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The “N” Word

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Numerous academics have been looked at as pariahs for uttering this word. This word has a pretty long history offending people. The word I’m talking about is natural. This “N” word—especially today—is extremely divisive in today’s society. If you say that something is ‘natural‘, are you taking away any accomplishments that one has done, all because it’s ‘natural‘?

Take what I’ve been writing about for the past three weeks: athletics. If you say that one is a “natural” at athletic competition, are you taking away the hard work it took for that specific athlete to accomplish his goal? No way. You’re acknowledging that that specific individual has something special that sets him apart from the average person. That’s not to say that hard work, determination, and confidence don’t matter; on the contrary. They DO matter. However, like I said with the Kalenjin Kenyan distance runners (who do have anatomical/physiologic advantages in regards to sprinting): you can take someone with elite genetics who has done elite training and put him up against someone who has subpar genetics (in terms of the athletic event) with elite training—the same training as the athlete with elite genetics—and the athlete with elite genetics/muscle fibers/physiology will constantly blow away the individual who is less genetically gifted.

People readily admit that certain races excel at certain physical activities whereas other races don’t fare as well. As I’ve extensively covered (and provided more than enough evidence/arguments for), the races differ in the number of muscle fibers which cause higher rates of obesity in blacks; this causes strength differences which then correlate with mortality. Finally, somatype is extremely important when speaking about athletics. Blacks have a mesomorphic somatype, which, along with their fiber typing and physiologic differences on average compared to whites, cause blacks to dominate most sporting events. However, when you say that certain races are “naturally more intelligent than others“, people all of a sudden have a bone to pick.

This “N” word when it comes to athletics is perfectly fine to use in our vocabulary, yet when we begin talking about intelligence differences—between races and individuals—all of a sudden we think that everyone is the same and that all brains are made the same. We believe that, although humans evolved genetically isolated for thousands of years and have incurred anatomic/physiologic differences, that one organ—the brain—is somehow exempt from the forces of natural selection. I can think of no traits that WON’T get selected for/against, and so I can think of no reason why the brain wouldn’t be under different selective pressures in Siberia/Northern Europe/the Americas/Africa/PNG/Australia.

However, as far as I can tell, we have not found any alleles that differ between populations. It was proposed in 2005 that the genes ASPM and Microcephalin influenced brain growth (Evans et al, 2005; Mekel-Brobov et al, 2005). However, two years later, Rushton, Vernon and Ann Bons (2007) showed that there was no evidence that Microcephalin and ASPM were associated with general mental ability (GMA), head circumference or altruism. Peter Frost cites Woodley et al, (2014) showing that the correlation between microcephalin and IQ is .79, whereas the correlation with ASPM and IQ was .254. Woodley et al (2014) also show there is a correlation between Disability Adjusted Life Years (DALY) and Microcephalin. The reasoning is that Microcephalin may improve the body’s immune response to viral infections, enabling humans to live in larger societies and thus get selected for higher IQ. Since the allele seems to give better disease resistance, then, over time, selection for higher intelligence can be selected for since fewer people are dying from disease due to increased resistance.

Nevertheless, the debate is still out on this allele. However, the data does look good in that we may have found certain polymorphisms that differ between populations which may explain some racial differences in intelligence. (For more information on IQ alleles, see Race and IQ: the Case for Genes).

Now, we are beginning to have some good evidence pile up showing that there are population differences in these alleles, and that they do predict intelligence. Racial differences in intelligence aren’t accepted by mainstream science and the public at large (obviously) like physiologic/anatomic differences are between human populations. Populations are split for thousands of years. They evolve different anatomy/physiology based on the environment. So, then, why wouldn’t psychological differences appear between the races of Man, when other, physical changes occurred from the OoA migration? It literally makes no sense.

People readily admit that athleticism is largely “natural“, yet when someone says that differences in intelligence are largely due to genes they get shouted down and called a ‘racist’, as if that adds anything to the dialogue. People readily admit that individuals/races are “naturally” leaner/stronger/faster/have quicker reflexes. But if one just even hints at thinking about “natural” differences between populations when it comes to general mental ability, they will be shouted down and their careers will be ruined.

Why? Why are people so scared of the “N” word? Because people want to believe that what they do or do not accomplish comes down to them as an individual and only them. They don’t want to think about the complex interaction between genes x environment and how that shapes an individual’s life path. They only think about environment, and not any possible genetic factors. Certain people—mostly social science majors—deny that evolution had ANY impact on human behavior. The “N” word, especially in today’s society, is a completely divisive word. State that you hold hereditarian views (in terms of mental ability) in regards to differences between populations and athletic events and no one will bat an eye.

“Didn’t you see Usain Bolt blow away the competition and set a new world record in the 100m dash at 9.58 seconds?!”

“He’s naturally good, he was born a gifted athlete.”

No one will bat an eye if you say this. This is where the tables will be flipped if you say:

“Don’t you know that differences in intelligence are largely genetic in nature and no matter how much you ‘train the brain’ you’ll stay at that intelligence level?”

“Man, that’s racist. That shouldn’t be looked at. We are all the same and equal. Except when it comes to certain athletic events, then we are not equal and some populations have natural predispositions that help them win. Evolution stopped at the neck 100kya; the only parts of the body under selective pressure over the past 100kya is below the neck!”

People who say this need to explain exactly what shields the brain from selection pressures. Man originated in Africa, the descendants of the soon-to-be coalesced races spent tens of thousands of years in differing environments. You need to do different things to survive in different environments. Just as the races differ physically, they differ mentally as well. Evolution did not stop at the neck. Significant changes in the brain have occurred in the past 10,000 years. There was a trade-off with agriculture, in that it was responsible for the population explosion which was responsible for mutations that affect intelligence and thus get selected for.

The “N” word is not a scary word. It is, in fact, it’s just common sense. People need to realize that by accepting genetic explanations for black domination in sports, that they would then, logically, have to accept racial differences in intelligence. It makes no sense to accept evolutionary theories (even if you don’t know it) in regards to athletics and not accept the same evolutionary theories for racial differences in the brain. There are real differences between populations, in both anatomy/physiology and our mental faculties and brain organization. If you accept one, you have to accept the other.

Racial Differences in Somatype

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One’s somatype is, really, the first thing they notice. Somatypes are broken down into three categories: ectomorph (skinny build), endomorph (rounder, fatter build) and mesomorph (taller, more muscular build). Like numerous other traits, different races and ethnies fall somewhere in between these three soma categories. Africans are meso, while Europeans are endo, while East Asians are more endo than Europeans. Differences in somatype, too, lead to the expected racial differences in sports due to differing anatomy and fat mass.

History of somatyping

The somatype classification was developed by psychiatrist William Sheldon in the 1940s, while releasing a book in 1954 titled Atlas of Men: Somatotyping the Adult Male At All AgesHe theorized that one’s somatype could predict their behavior, intelligence, and where they place socially. Using nude posture photos from his Ivy League students, he grouped people into three categories based on body measurements and ratios—mesomorph, endomorph, and ectomorph. Clearly, his theory is not backed by modern psychology, but I’m not really interested in that. I’m interested in the somatyping.


The three somatypes are endomorph, mesomorph, and ectomorph. Each type has different leverages and body fat distribution. Endomorphs are rounder, with short limbs, a large trunk, carry more fat in the abdomen and lower body, large chest, wide hips, and has hardly any muscular definition, yet gain strength easily. Ectomorphs, on the other hand, are taller, lankier with longer limbs, a narrow chest, thin body, short trunk and has little muscle.

There are further subdivisions within the three main types, mesomorphic-endomorph (meso-dominant), mesomorph-endomorph (both types are equal with less ectomorphy), ectomorphic-mesomorph, endomorphic-mesomorph, endomorph-ectomorph, and ectomorphic-endomorph. This can be denoted as “7-1-1”, which would indicate pure endomorph, “1-7-1” would indicate pure mesomorph and “1-1-7” would be a pure ectomorph. Further breakdowns can be made such as “1.6-2.7-6.4”, indicating the somatype is ecto-dominant. On the scale, 1 is extremely low while 7 is extremely high. The races, however, fall along racial lines as well.

Racial differences in somatype

West Africans and their descendants are the most mesomorphic. They also have the highest amount of type II muscle fibers which is a leading cause of their success in sporting events which call for short bursts of speed. Due to having longer limbs, they have a longer stride and can generate more speed. West Africans also have the narrowest hips out of all of the races (Rushton, 1997: 163) which further leads to their domination in sprinting competitions and events that take quick bursts of speed and power. However much success their morphology lends them in these types of competitions, their somatype hampers them when it comes to swimming. The first black American qualified for the Olympic swimming team in the year 2000. This is due to a narrower chest cavity and denser, heavier bones.

East Africans are most ectomorphic which you can see by their longer limbs and skinnier body. They have an average BMI of 21.6, one of the lowest in the world. Their low BMI, ectomorphic somatype and abundance of slow twitch muscle fibers are why they dominate in distance running events. Many explanations have been proposed to explain why East Africans (specifically Kenyans and Ethiopians) dominate distance running. The main factor is their somatype (ectomorphic) (Wilbur and Pitsiladis, 2012). The authors, however, downplay other, in my opinion, more important physiologic characteristics such as muscle fiber typing, and differences in physiology. Of course their somatype matters for why they dominate, but other important physiologic characteristics do matter. They clearly evolved together so you cannot separate them.

