white differences in testosterone, Richard et al (2014) showed a 2.5 to 4.9 percent difference in free testosterone and concluded that that difference was not enough to account for the racial disparity in prostate cancer. So it’s either black Americans have lower levels of IGFBP-3 or diet/environmental factors that cause this racial disparity in prostate cancer, not testosterone.

Rohrmann et al (2007) showed that testosterone differences between blacks (n=363) and whites (n=674) did not noticeably differ (5.29 ng/ml and 5.11 ng/ml respectively). Mexican Americans (n=376) , on the other hand, showed a higher average rate (5.48 ng/ml) over both cohorts. Blacks had higher levels of estradiol than whites (40.80 pg/nl and 35.46 pg/nl respectively). Blacks also had a higher level of sex hormone-binding globulin (SHGB) (36.49 nmol/liter) than whites (34.91 nmol/liter) and Mexican Americans (34.91 nmol/liter). That may account for some of the racial disparity in prostate cancer, but it’s not testosterone (which shows that ‘higher levels of testosterone’ as PP says, isn’t proof of any racial differences in penis size).

The Kinsey data is nonrepresentative and nonrandom. We have comparative sizes for certain ethnies, and the only statistical difference is between Nigerians and Koreans and Czechs. Rushton and Boegart didn’t mention that blacks danced less than white college students, blacks are more prudish regarding nudity, more likely to have a prostitute as a sexual partner and less likely to want large families (Weizmann et al, 1990). A study on certain CAG repeats shows that Africans cluster with East Asians on two measures, contradicting Lynn’s hypothesis. French Army Surgeon, lol (see Weizman et al 1990 from above):

This work is filled with internal contradictions. For example, an average African Negro penis is said to be 7 3/4 to 8 inches long on p. 56, while on p. 242 it is stated that it “generally exceeds” 9 inches. Similarly, while the French Army surgeon announces on p. 56 that he once discovered a 12-inch penis, an organ of that size becomes “far from rare” on p. 243. As one might presume from such a work, there is no indication of the statistical procedures used to compute averages, what terms such as “often” mean, how subjects were selected, how measurements were made, what the sample sizes were, etc.

I think I’ve shown that there are no “””racial””” differences in size with the Veale et al 2014 study and the Orakwe and Ebuh (2007) study. As far as I see, two statistical differences exist between Nigerians and Koreans and Czechs. But there’s not enough “””quality data””” to say “this race bigger than that race”. To believe there are racial differences in penis size or that there is even an inverse relationship between penis size and brain size takes a huge leap of faith to believe.

There are, without a doubt, average differences in a lot of things between races; hormones being one of them. Any differences  between races in IGF-1 have no effect on penis size (IGF-1 is, however, one reason why black girls reach menarche at a younger age than white girls. Will write more on that in the future.). Africans were more similar to Asians that Caucasians on two of the five androgen indicators that Dutton (2015) tested. The Kinsey data is nonrepresentative and nonrandom and that is what PP continuously references. I’m highly skeptical leading towards no based on my knowledge of hormones and how they work in the human body. Testosterone does not explain any racial differences in penis size, and does not explain any differences in prostate cancer acquisition (though, other hormones do).