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The “N” Word

1300 words

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.

Somatypes

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.

Conclusion

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.

References

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.

Conclusion

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.

References

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.

Conclusion

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.)

References

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>2.0.co;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

1700 words

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.

References

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

The Testosterone and Fertility Conundrum: A Western Perspective

2750 words

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

References

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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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

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SAT and KFC

by Scott Jameson

700 words

For my first post on this blog, I thought I’d talk about something relevant to the mission of the blog: Political Correctness. I’m very grateful to RaceRealist for inviting me to hop on board here (although I should put out the categorical disclaimer that me posting here is not in and of itself an endorsement of any given thing he’s said over the years).

This is going to be something of an opinion essay about why denying reality is silly: because you still have to live in it. Most of my content is going to be more empirically driven, as you’re used to on this blog. Bear with me.

The SAT’s name change story is a classic case of “Political Correctness,” and is mirrored by KFC’s story of adapting to new nutritional standards. For those out of the loop: after the public realized how unhealthy fried foods are, Kentucky Fried Chicken changed its name to KFC. The point was to make the unhealthy nature of the food one conceptual extrapolation away from the name itself, in hopes that the public would not bother to recall what the “F” stood for.

SAT originally stood for “Scholastic Aptitude Test.” It was (and is) a test to determine how apt you are for scholarly endeavors. Put bluntly, it’s a somewhat sloppy IQ test oriented towards scholarly settings in particular. Of course, that name was too accurate, so it fell out of favor. The public does not want to live in a world wherein poor students are less apt than rich students and Black students are less apt than White students, and so the Scholastic Aptitude Test became the Scholastic Assessment Test. In order to be offended by that, you have to remember that what’s being assessed is aptitude and that nothing has changed. Like “KFC,” it was one conceptual extrapolation away from the reality at hand. Most people were probably too harebrained to see through that.

For some reason, they kept rolling with it. It became an alleged Reasoning Test, and then simply a series of letters that used to be an abbreviation: “the SAT,” no doubt an homage to The Colonel and the chicken he hawks. They’re both just a series of letters now – the unpleasant realities contained therein have been conceptually sterilized. Like the SAT, the nutritional content of the chicken hasn’t changed as much as the name has.

You may suspect that I’m simply flinging excrement in the general direction of The College Board, but there’s a point to what I’m saying here. What we call “Political Correctness” is a pervasive scrubbing of reality out of the consciousness of the public at large, especially the young. There was a time when people were allowed to say things like “I do not enjoy living around Blacks/Whites/Hispanics/whomever.” “Political Correctness” entered from stage left, and then Boomers had to say “bad schools” and “bad neighborhood” instead. Odds are, the Boomers understood the connotative meanings, at least at first. But if you asked millennials what those terms are, I’d bet on most of them actually being ignorant enough to think that the schools are themselves the problem. Nobody ever pointed out to these kids that almost all of the “bad schools” – the schools with low average test scores – are simply full of Hispanics (Mestizos) and African Americans who have low average test scores regardless of what school they’re in, and that the supermajority of all of the “good schools” aren’t. Anyone who doesn’t know this has been deliberately rendered ignorant of a reality that is important to their lives.

What we call “Political Correctness” is in fact the successful, systematic obfuscation of reality, and having reality perpetually hidden from you is dangerous. That is why we at this blog are NotPoliticallyCorrect. As long as I’m here, I can promise you my best attempt at discovering and conveying the truth in the NotPoliticallyCorrect fashion exemplified thus far by RaceRealist: bringing you interesting truths, obscure truths, and of course, controversial truths.

*****

I’m not the first to make the SAT-KFC comparison, by the way. After I wrote this article, I looked around for sources only to dredge this up.

Psychology, Anti-Hereditarianism, and HBD

3800 words

Abstract

The denial of human nature is extremely prevalent, most noticeably in our institutions of higher learning. To most academics, the fact that there could be population differences that are genetic in nature is troubling for many people. However, denying genetic/biological causes for racial differences is 1) intellectually dishonest; 2) will lead to negative health outcomes for populations due to the assumption that all human populations are the same; and 3) the ‘lie of equality’ will not allow all human populations to reach their ‘potential’ to be as good as they can be due to the fact that implicit assumption that all human populations are the same. Anti-hereditarians fully deny any and all genetic explanations for human differences, believing that human brain evolution somehow halted around 50-100 kya. Numerous studies show that race is a biological reality; it doesn’t matter what we call the clusters as those are the social constructs. The contention is that ‘all brains are the same color’ (Nisbett, 2007; for comment see my article Refuting Richard Nisbett), and that evolution in differing parts of the world for the past 50,000 years was not enough for any meaningful population differences between people. But to accept that means you must accept the fact that the brain is the only organ that is immune to natural selection. Does that make any sense? I will show that these differences do exist and should be studied, as free of any bias as possible, with every possible hypothesis being looked at and not discarded.

Evolution is true. It’s not ‘only a theory’ (as some anti-evolutionists contend). Anti-evolutionists do not understand the definition of the word ‘theory’. Richard Dawkins (2009) wrote that a theory is a scheme or system of ideas or statements held as an explanation or account of a group of facts or phenomena. This is in stark contrast to the layperson’s definition of the word theory, which means ‘just a guess’. Evolution is a fact. What biologists argue with each other about is the mechanisms behind evolution, for any quote-mining Creationists out there.