Europeans are more endo than East Africans and West Africans but less so than East Asians. Europeans have a strong upper body, broad shoulders, longer and thicker trunk and shorter extremities along with 41 percent slow twitch fibers compared to blacks’ 33 percent slow twitch fibers. This is why Europeans dominate power sports such as powerlifting and the World’s Strongest Man. Eighty to 100 percent of the differences in total variation in height, weight, and BMI between East Asians and Europeans are associated with genetic differences (Hur et al, 2008). If the variation between East Asians and Europeans on height, weight and BMI are largely attributed to genetic factors, then the same, I assume, should be true for Africans and Europeans/East Asians.

East Asians are the most endomorphic race and have lighter skeletons and more body fat. They have short arms and legs with a large trunk, which is a benefit when it comes to certain types of lifting movements (such as Olympic lifting, where East Asians shine) but hampers them when it comes to sprinting and distance running (although they have higher rates of type I fibers). East Asians also have more body fat at a lower BMI which is further evidence for the endomorphic somatype. This is also known as ‘TOFI’, ‘Thin on the Outside, Fat on the Inside’. Chinese and Thai children had a higher waist circumference and higher trunk fat deposits than Malay and Lebanese children (Liu et al, 2011). This is a classic description of the endomorphic individual.

Human hands and feet are also affected by climate. Climatic variation played a role in shaping the racial somatic differences we see today. The differences seen in hands and feet “might be due to the presence of evolutionary constraints on the foot to maintain efficient bipedal locomotion” (Betti et al, 2015).

Black-white differences in somatype

Fifty percent of the variability in lean mass is due to genetic factors (Arden and Specter, 1997) with the heritability of stature 85 percent in a meta-analysis (Peeters et al, 2009). Racial differences in somatype are also seen at a young age (Malina, 1969). Blacks had better muscular development and less fat-free mass at an early age. Vickery et al (1988) argued that since blacks have thinner skin folds that caliper measurements testing differences in body fat would be skewed. Malina (1969) also reports the same. Note that Malina’s paper was written in 1969, literally right before it got pushed on the American populace that fat was bad and carbohydrates were good.

Looking at the two tables cited by Malina (1969) on somatype we can see the difference between blacks and whites.

Data from Malina, (1969: 438) n Mesomorph Ectomorph Endomorph
Blacks 65 5.14 2.99 2.92
Whites 199 4.29 2.89 3.86
Data from Malina (1969: 438) Blacks Whites
Thin-build body type 8.93 5.90
Submedium fatty development 48.31 29.39
Medium fleshiness 33.69 43.63
Fat and very fat categories 9.09 21.06

Since this data was collected literally before we went down the wrong path and wrongly demonized fat and (wrongly) championed carbohydrates, this is an outstanding look at somatype/fat mass before the obesity epidemic. There is a clear trend, with blacks being more likely to have lower levels of fat-free body mass while also more likely to be mesomorphic. This is a ton of implications for racial differences in sports.

Somatype is predicated on lean mass, stature, bone density and fat-free body mass. Since racial differences appear in somatype at an early age, there is a great chance that the differences in somatype are genetic in nature.

College (American) football players are more likely to be endo-mesomorphs while high-school football players were more likely to be mesomorphs (Bale et al, 1994). This partly explains black over representation in football. Further, basketball, handball, and soccer players in Nigeria were taller, heavier, and had lower percent body fat than other athletic groups (Mazur, Toriola, and Igobokwe, 1985). Somatic differences have a lot to do with domination in sports competition.

Somatic differences are also seen in boxing. Elite boxers are more likely to have a mesomorphic somatype compared to non-athletes. Higher weight divisions were also more likely to be mesomorphic and endomorphic than the lower weight divisions which skewed ectomorphic (Noh et al, 2014). Blacks do well in boxing since they have a more mesomorphic somatype. Due to their higher levels of type II fibers, they can be quicker and throw more forceful punches which translates to boxing success.


Racial differences in somatype are another key to the puzzle to figure out why the races differ in elite sporting competition. The races evolved in different geographic locations which then led to differences in somatype. West African sports dominance is explained by their somatype, muscle fiber type, and physiology. The same can be said for Europeans in strength sports/powerlifting sports, and East Asians with ping-pong and some strength sports (though, due to lower muscle mass they are the least athletic of the races). I am not, of course, denying the impact of determination to succeed or training of any kind. What one must realize, however, is that one with the right genetic makeup/somatype and elite training will, way more often than not, outperform an individual with the wrong genetic makeup/somatype and elite training. These inherent differences between races explain the disparities in elite sporting competitions.


Arden, N. K., & Spector, T. D. (1997). Genetic Influences on Muscle Strength, Lean Body Mass, and Bone Mineral Density: A Twin Study. Journal of Bone and Mineral Research,12(12), 2076-2081. doi:10.1359/jbmr.1997.12.12.2076

Bale P, Colley E, Mayhew JL, et al. Anthropometric and somatotype variables related to strength in American football players. J Sports Med Phys Fitness 1994;34:383–9

Betti, L., Lycett, S. J., Cramon-Taubadel, N. V., & Pearson, O. M. (2015). Are human hands and feet affected by climate? A test of Allen’s rule. American Journal of Physical Anthropology,158(1), 132-140. doi:10.1002/ajpa.22774

Hur, Y., Kaprio, J., Iacono, W. G., Boomsma, D. I., Mcgue, M., Silventoinen, K., . . . Mitchell, K. (2008). Genetic influences on the difference in variability of height, weight and body mass index between Caucasian and East Asian adolescent twins. International Journal of Obesity,32(10), 1455-1467. doi:10.1038/ijo.2008.144

Liu, A., Byrne, N. M., Kagawa, M., Ma, G., Kijboonchoo, K., Nasreddine, L., . . . Hills, A. P. (2011). Ethnic differences in body fat distribution among Asian pre-pubertal children: A cross-sectional multicenter study. BMC Public Health,11(1). doi:10.1186/1471-2458-11-500

Malina, R. M. (1969). Growth and Physical Performance of American Negro and White Children: A Comparative Survey of Differences in Body Size, Proportions and Composition, Skeletal Maturation, and Various Motor Performances. Clinical Pediatrics,8(8), 476-483. doi:10.1177/000992286900800812

Mathur, D. N., Toriola, A. L., & Igbokwe, N. U. (1985). Somatotypes of Nigerian athletes of several sports. British Journal of Sports Medicine,19(4), 219-220. doi:10.1136/bjsm.19.4.219

Noh, J., Kim, J., Kim, M., Lee, J., Lee, L., Park, B., . . . Kim, J. (2014). Somatotype Analysis of Elite Boxing Athletes Compared with Nonathletes for Sports Physiotherapy. Journal of Physical Therapy Science,26(8), 1231-1235. doi:10.1589/jpts.26.1231

Peeters, M., Thomis, M., Beunen, G., & Malina, R. (2009). Genetics and Sports: An Overview of the Pre-Molecular Biology Era. Genetics and Sports Medicine and Sport Science, 28-42. doi:10.1159/000235695

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

Vickery SR, Cureton KJ, Collins MA. Prediction of body density from skinfolds in black and white young men. Hum Biol 1988;60:135–49.

Wilber, R. L., & Pitsiladis, Y. P. (2012). Kenyan and Ethiopian Distance Runners: What Makes Them so Good? International Journal of Sports Physiology and Performance,7(2), 92-102. doi:10.1123/ijspp.7.2.92

Possibly Retracting My Article on HBD and Baseball

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I am currently reading Taboo: Why Black Athletes Dominate Sports and Why We’re Afraid To Talk About It and came across a small section in the beginning of the book talking about black-white differences in baseball. It appears I am horribly, horribly wrong and it looks like I may need to retract my article HBD and Sports: Baseball. However, I don’t take second-hand accounts as gospel, so I will be purchasing the book that Entine cites, The Bill James Baseball Abstract 1987 to look into it myself and I may even do my own analysis on modern-day players to see if this still holds. Nevertheless, at the moment disregard the article I wrote last year until I look into this myself.

Excerpt from Taboo: Why Black Athletes Dominate Sports and Why We’re Afraid To Talk About It:

Baseball historian Bill James, author of dozens of books on the statistical twists of his favorite sport believes this trend [black domination in baseball] is not a fluke. In an intriguing study conducted in 1987, he compared the careers of hundreds of rookies to figure out what qualities best predict who would develop into stars. He noted many intangible factors, such as whether a player stays fit or is just plain lucky. The best predictors of long-term career success included the age of the rookie, his defensive position as a determinant in future hitting success (e.g., catchers fare worse than outfielders), speed, and the quality of the player’s team. But all of these factors paled when compared to the color of the player’s skin.

“Nobody likes to write about race,” James noted apologetically. “I thought I would do a [statistical] run of black players against white players, fully expecting that it would show nothing in particular or nothing beyond the outside range of chance, and I would file it away and never mention that I had looked at the issue at all.

James first compared fifty-four white rookies against the same number of black first-year players who had comparable statistics. “The results were astonishing,” James wrote. The black players:

* went on to have better major-league careers in 44 out of 54 cases

* played 48 percent more games

* had 66 percent more major league hits

* hit 93 percent more triples

* hit 66 percent more home runs

* scored 69 percent more runs

* stole 400 more bases (Entine, 2000: 22-23)

Flabbergasted at what he found, James ran a second study using forty-nine black/white comparisons. Again, blacks proved more durable, retained their speed longer, and were consistently better hitters. For example, he compared Ernie Banks, a power hitting shortstop for the Chicago Cubs, and Bernie Allen who broke in with Minnesota. They both reached the majors when they were twenty-three years old, were the same height and weight, and were considered equally fast. Over time, Allen bombed and Banks landed in the Hall of Fame. (Entine, 2000: 24)

In an attempt to correct for possible bias, James compared players with comparable speed statistics such as the number of doubles, triples, and stolen bases. He ran a study focused on players who had little speed. He analyzed for “position bias” and made sure that players in the same eras were being compared. Yet every time he crunched the numbers, the results broke down across racial lines. When comparing home runs, runs scored, RBIs or stolen bases, black players held an advantage a startling 80 percent of the time. “And I could identify absolutely no bias to help explain why this should happen,” James said in disbelief.

James also compared white Hispanic rookies whom he assumed faced an uphill battle similar to that for blacks, with comparable groups of white and black players. The blacks dominated the white Latinos by even more than they did white North Americans, besting them in 19 of the 26 comparisons. Blacks played 62 percent more games, hit 192 more home runs, drove in 125 percent more runs, and stole 30 percent more bases.

So why have blacks become the stars of baseball far out of proportion to their relative numbers? James eventually concluded that there were two possible explanations: “Blacks are better athletes because they are born better athletes, which is to say that it is genetic, or that they are born equal and become better athletes. (Entine, 2000: 24-25)

Black-White Differences in Muscle Fiber and Its Role In Disease and Obesity

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How do whites and blacks differ by muscle fiber and what does it mean for certain health outcomes? This is something I’ve touched on in the past, albeit briefly, and decided to go in depth on it today. The characteristics of skeletal muscle fibers dictate whether one has a higher or lower chance of being affected by cardiometabolic disease/cancer. Those with more type I fibers have less of a chance of acquiring diabetes while those with type II fibers have a higher chance of acquiring debilitating diseases. This has direct implications for health disparities between the two races.

Muscle fiber typing by race

Racial differences in muscle fiber typing explain differences in strength and mortality. I have, without a shadow of a doubt, proven this. So since blacks have higher rates of type II fibers while whites have higher rates of type I fibers (41 percent type I for white Americans, 33 percent type I for black Americans, Ama et al, 1985) while West Africans have 75 percent fast twitch and East Africans have 25 percent fast twitch (Hobchachka, 1988). Further, East and West Africans differ in typing composition, 75 percent fast for WAs and 25 percent fast for EAs, which has to do with what type of environment they evolved in (Hochhachka, 1998). What Hochhachka (1998) also shows is that high latitude populations (Quechua, Aymara, Sherpa, Tibetan and Kenyan) “show numerous similarities in physiological hypoxia defence mechanisms.” Clearly, slow-twitch fibers co-evolved here.

Clearly, slow-twitch fibers co-evolved with hypoxia. Since hypoxia is the deficiency in the amount of oxygen that reaches the tissues, populations in higher elevations will evolve hypoxia defense mechanisms, and with it, the ability to use the oxygen they do get more efficiently. This plays a critical role in the fiber typing of these populations. Since they can use oxygen more efficiently, they then can become more efficient runners. Of course, these populations have evolved to be great distance runners and their morphology followed suit.

Caesar and Henry (2015) also show that whites have more type I fibers than blacks who have more type II fibers. When coupled with physical inactivity, this causes higher rates of cancer and cardiometabolic disease. Indeed, blacks have higher rates of cancer and mortality than whites (American Cancer Society, 2016), both of which are due, in part, to muscle fiber typing. This could explain a lot of the variation in disease acquisition in America between blacks and whites. Physiologic differences between the races clearly need to be better studied. But we first must acknowledge physical differences between the races.

Disease and muscle fiber typing

Now that we know the distribution of fiber types by race, we need to see what type of evidence there is that differing muscle fiber typing causes differences in disease acquisition.

Those with fast twitch fibers are more likely to acquire type II diabetes and COPD (Hagiwara, 2013); cardiometabolic disease and cancer (Caesar and Henry, 2015); a higher risk of cardiovascular events (Andersen et al, 2015, Hernelahti et al, 2006); high blood pressure, high heart rate, and unfavorable left ventricle geometry leading to higher heart disease rates and obesity (Karjalainen et al, 2006) etc. Knowing what we know about muscle fiber typing and its role in disease, it makes sense that we should take this knowledge and acknowledge physical racial differences. However, once that is done then we would need to acknowledge more uncomfortable truths, such as the black-white IQ gap.

One hypothesis for why fast twitch fibers are correlated with higher disease acquisition is as follows: fast twitch fibers fire faster, so due to mechanical stress from rapid and forceful contraction, this leads the fibers to be more susceptible to damage and thus the individual will have higher rates of disease. Once this simple physiologic fact is acknowledged by the general public, better measures can be taken for disease prevention.

Due to differences in fiber typing, both whites and blacks must do differing types of cardio to stay healthy. Due to whites’ abundance of slow twitch fibers, aerobic training is best (not too intense). However, on the other hand, due to blacks’ abundance of fast twitch fibers, they should do more anaerobic type exercises to attempt to mitigate the diseases that they are more susceptible due to their fiber typing.

Black men with more type II fibers and less type I fibers are more likely to be obese than ‘Caucasian‘ men are to be obese (Tanner et al, 2001). More amazingly, Tanner et al showed that there was a positive correlation (.72) between weight loss and percentage of type I fibers in obese patients. This has important implications for African-American obesity rates, as they are the most obese ethny in America (Ogden et al, 2016) and have higher rates of metabolic syndrome (a lot of the variation in obesity does come down food insecurity, however). Leaner subjects had higher proportions of type I fibers compared to type II. Blacks have a lower amount of type I fibers compared to whites without adiposity even being taken into account. Not surprisingly, when the amount of type I fibers was compared by ethnicity, there was a “significant interaction” with ethnicity and obesity status when type I fibers were compared (Tanner et al, 2001). Since we know that blacks have a lower amount of type I fibers, they are more likely to be obese.

In Tanner et al’s sample, both lean blacks and whites had a similar amount of type I fibers, whereas the lean blacks possessed more type I fibers than the obese black sample. Just like there was a “significant interaction” between ethnicity, obesity, and type I fibers, the same was found for type IIb fibers (which, as I’ve covered, black Americans have more of these fibers). There was, again, no difference between lean black and whites in terms of type I fibers. However, there was a difference in type IIb fibers when obese blacks and lean blacks were compared, with obese blacks having more IIb fibers. Obese whites also had more type IIb fibers than lean whites. Put simply (and I know people here don’t want to hear this), it is easier for people with type I fibers to lose weight than those with type II fibers. This data is some of the best out there showing the relationship between muscle fiber typing and obesity—and it also has great explanatory power for black American obesity rates.


Muscle fiber differences between blacks and whites explain disease acquisition rates, mortality rates (Araujo et al, 2010), and differences in elite sporting competition between the races. I’ve proven that whites are stronger than blacks based on the available scientific data/strength competitions (click here for an in-depth discussion). One of the most surprising things that muscle fibers dictate is weight loss/obesity acquisition. Clearly, we need to acknowledge these differences and have differing physical activity protocols for each racial group based on their muscle fiber typing. However, I can’t help but think about the correlation between strength and mortality now. This obesity/fiber type study puts it into a whole new perspective. Those with type I fibers are more likely to be physically stronger, which is a cardioprotectant, which then protects against all-cause mortality in men (Ruiz et al, 2008; Volaklis, Halle, and Meisenger, 2015). So the fact that black Americans have a lower life expectancy as well as lower physical strength and more tpe II fibers than type I fibers shows why blacks are more obese, why blacks are not represented in strength competitions, and why blacks have higher rates of disease than other populations.The study by Tanner et al (2001) shows that there obese people are more likely to have type II fibers, no matter the race. Since we know that blacks have more type II fibers on average, this explains a part of the variance in the black American obesity rates and further disease acquisition/mortality.

The study by Tanner et al (2001) shows that there obese people are more likely to have type II fibers, no matter the race. Since we know that blacks have more type II fibers on average, this explains a part of the variance in the black American obesity rates and further disease acquisition/mortality.

Differences in muscle fiber typing do not explain all of the variance in disease acquisition/strength differences, however, understanding what the differing fiber typings do, metabolically speaking, along with how they affect disease acquisition will only lead to higher qualities of life for everyone involved.


Araujo, A. B., Chiu, G. R., Kupelian, V., Hall, S. A., Williams, R. E., Clark, R. V., & Mckinlay, J. B. (2010). Lean mass, muscle strength, and physical function in a diverse population of men: a population-based cross-sectional study. BMC Public Health,10(1). doi:10.1186/1471-2458-10-508

Andersen K, Lind L, Ingelsson E, Amlov J, Byberg L, Miachelsson K, Sundstrom J. Skeletal muscle morphology and risk of cardiovascular disease in elderly men. Eur J Prev Cardiol 2013.

Ama PFM, Simoneau JA, Boulay MR, Serresse Q Thériault G, Bouchard C. Skeletal muscle characteristics in sedentary Black and Caucasian males. J Appl Physiol 1986: 6l:1758-1761.

American Cancer Society. Cancer Facts & Figures for African Americans 2016-2018. Atlanta: American Cancer Society, 2016.

Ceaser, T., & Hunter, G. (2015). Black and White Race Differences in Aerobic Capacity, Muscle Fiber Type, and Their Influence on Metabolic Processes. Sports Medicine,45(5), 615-623. doi:10.1007/s40279-015-0318-7

Hagiwara N. Muscle fibre types: their role in health, disease and as therapeutic targets. OA Biology 2013 Nov 01;1(1):2.

Hernelahti, M., Tikkanen, H. O., Karjalainen, J., & Kujala, U. M. (2005). Muscle Fiber-Type Distribution as a Predictor of Blood Pressure: A 19-Year Follow-Up Study. Hypertension,45(5), 1019-1023. doi:10.1161/01.hyp.0000165023.09921.34

Hochachka, P.W. (1998) Mechanism and evolution of hypoxia-tolerance in humans. J. Exp. Biol. 201, 1243–1254

Karjalainen, J., Tikkanen, H., Hernelahti, M., & Kujala, U. M. (2006). Muscle fiber-type distribution predicts weight gain and unfavorable left ventricular geometry: a 19 year follow-up study. BMC Cardiovascular Disorders,6(1). doi:10.1186/1471-2261-6-2

Ogden C. L., Carroll, M. D., Lawman, H. G., Fryar, C. D., Kruszon-Moran, D., Kit, B.K., & Flegal K. M. (2016). Trends in obesity prevalence among children and adolescents in the United States, 1988-1994 through 2013-2014. JAMA, 315(21), 2292-2299.

Ruiz, J. R., Sui, X., Lobelo, F., Morrow, J. R., Jackson, A. W., Sjostrom, M., & Blair, S. N. (2008). Association between muscular strength and mortality in men: prospective cohort study. Bmj,337(Jul01 2). doi:10.1136/bmj.a439

Tanner, C. J., Barakat, H. A., Dohm, G. L., Pories, W. J., Macdonald, K. G., Cunningham, P. R., . . . Houmard, J. A. (2001). Muscle fiber type is associated with obesity and weight loss. American Journal of Physiology – Endocrinology And Metabolism,282(6). doi:10.1152/ajpendo.00416.2001

Volaklis, K. A., Halle, M., & Meisinger, C. (2015). Muscular strength as a strong predictor of mortality: A narrative review. European Journal of Internal Medicine,26(5), 303-310. doi:10.1016/j.ejim.2015.04.013

Racial Differences in Muscle Fiber Typing Cause Differences in Elite Sporting Competition

1050 words

Blacks are, on average, better at sports than whites. Why? The answer is very simple: muscle fiber typing. Most individuals have an even proportion of muscle fibers, skewing about 5 to 10 percent less on type II fibers. However, when it comes to elite competition, race—and along with it muscle fiber typing—come into play more. Who is stronger? Why? Who is faster? Why? Who is better at endurance running? Why? The answers to these questions lie in muscle fiber typing, somatype, and, of course, grit and determination. Today I will provide yet more evidence for my argument that whites are stronger than blacks.

Muscle fiber typing by race

I’ll be quick here since I’ve covered this extensively.

Blacks have more type II muscle fibers in comparison to whites who have more type I muscle fibers. This difference in fiber typing causes differences in aerobic capacity which lead to higher rates of cardiorespiratory diseases such as type II diabetes, heart disease, and hypertension.

There are two types of muscle fibers with two divisions: Type I and Type II with the divisions being in the slow twitch fiber, further broken down into Type IIa and Type II x. Type I fibers fire slowly and possess greater aerobic metabolic capacity due to higher levels of lipid, myoglobin, mitochondrial and capillary content. Type II fibers, on the other hand, fire faster, have reduced aerobic capacity (and all that comes with it) and are better equipped for anaerobic activity (explosive sports). Type IIa possesses more aerobic potential than IIx, but less anaerobic potential than type I fibers. Some evidence exists showing that it’s possible to train type II fibers to have a similar aerobic capacity to type I, but I don’t really buy that. It is possible to make aerobic capacity similar to the aerobic capacity that type I fibers have, but type II will not be fully like them.

Blacks have more type II fibers while whites have more type I fibers. Type II fibers predispose people to a myriad of cardiometabolic diseases which are also associated with grip strength.

Differences in fiber typing in elite athletes

Now comes the fun part. How do muscle fibers differ between elite athletes? A few studies have been done but, as expected in physiology studies, they have a low n, but they still do show physiologic differences when compared to the control subjects, physiologic differences that were predicted due to what we know about muscle fiber typing.

Type IIa fibers possess more aerobic potential than IIx, therefore, power lifters have a higher proportion of IIa fibers compared to IIx fibers. It should also be noted that powerlifters have the same amount of type I fibers as the general population (Fry et al, 2003a), so knowing this fact, since blacks have a lower proportion of type I muscle fibers as noted in Caeser et al (2015), this explains why there are very few black power lifters: they have the opposite type II fiber type while having less type I fiber.

Furthermore, Olympic lifters also use a higher percentage of type IIa fibers (Fry et al, 2003b). This also explains the lower amount of blacks in weight lifting as well. Fiber types don’t explain everything, but at elite levels, they do mean a lot and looking at the racial variation explains racial differences in elite sporting competition.

Explaining racial differences in sprinting competitions is easy as well. Type IIx fibers combined with the ACTN3 gene=elite human performance (Mills et al, 2001). The gene ACTN3 was discovered to explain explosive power, and it just so happened to vary by race. William Saletan writes:

the relative frequency of the X allele is 0.52 in Asians, 0.42 in whites, 0.27 in African-Americans, and 0.16 in Africans. If you break out the data further, the frequency of the XX genotype is 0.25 in Asians, 0.20 in European whites, 0.13 in African-Americans, and 0.01 in African Bantu. Conversely, the frequency of RR (the genotype for speed and power) is 0.25 in Asians, 0.36 in European whites, 0.60 in African-Americans, and 0.81 in African Bantu. Among Asians, you can expect to find one RR for every XX. Among whites, you can expect nearly two RRs for every XX. Among African-Americans, you can expect more than four RRs for every XX.

This allele is responsible for explosive power. Explosive power is needed to excel in events such as sprinting, football, basketball and other sports where power is needed in short bursts. However, where blacks have an advantage in explosive power sports, the advantage is lost once events like swimming, power lifting (described above), Olympic lifting (differing fiber type) etc.


Racial differences in elite sporting competition come down to a lot of genetic factors, largely influenced by hormones, genes, and muscle fiber typing. Population variation between known fiber typings/hormones/genes that affect certain types of athletic performance explains a lot of the variation within, and especially between populations. Due to anatomical differences, blacks excel at some sports and suffer at others. The same also holds for whites; there is considerable variation in somatype, some somatypes are better for strongman/powerlifting competitions than others. These differences affect the outcomes of elite sporting competition as well.

Blacks have a higher amount of type II fibers, which accounts for a lot of their disease acquisition (Caesar et al, 2015). Due to this physiologic difference, this is why blacks excel at some sports, and not others.

Once again: Blacks are not stronger than whites.

(Note: Click here for discussion on Kenyan distance running.)


Ceaser, T., & Hunter, G. (2015). Black and White Race Differences in Aerobic Capacity, Muscle Fiber Type, and Their Influence on Metabolic Processes. Sports Medicine,45(5), 615-623. doi:10.1007/s40279-015-0318-7

Fry, A. C., Webber, J. M., Weiss, L. W., Harber, M. P., Vaczi, M., & Pattison, N. A. (2003). Muscle Fiber Characteristics of Competitive Power Lifters. The Journal of Strength and Conditioning Research,17(2), 402. doi:10.1519/1533-4287(2003)017<0402:mfcocp>;2

Fry, A. C., Schilling, B. K., Staron, R. S., Hagerman, F. C., Hikida, R. S., & Thrush, J. T. (2003). Muscle Fiber Characteristics and Performance Correlates of Male Olympic-Style Weightlifters. Journal of Strength and Conditioning Research,17(4), 746-754. doi:10.1519/00124278-200311000-00020

Mills, M., Yang, N., Weinberger, R., Vander Woude, D., Beggs, A., Easteal, S., & North, K. (2001). Differential expression of the actin-binding proteins, alpha-actinin-2 and -3, in different species: implications for the evolution of functional redundancy. Human Molecular Genetics,10(13), 1335-1346. doi:10.1093/hmg/10.13.1335

Racial Differences in Grip Strength

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Strength differences between the races are of big interest to me. Not only due to the evolutionary perspective, but also due to how it relates to health and disease. Hand grip strength (HGS) in men is a good predictor of: Parkinson’s disease (Roberts et al, 2015); lower cardiovascular health profile (Lawman et al, 2016); Alzheimer’s disease (Buchman et al, 2007) and other chronic diseases in men, not in women (Cheung et al, 2013). HGS also predicts diabetes and hypertension (Mainous 3rd et al, 2015), as well as death from all causes, cardiovascular disease (CVD) and cancer in men (Gale et al, 2006). Due to these associations, the study of HGS in men is well warranted. However, here too, we find racial differences and they just so happen to follow trends and corroborate with other data on the mortality of men with lower grip strength.

Araujo et al (2010) obtained data from the Boston Community Health/Bone (BACH/Bone) Survey which included 1,219 randomly selected black, white and ‘Hispanic’ men to assess lean mass, muscle strength, and physical function. Though out of this sample, 10 men didn’t have a DXA performed and 49 men missing data on lean mass, fat mass and Physical Activity for the Elderly (PASE), which left 1,157 men to be analyzed. These studies, however, leave a lot to be desired in how they measure strength (for the purposes that I’m interested in) but they will have to do, for now. Unlike the bench pressing study I wrote about yesterday in which calipers were used to assess body fat, in this study they measured body fat with the DXA scan to assess lean mass. That way, there won’t be any potential confounds, possibly skewing lean mass/fat comparisons. The age of the cohort ranged from 30 to 79 with a mean age of 48.

Table 1 shows the results of the DXA scan, anthropometric data and lean and fat mass. Blacks’ mean lean mass of 124 pounds (mean weight 193 pounds), ‘Hispanics” lean mass was 114 pounds (mean weight 179 pounds) and whites had a mean lean mass of 122 pounds (mean weight 196 pounds). Blacks had a mean grip strength of 89.826 pounds while ‘Hispanics’ had a mean grip strength of 82.698 pounds and whites had a mean grip strength of 88.528 pounds. Blacks had a higher lean mass index than whites by 5 percent, but had a composite physical function score 20 percent lower than whites.

White men had a 25 percent higher average composite physical functioning score, which, when indexed by lean mass and grip, white men had grips 10 percent stronger. White men also scored higher on physical function and lean mass. White men had lower levels of lean muscle mass than blacks and ‘Hispanics’ after controlling for confounding factors, yet whites were still stronger. Since lean mass is related to strength, blacks and ‘Hispanics’ should have had a stronger grip, yet they didn’t. Why?

The authors stated that the reason was unknown since they didn’t test for muscle quality or strength exerted for each unit of muscle. I have proven that whites, on average, are stronger than blacks. If the it were true that blacks were stronger, which is what you see upon first glance viewing table 1 of Araujo et al (2010), then the black population would have lower rates of morbidity and mortality due to higher levels of strength. The black population doesn’t have lower levels of morbidity or mortality. Therefore blacks are not stronger than whites.

Muscular strength is associated with mortality in men (Ruiz et al, 2008; Volaklis, Halle, and Meisenger, 2015), so if the strongest race of men has lower incidences of the above diseases mentioned above along with a higher life expectancy, then there is a good chance that muscular strength is a good predictor of disease within and between race and ethnicity as well. Muscular strength is inversely associated with death from all causes and cancer in men even after adjusting for cardiorespiratory factors. The findings from Ruiz et al (2008) are valid for young and old men (aged 20-82), as well as normal and overweight men.

There are clear associations between muscular strength/hand grip strength and mortality. These differences in mortality are also seen in the United States between race. In 2012, the death rate for all cancer combined was 24 percent higher in black men than in white men. Life expectancy is lower for blacks at 72.3 years compared to 76.7 years for white men (American Cancer Society, 2016). As shown above, men with lower levels of muscular strength have a higher risk of mortality.

As I have asserted in the past, blacks have differing muscle fiber typing (type II) on average when compared to whites (who have type I fibers). Type II muscle fibers are associated with a reduced Vo2 max, which has implications for the health of black Americans. Blacks have lower aerobic capacity along with a greater percentage of type II skeletal muscle fiber (Caesar and Hunter, 2015).

Slow twitch fibers fire through aerobic pathways. Fast twitch (Type II) fibers fire through anaerobic pathways and tire quicker than slow twitch. Each fiber fires off through different pathways, whether they be anaerobic or aerobic. The body uses two types of energy systems, aerobic or anaerobic, which then generate Adenosine Triphosphate, better known as ATP, which causes the muscles to contract or relax. Depending on the type of fibers an individual has dictates which pathway muscles use to contract which then, ultimately, dictate if there is high muscular endurance or if the fibers will fire off faster for more speed.

Differences in muscle fiber typing explain why whites had a stronger grip than non-whites in the BACH/Bone survey. Testing the fiber typings of the three ethnies would have found a higher percentage of type II fibers in blacks, which would account for the lower grip strength despite having higher levels of lean mass when compared to whites.

The apparent ‘paradox’ seen in Araujo et al (2010) is explained by basic physiology. However, in our politically correct society, such differences may be suppressed and thusly people won’t be able to receive the help they need. Race is an extremely useful marker in regards to medicine. By denying average racial differences in numerous anatomical/metabolic/physiologic traits, we deny people the right help they need. Common sense dictates that if such relationships are found, then further research must occur in order to find the cause and a possible solution to the problem.

This study by Araujo et al shows that we need to pay more attention to race when it comes to disease. By denying racial differences we are dooming people to a lower quality of life due to the implicit assumption that we are all the same on the inside (farrrrr from the truth). These average differences in metabolism, anatomy, and physiology do account for some of the variation in disease between race and ethnicity, so this warrants further research. If only we, as a country, can acknowledge racial differences and get people the correct help. Maybe one day we can stop assuming that all races are equal on the inside and when you notice a trend within a particular racial group you find out the cause and whether or not there is any way to ameliorate it.

Muscular strength adds to the protective effect of cardiorespiratory fitness and risk of death in men. That blacks have lower levels of strength than whites, have different muscle fiber typing than whites on average, a lower life expectancy than whites, and higher rates of cancer show that they do not have the physical strength that whites do. What really seals the deal is the fact that blacks have more type II muscle fibers (Caesar and Hunter, 2015). Muscular strength/grip strength is a great predictor of disease in men. Since blacks have lower grip strength yet higher levels of lean mass compared to whites, this show that the difference is due to muscle fiber typing, which, as I have covered in the past, are also associated with cardiometabolic disease and obesity.

Blacks have the highest rate of obesity in America. Looking at obesity rates in America, we see that 69 percent of black men are overweight or obese (remember that black Americans with more African ancestry are less likely to be obese), 71.4 percent of white men are overweight or obese, and 78.6 percent of ‘Hispanic’ men are overweight or obese (Ogden et al, 2016).

Blacks are not stronger than whites. I have compiled enough data to prove that fact. This adds further support for my contention.


American Cancer Society. Cancer Facts & Figures for African Americans 2016-2018. Atlanta: American Cancer Society, 2016.

Araujo, A. B., Chiu, G. R., Kupelian, V., Hall, S. A., Williams, R. E., Clark, R. V., & Mckinlay, J. B. (2010). Lean mass, muscle strength, and physical function in a diverse population of men: a population-based cross-sectional study. BMC Public Health,10(1). doi:10.1186/1471-2458-10-508

Buchman, A. S., Wilson, R. S., Boyle, P. A., Bienias, J. L., & Bennett, D. A. (2007). Grip Strength and the Risk of Incident Alzheimer’s Disease. Neuroepidemiology,29(1-2), 66-73. doi:10.1159/000109498

Ceaser, T., & Hunter, G. (2015). Black and White Race Differences in Aerobic Capacity, Muscle Fiber Type, and Their Influence on Metabolic Processes. Sports Medicine,45(5), 615-623. doi:10.1007/s40279-015-0318-7

Cheung, C., Nguyen, U. D., Au, E., Tan, K. C., & Kung, A. W. (2013). Association of handgrip strength with chronic diseases and multimorbidity. Age,35(3), 929-941. doi:10.1007/s11357-012-9385-y

Gale, C. R., Martyn, C. N., Cooper, C., & Sayer, A. A. (2006). Grip strength, body composition, and mortality. International Journal of Epidemiology,36(1), 228-235. doi:10.1093/ije/dyl224

Lawman, H. G., Troiano, R. P., Perna, F. M., Wang, C., Fryar, C. D., & Ogden, C. L. (2016). Associations of Relative Handgrip Strength and Cardiovascular Disease Biomarkers in U.S. Adults, 2011–2012. American Journal of Preventive Medicine,50(6), 677-683. doi:10.1016/j.amepre.2015.10.022

Mainous, A. G., Tanner, R. J., Anton, S. D., & Jo, A. (2015). Grip Strength as a Marker of Hypertension and Diabetes in Healthy Weight Adults. American Journal of Preventive Medicine,49(6), 850-858. doi:10.1016/j.amepre.2015.05.025

Ogden C. L., Carroll, M. D., Lawman, H. G., Fryar, C. D., Kruszon-Moran, D., Kit, B.K., & Flegal K. M. (2016). Trends in obesity prevalence among children and adolescents in the United States, 1988-1994 through 2013-2014. JAMA, 315(21), 2292-2299.

Roberts, H. C., Syddall, H. E., Butchart, J. W., Stack, E. L., Cooper, C., & Sayer, A. A. (2015). The Association of Grip Strength With Severity and Duration of Parkinson’s. Neurorehabilitation and Neural Repair,29(9), 889-896. doi:10.1177/1545968315570324

Ruiz, J. R., Sui, X., Lobelo, F., Morrow, J. R., Jackson, A. W., Sjostrom, M., & Blair, S. N. (2008). Association between muscular strength and mortality in men: prospective cohort study. Bmj,337(Jul01 2). doi:10.1136/bmj.a439

Volaklis, K. A., Halle, M., & Meisinger, C. (2015). Muscular strength as a strong predictor of mortality: A narrative review. European Journal of Internal Medicine,26(5), 303-310. doi:10.1016/j.ejim.2015.04.013

Muscular Strength By Gender and Race

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It’s a known fact that men are stronger, but how much stronger are we really than women? Strength does vary by race as I have covered here extensively. However, I took another look at the only paper that I can find in the literature on black/white strength on the bench press and found one more data point that lends credence to my theory on racial differences in strength.

Strength and gender

Men are stronger than women. No one (sane) denies this. There are evolutionary reasons for this, main reason being, women selected us for higher levels of testosterone, along with differences in somatype. Now, what is not known by the general public is just how much stronger the average man is compared to the average woman.

Miller et al (2008) studied the fiber type and area and strength of the biceps brachii and vastus lateralis in 8 men and 8 women. They were told to do two voluntary tests of strength, using elbow flexion (think biceps curl) and knee extension. (Note: I am assuming they are exercises similar to biceps curls and knee extension, as the authors write that they had custom-made equipment from Global Gym.) They also measured motor unit size, number, and activation during both movements.

The women had 45 percent smaller muscle cross-section area (CSA) in the brachii, 41 percent in the total elbow flexor, 30 percent in the vastus laterus, and 25 percent smaller knee extensors. The last point makes sense, since women have stronger lower bodies compared to their upper bodies (as you can see).

Men were significantly stronger in both upper and lower body strength. In the knee extension, women was 62 and 59 percent of male 1RM and maximal voluntary isometric contraction (MVC) respectively. As for elbow strength, women were 52 percent as strong as men in both 1RM and MVC. Overall, women were 70 and 80 percent as strong as men in the arms and the legs. This is attributed to either men’s bigger fibers or men putting themselves into more physical situations to have bigger fibers to be stronger (…a biological explanation makes more sense). However, no statistical difference between muscle fibers was found between gender, lending credence to the hypothesis that men’s larger fibers are the cause for greater overall upper-body strength.

The cause for less upper-body strength in women is due the distribution of women’s lean tissue being smaller. Women, as can be seen in the study, are stronger in terms of lower limb strength and get substantially weaker when upper-body strength is looked at.

Other studies have shown this stark difference between male and female strength. Men have, on average, 61 percent more total muscle mass than women, 75 percent more arm muscle mass, which translates approximately into a 90 percent greater upper body strength in men. 99.9 percent of females fall below the male mean, meaning that sex accounts for 70 percent of human variation in muscle mass and upper-body strength in humans (Lassek and Gaulin, 2009). Women select men for increased muscular size, which means increased testosterone, but this is hard to maintain so it gets naturally selected against. There is, obviously, a limit to muscle size and how many kcal you can intake and partition enough kcal to your growing muscles. However, women are more attracted to a muscular, mesomorphic phenotype (Dixson et al, 2009) so selection will occur by women for men to have a larger body type due to higher levels of testosterone.

Strength and race

The only study I know of comparing blacks and whites on a big three lift (bench pressing) is by Boyce et al (2014). They followed a sample of 13 white female officers, 17 black female officers, 41 black male officers and 238 white male officers for 12.5 years, assessing bench pressing strength at the beginning and the end of the study. The average age of the sample was 25.1 for the 41 black males and 24.5 for the 237 white males. The average age for the black women was 24.9 and the average for white women was 23.9. This is a longitudinal study, and the methodology is alright, but I see a few holes.

An untrained eye looking at the tables in the study would automatically think that blacks are stronger than whites at the end of the study. At the initial recruitment, the black mean weight was 187 pounds and they benched 210 pounds. They benched 1.2 times their body weight. Whites weighed 180 pounds and benched 185 pounds. They benched 1.02 times their body weight. Black women weighed 130 pounds at initial recruitment and benched 85 pounds, benching .654 times their body weight. White women weighed 127 pounds at initial recruitment and bench 82 pounds, benching .646 times their body weight. Right off the bat, you can see that the difference between black and white women is not significant, but the difference between blacks and whites is.

At the follow-up, the black sample weighed 224 pounds and benched 240 pounds while the whites weighed 205 pounds benching 215 pounds. Looking at this in terms of strength relative to body weight, we see that black males benched 1.07 times their body weight while whites benched 1.04 times their body weight. A very slight difference favoring black males. However, there were more than 5 times the amount of whites in comparison to blacks (41 compared to 238), so I can’t help but wonder if the smaller black sample compared to the white sample may have anything to do with it.

Black women weighed 150 pounds at the follow-up, benching 99 pounds while white women weighed 140 pounds benching 90 pounds. So black women benched 6.6 times their body weight while white women benched .642 times their body weight.

Another thing we have to look at is black body weight compared to bench press decreased in the 12 years while white body weight compared to bench press was diverging with the black bench press compared to body weight.

Furthermore, this study is anomalous as the both cohorts gained strength into their late 30s (testosterone begins to decline at a rate of 1-2 percent per year at age 25). It is well known in the literature that strength begins to decrease at right around 25 years of age (Keller and Englehardt, 2014).

Another pitfall is that, as they rightly point out, they used skin caliper measuring on the black cohort. It has been argued in the literature that blacks should have a different BMI scale due to differing levels of fat-free body mass (Vickery et al, 1988). Remember that black American men with more African ancestry are less likely to be obese, which is due to levels of fat-free body mass. Since fat-free mass is most likely skewed, I shouldn’t even look at the study. I do believe that black Americans should have their own BMI scale; they’re physiologically different enough from whites—though the differences are small—they lead to important medical outcomes. This is why race most definitely should be implemented into medical research. The authors rightly state that when further research is pursued the DXA scan should be used to assess fat-free body mass.

Unfortunately, the authors did not have access to the heights of the cohort due to an ongoing court case on the department for discrimination based on height. So, unfortunately, this is the only anthropometric value that could not be assessed and is an extremely important variable. Height can be used to infer somatype. Somatype can then be used to infer limb length. Longer limbs increase the ROM, in turn, decreaseing strength. The missing variable of height is a key factor in this study.

Finally, and perhaps most importantly, they assessed the strength of the cohort on a Smith Machine Bench Press.

  • The Smith Machine is set on a fixed range of motion; not all people have the same ROM, so assessing strength on a smith machine makes no sense.
  • To get into position for the Smith Machine, since the bar path is the same, you need to get in pretty much the same position as everyone else. I don’t need to explain the anatomical reasons why this is a problem in regards to testing a 1RM.
  • An Olympic bar weighs 45 pounds, but numerous Smith Machines decreases the weight by 10-20 pounds.
  • Since the individual is not able to stabilize the bar due to the machine, the chest, triceps, and biceps are less activated during the Smith Machine lift (Saeterbakken et al, 2011)


Due to all of these things wrong with the study, especially the Smith Machine bench press, it’s hard to actually gauge the true strength of the cohort. Depending on the brand, Smith Machines can decrease the load by 10-30 pounds. Combined with the unnatural, straight-line bar path of the movement, it’s not ideal for a true strength test.


Gender differences in strength have a biological basis (obviously) and are why women shouldn’t be able to serve in the military and transgendered people shouldn’t be able to compete with ‘the gender they feel that they are’ (coming in the future).

The more interesting topic is the one on racial differences in strength. The untrained eye may read that paper and walk away assuming that the average black person is somehow stronger than the average white person. However, this study is anomalous since the cohort gained strength into their 30s when the literature shows otherwise. The biggest problem with the study is the Smith Machine bench press. It is not a natural movement and decreases muscle activation in key areas of the chest and triceps which aid in power while doing a regular bench press. Due to this, and the other problems I pointed out, I can’t accept this study.

Of course, height not being noted is not the fault of the researchers, but more questions would be answered if we knew the heights of the officers—which is an extremely critical variable. White males also gained more lean mass over the course of the study compared to blacks—47 percent and 44 percent respectively—which, as I pointed out, is anomalous.

There is more to HBD than IQ differences. I contend that somatype differences between the races are much more interesting. I will be writing about that more in the future. 

Furthermore, for anyone with any basic physiology and anatomy knowledge, they’d know that different leverages affect strength. The races differ in somatype on average and thusly have different leverages. This is one out of many reasons why there are racial differences in strength and elite sports. Leverages and muscle fiber typing. 

My points on racial differences in strength still hold; the anthropmetric data backs me upelite sporting events back me up. My theory as a whole to racial differences in sports is sound, and this study does nothing to make me think twice about it. There are way too many confounds for me to even take it seriously when reevaluating my views on racial differences in strength. This study was garbage to assess absolutely strength due to the numerous things wrong with it. I await a more robust study with actual strength exercises, not one done on an assisted machine. 


Boyce, R. W., Willett, T. K., Jones, G. R., & Boone, E. L. (2014). Racial Comparisons in Police Officer Bench Press Strength over 12.5 Years. Int J Exerc Sci 7 (2), 140-151.

Dixson, B. J., Dixson, A. F., Bishop, P. J., & Parish, A. (2009). Human Physique and Sexual Attractiveness in Men and Women: A New Zealand–U.S. Comparative Study. Archives of Sexual Behavior,39(3), 798-806. doi:10.1007/s10508-008-9441-y

Keller K, Engelhardt M. Strength and muscle mass loss with aging process. Age and strength loss. MLTJ. 2013;3(4):346–350.

Lassek, W. D., & Gaulin, S. J. (2009). Costs and benefits of fat-free muscle mass in men: relationship to mating success, dietary requirements, and native immunity. Evolution and Human Behavior,30(5), 322-328. doi:10.1016/j.evolhumbehav.2009.04.002

Miller, A. E., Macdougall, J. D., Tarnopolsky, M. A., & Sale, D. G. (1993). Gender differences in strength and muscle fiber characteristics. European Journal of Applied Physiology and Occupational Physiology,66(3), 254-262. doi:10.1007/bf00235103

Saeterbakken, A. H., Tillaar, R. V., & Fimland, M. S. (2011). A comparison of muscle activity and 1-RM strength of three chest-press exercises with different stability requirements. Journal of Sports Sciences,29(5), 533-538. doi:10.1080/02640414.2010.543916

Vickery SR, Cureton KJ, Collins MA. Prediction of body density from skinfolds in black and white young men. Hum Biol 1988;60:135–49.

Brain Size Increased for Expertise Capacity, not IQ

2000 words

One of the HBD’s supposed biggest findings is that IQ increases as a function of distance from the equator. The theory holds that those groups who experienced colder winters were selected for levels of higher and they passed on their high IQ genes. Cold winter theory is supposed to explain why some races have higher levels of achievement and IQ than others. However, after a conversation with PumpkinPerson about cold winter theory and tool use, something clicked in my head: the real reason for the increase in brain size in peoples further from the equator wasn’t for IQ, but expertise capacity. I will go through the reasons how and why our brain size increased for the capacity for expertise and not IQ and hopefully put the cold winter theory to rest for good.

Tool complexity/use and brain size

PumpkinPerson is one of the biggest champions of the cold winter theory, writing: “I don’t even understand how one can believe in racially genetic differences in IQ without also believing that cold winters select for higher intelligence because of the survival challenges of keeping warm, building shelter, and hunting large game.” He wrongly assumes that climate theories are the only explanation for racial gaps in intelligence when other theories (such as differing types of sexual selection) could explain the gap just as well. However, since Rushton and Lynn have pushed this theory for 30+ years, it’s still engrained in the minds of some people. It is hard to change your views in the face of contrary data, but for those of my readers who are proponents of cold winters increasing IQ, I hope tonight I can sway you into believing that brain size increased as a function of climate and tool-making, not for IQ.

In his article he cites Richard Lynn (2006: 148), saying:

… hunter-gatherer peoples in tropical and subtropical latitudes such as the Amazon basin and New Guinea typically have between 10 and 20 different tools, whereas those in the colder northern latitudes of Siberia, Alaska, and Greenland have between 25 and 60 different tools. In addition, peoples in cold northern environments make more complex tools, involving the assembly of components, such as hafting a sharp piece of stone or bone onto the end of a spear and fixing a stone axe  head onto a timber shaft.

I, of course, don’t doubt that peoples in cold northern environments need more (and complex) tools compared to those in tropical climes. But I look at it from a different point of view.

This is based on the research of Terrence (1983) and his study on time budgeting and hunter-gathering technology. The data does show that the number of tools correlates to latitude, but he leaves out that it also correlates with mobile and immobile and diet. That’s a pretty big factor. Of course, the type of animals around and what you need to do to kill/extract the meat involves a certain type of complex tool. In northern environments, a few more tools are needed to survive, so what? That doesn’t really mean anything. The whole brain-size/IQ latitude cold winter theory can be explained in another way.

Tool use increased our brain size throughout our evolutionary history, so with Arctic peoples living in cold climes where having a bigger brain is advantageous, they already had more neural columns for expertise capacity. The construction of complex tools increased brain size along with the colder climate. If tool use can explain part of the increase in our brain size over 3 million years, why can’t it partly explain why Arctic peoples—who use more (and complex) tools—larger brains over those further from the Arctic? Because brain size increased for expertise capacity, not IQ. Since they had bigger brains they were able to master the creation of complex tools, which further increased their brain size along with colder climates. Those who could make better tools could pass their genes, selecting for bigger brains.

Brain size increased for expertise capacity, not IQ

Table 3.1 in Torrence (1983) makes reference to technounits, a way to gauge the complexity of a particular item (Collard et al, 2011). Those in northerly climes do have tools with higher technounits, however, that’s showing that what is needed to construct the tools is a high capacity for expertise.

Skoyles (1999) posits that brain size increased for expertise capacity, not IQ. Bigger brains cause extreme complications during birth, calling for Caesarian sections (which is driving the evolution of bigger heads), so selection for bigger brains must have been advantageous in another way. Skoyles cites studies showing that microcephalics have brains in the average range of Erectus while having IQs in the normal/above average range. This implies that Erectus could have had IQs in our range, and that selection for bigger heads was caused by something else—the need for expertise.

Even then, the correlation between brain size and IQ cannot be invoked here. A .33-.4 correlation between brain size and IQ still leaves a lot of room for people to have brain sizes in the range of Erectus and still have above average IQs. Assuming a correlation of .51, that leaves 74 percent of the brain size/IQ correlation unexplained. This leaves a lot of room for other explanations for the remaining variance.

So if you think of the implications of Skoyles’ (1999) paper in regards to human races and the quote provided from Lynn (2006), you can look at it as Arctic peoples needed to be able to learn how to make complex tools which required a certain amount of expertise. Acquiring certain types of expertise does lead to certain local changes in the brain due to environmental demands, for instance in racecar drivers (Bernardi et al, 2013) and in taxi drivers in London who were “on The Knowledge” (Maguire et al, 2000). Tool use did cause increases in our brain size in our ancestral past, so the fact that Arctic peoples have bigger brains but lower IQs is explained by brain size being selected for expertise (their expertise to make their numerous tools) and cold climates but cold temperatures do NOT explain intelligence differences between the races.


Indeed, there is evidence that ‘chunks’ form in the brain due to certain types of expertise (Gobet and Simon, 1998). In their study, Gobet and Simon showed that Chess masters used significantly more chunks, extending the chunking theory ” to take account of the evidence for large retrieval structures (templates) in long-term memory.” This study is direct evidence for Skoyles’ contention on “informational chunks (Skoyles, 1999) lending credence to the claim that people who master something have more information stored in their ‘chunks’.

Furthermore, high and low skill employees organize their conceptual knowledge about a problem differently (Lamberti and Newsome, 1989). Low-skilled workers performed much faster on the tasks that needed concrete information organization whereas high-skilled workers were better on the more abstract concepts. Overall, both high- and low-skilled workers processed the same information differently. This study has nothing to do with IQ itself, just how high- and low-skilled workers process information differently (which may come down to ‘chunks’ in the brain).

Chase and Simon (1973) show that the amount of information extracted during a memory and perception task is directly related to the amount of time the individual has played chess. They state that chess skill is “reflected in the speed with which chunks are perceived in the perception task and the size of the chunks in the memory task.” Of course, you can’t just throw anyone into a chess game who has never played before—IQ be damned—and expect them to do well. You need to hone your strategy and skill over time by noticing all types of moves, thinking ahead and guessing what your opponent will do ahead of time. This all takes time playing the game, and since people who have played longer can more easily tap into the ‘chunks’, this shows that chess skill is largely a function of time spend playing (note: IQ is still important, of course. Just, practice makes perfect and one with practice and a low IQ will beat someone with no/little practice and a high IQ).

Expertise does, indeed, take deliberate practice. Practice DOES make perfect.


Our brains increased evolutionarily speaking as to acquire more expertise. Bigger brains (and therefore bigger heads) cause problems with childbirth and so natural selection must have selected bigger brains since they increase expertise capacity. The fact that there are numerous people in the world with Erectus-sized brains and IQs in the normal/above average range lends credence to the claim. Erectus could have possibly had intelligence level near our own. But what really needs to be thought about here is this: It just so happens that the brain size increase corresponds with the beginnings of our modern gait and pelvis (Lieberman et al, 2006). The beginnings of cultural acquisition and transference began around that time (Herculano-Houzel and Kaas, 2011) and so our brain size would have increased due to cooking allowing us to have the energy for a bigger brain with more neurons.

Of course Erectus would need to become an expert with the new-found technology he acquired. Over time, the more ‘expert’ Erectus would have passed their genes on, both for increased brain size and expertise, and the hominin brain size then increased.

Looking at racial differences in brain size while thinking about how expertise capacity increases brain size and thinking about tool use/complexity of Arctic peoples is an alternate (and in my opinion) better theory of explaining racial differences in brain size. I obviously don’t believe that brain size differences cause IQ differences, the brain size differences are a function of climate and tool use/complexity. To make complex tools you need a sort of ‘expertness’, which, as Skoyles argues, causes brain size to increase. This explains the so-called anomalous Inuits with a brain size equal to that of East Asians but with an IQ in the low 90s.

Put simply, complex tools+cold winters+ cooked food=big brains. Cold climates DO NOT by themselves CAUSE higher levels of g. It’s just a correlation, it does not mean that it is causal. Big brains retain heat better in the cold whereas smaller heads cool better. That’s the reason for racial brain size differences, but climate and brain size in and of themselves do not CAUSE racial differences in IQ.

I now believe that sexual selection is a cause for racial differences in IQ, but that’s for another day.


Bernardi, G., Ricciardi, E., Sani, L., Gaglianese, A., Papasogli, A., Ceccarelli, R., . . . Pietrini, P. (2013). How Skill Expertise Shapes the Brain Functional Architecture: An fMRI Study of Visuo-Spatial and Motor Processing in Professional Racing-Car and Naïve Drivers. PLoS ONE,8(10). doi:10.1371/journal.pone.0077764

Chase, W. G., & Simon, H. A. (1973). Perception in chess. Cognitive Psychology,4(1), 55-81. doi:10.1016/0010-0285(73)90004-2

Collard, M., Buchanan, B., Morin, J., & Costopoulos, A. (2011). What Drives the Evolution of Hunter–Gatherer Subsistence Technology? A Reanalysis of the Risk Hypothesis with Data from the Pacific Northwest. Culture Evolves, 341-358. doi:10.1093/acprof:osobl/9780199608966.003.0020

Dr. John R. Skoyles (1999) HUMAN EVOLUTION EXPANDED BRAINS TO INCREASE EXPERTISE CAPACITY, NOT IQ. Psycoloquy: 10(002) brain expertise

Gobet, F., & Simon, H. A. (1998). Expert Chess Memory: Revisiting the Chunking Hypothesis. Memory,6(3), 225-255. doi:10.1080/741942359

Herculano-Houzel, S., & Kaas, J. H. (2011). Gorilla and Orangutan Brains Conform to the Primate Cellular Scaling Rules: Implications for Human Evolution.

Lamberti, D. M., & Newsome, S. L. (1989). Presenting abstract versus concrete information in expert systems: what is the impact on user performance? International Journal of Man-Machine Studies,31(1), 27-45. doi:10.1016/0020-7373(89)90031-x

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

Lynn, R. (2006). Race differences in intelligence: An evolutionary analysis. Augusta, Ga.: Washington Summit Publishers.

Maguire, E. A., Gadian, D. G., Johnsrude, I. S., Good, C. D., Ashburner, J., Frackowiak, R. S., & Frith, C. D. (2000). Navigation-related structural change in the hippocampi of taxi drivers. Proceedings of the National Academy of Sciences,97(8), 4398-4403. doi:10.1073/pnas.070039597

Torrence, R. (1983). Time budgeting and hunter-gatherer technology. In G. Bailey (Ed.). Hunter-Gatherer Economy in Prehistory: A European Perspective. Cambridge, Cambridge University Press.

Evolution and IQ Linkfest II

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Why Grit Is More Important Than IQ When You’re Trying To Become Successful (Psychologist Angela Duckworth states that what matter for future life success isn’t IQ, SAT scores, or even graduating from a top college. What matters most for life success is a blend of perseverance and passion that she calls ‘grit’, in her book Grit: The Power of Passion and PerseveranceAccording to Duckworth, grittiness is passion, and being passionate about something will make you successful is persevering in the face of adversity; i.e., something not working out in your favor and you continue to go at it. She thought of two equations: talent x effort=skill, skill x effort=achievement. Talent is how quickly skills improve when effort is invested, whereas achievement occurs when you take the skills you acquired and put them to use. I’ll buy the book and read it and see what else she says.)

How Skill Expertise Shapes the Brain Functional Architecture: An fMRI Study of Visuo-Spatial and Motor Processing in Professional Racing-Car and Naïve Drivers (Brain functional architecture sustaining visuo-motor processing in racecar drivers “undergoes both ‘quantitative’ and ‘qualitative’ modifications that are evident even when the brain is engaged in relatively simple, non-demanding tasks.” Pretty much, get good at something, like really good, and your brain will change in size and mass.)

Acquiring ‘‘the Knowledge’’ of London’s Layout Drives Structural Brain Changes (Specific and enduring structural brain changes in adults “can be induced by biologically relevant behaviors engaging higher cognitive functions such as spatial memory.” Yet more evidence that becoming an ‘expert’ in something leads to substantial brain changes—which are permanent.)

Autism genes conserved during human evolution to make us smarter, say scientists (We were selected to be autistes since it was beneficial in our ancestral past. Autism is also associated with intellectual achievement.)

A model for brain life history evolution (As adult brain mass increases, so does skill, assumming the costs of maintaining brain mass and memories stay constant. This could be a cause for our larger brains. We know that our brains consume 20 ro 25 percent of our daily kcal, so in our evolutionary past, those who couldn’t amass the kcal to power the ever-growing brain would have died. González-Forero says that as we became proficient with tools, then our brain size began to increase. I have cited a few studies saying that over the past month.)

Lessons from Making Brain Soup (Learn about Herculano-Houzel and Lent’s 2005 Isotropic Fractionator—a machine that allows single cells in ‘brain soup’ to be counted as to get an accurate estimate of neurons.)

Numbers of neurons as biological correlates of cognitive capability (Body mass is a poor predictor of neurons, number of brain stem neurons estimates the capacity for processing bodily signals, mass of the cortex is a poor predictor of neuronal amount, the bird pallium packs more neurons than primate cortices of similar mass and finally the number of neurons in the cortex or pallium correlate directly with intelligence. Herculano-Houzel is blazing a new path in the field of neuroscience, with a novel way of looking at the brain showing that our brains are only scaled-up primate brains in terms of its neuronal composition.)

Creative People Have Better-Connected Brains, Scans Reveal (Highly creative people have more connections on the right and left sides of their brains, suggesting that creativity is biological in nature.)

Genetics Play a Role in Social Anxiety Disorder, Study Finds (Like most disorders, genetics plays a role. Whether it’s small or large, more often than not, genetics will always have at least a bit to say.)

Peer-review activists push psychology journals towards open data (An APA editor will not step down for stating that he won’t publish papers in which the authors don’t let their dataset become public. This is a great move. Why publish something that may possibly be garbage?)

We Look Like Our Names: The Manifestation of Name Stereotypes in Facial Appearance. (This is an interesting one, and one I’ve wondered my whole life since people have told me that ‘I don’t physically look’ how my name is. The researchers state that “facial appearance represents social expectations of how a person with a specific name should look.” Social tags influence one’s facial appearance.)

Greater insight into basic biology of pain will reveal non-addictive remedies (We need to better understand pain physiology, drug development and the individual response to pain in order to develop non-addictive drugs.)

Researchers Discover How Animals Measure Annual Time to Reproduce (The pituitary gland mediates when some mammals start reproducing. The length of the day is noticed in most animals by the pineal gland in the brain.

Does Cannabis Use Lower Your IQ? (No it does not. Recent longitudinal studies show that smoking marijuana does not lead to cognitive decline.

Reader’s Corner: Do we really understand animal intelligence? “Are We Smart Enough to Know How Smart Animals Are?” (We do not understand animal intelligence and we are not smart enough to know how smart animals are. We have an anthropocentric view of evolution, and thusly, we attempt to put our cognitive traits onto other animals when they are adapted for other areas. Herculano-Houzel’s research will begin to detangle this.)

Can Animals Acquire Language? (Evidence says no. However, I’m sure a few readers have heard of Koko the gorilla. She’s able to do sign language and has an estimated IQ of 75 to 95 on the Cattell Infant Intelligence Scale (pg. 99))

Dogs, toddlers show similarities in social intelligence (There is a g factor for dogs. The authors state that the similarities between child and dog intelligence could come down to ‘survival of the friendliest’. I’ll write about this soon.)

How Humans Became Intelligent (Cognitive neuroscientist and philosopher Daniel Dennet sees human consciousness as memetics and genetics. That is, we learn from others and what we are able to learn from others comes down to our genes. I will buy this book as well.)

The Testosterone and Fertility Conundrum: A Western Perspective

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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.


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