We know that evolution is a fact and it is the only game in town (Dawkins, 2009) to explain the wide diversity and variation we see on our planet. However, numerous scholars deny the effect of evolution on human behavior (most residing in the social sciences, but other prominent biologists have denied (or implied there were no differences between us and our ancestors) the effect of human evolution on behavior and cognition; Gould 1981, 1996, for a review of Gould 1996, see my article Complexity, Walls, 0.400 Hitting and Evolutionary “Progress” and Stephen Jay Gould and Anti-Hereditarianism; Mayr 1963; see Cochran and Harpending 2009). A prominent neuroscientist, who I have written about here, Herculano-Houzel, implied that Neanderthals and Antecessor may have been just as intelligent as we are due to a neuronal count in a similar range to ours (Herculano-Houzel 2013). This raises an interesting question (which I have tackled here and will return to in the future): did our recent hominin ancestors at least have the capacity for similar intellect to ours (Villa and Roebroeks, 2014; Herculano-Houzel and Kaas, 2011)? It is interesting that neuronal scaling rules hold for our extinct ancestors, and this question is most definitely worth looking into.

Whatever the case may be in regards to recent human evolution and our extinct hominin ancestors, human evolution has increased in the past 10,000 years (Cochran and Harpending, 2009; Wade, 2014). This is due to the dispersal of Anatomical Modern Humans (AMH) OoA around 70 kya; and with this geographical isolation, populations began to diverge with no interbreeding with each other. However, this is noticed most in ‘Native’ Americans, who show no gene flow with other populations due to being genetically isolated (Villena et al, 2000). Who’s to say that evolution stops at the neck, and no further evolution occurs on the brain? Is the brain itself exempt from the laws of natural selection? We know that there is no/hardly any gene flow between populations before the advent of modern-day technology and vehicles; we know that humans differ on morphological and anatomical traits, why are genetic differences out of the question, especially when genetic differences may explain, in part, some of the variation between populations?

We know that evolution is true, without a reasonable doubt. So why, do some researchers contend, is the human brain exempt from such selective pressures?

A theoretical article by Winegard, Winegard, and Boutwell (2017) was just released on January 17th. In the article, they argue that social scientists should integrate HBD into their models. Social scientists do not integrate genetics into their models, and the longer one studies social sciences, the more likely it is they will deny human nature, regardless of political leaning (Perry and Mace, 2010). This poses a problem. By completely ignoring a huge variable (possible genetic differences), this has the potential to harm people’s health, as race is a very informative marker when discussing diseases acquisition as well as whether certain drugs will work on two individuals of different races (Risch et al, 2002; Tang et al, 2005; Wade, 2014). People who deny the usefulness of race, even in a medical context, endanger the lives of individuals from different races/ethnies since they assume that all humans are the same inside, despite ‘superficial differences’ between populations.

The notion that all human populations—genetic isolation and evolution in differing ecosystems/climates/geographic locales be damned—is preposterous to anyone who has a true understanding of evolution. Why should man’s brain be the only organ on earth exempt from the forces of natural selection? Why do egalitarians assume that all humans are the same and have the same psychological faculties compared to other humans, despite the fact that rapid evolution has occurred within the human species within the last 10,000 years?

To see some of the most obvious ways to see natural selection in action in human populations, one should look to the Inuits (Fumagalli, 2015; Daanen and Lichtenbelt, 2016; NIH, 2015; Cardona et al, 2014; Tishkoff, 2015; Ford, McDowell, and Pierce, 2015; Galloway, Young, and Bjerregaard, 2012; Harper, 2015). Global warming is troubling to some researchers, with many researchers suggesting that global warming will have negative effects on the health and food security of the Inuit (Ford et al, 2014, 2016; Ford, 2012, 2009; Wesche, 2010; Furgal and Seguin, 2006; McClymont and Myers, 2012; Petrasek et al, 2015; Rosol, Powell-Hellyer, and Chan, 2016; Petrasek, 2014; WHO, 2003). I could go on and on citing journal articles for both claims, but you get the point already. The main point is this: we know the Inuit have evolved for their climate, and a (possible) climate change would then have a negative effect on their quality of life due to their adaptations to the cold weather climate. However, egalitarians still contend, with these examples and numerous others I could cite, that any and all differences within and between human populations can be explained by socio-cultural factors and not any genetic ones.

One of the best examples of genetic isolation in a geographic locale that is the complete opposite from the environment of evolutionary adaptedness (EEA; Kanazawa, 2004), the African savanna in which we evolved in. I did entertain the idea of the Savanna hypothesis, and while I do believe that it could explain a lot of the variance in IQ between countries (Kanazawa, 2007), his hypothesis doesn’t make sense with what we know about human evolution over the past 10,000 years.

The most obvious differences we can see between populations is differences in skin color. Skin color does not signify race, per se, but it is a good indicator. Skin color is an adaptation to UV radiation (Jablonski and Chaplin, 20102000; Juzenienne et al, 2009; Jeong and Rienzo, 2015; Hancock, et al, 2010; Kita and Fraser, 2016; Scheinfeldt and Tishkoff, 2013), and is therefor and adaptation based on climate. Dark skin is a protectant from skin cancer (Brenner and Hearing, 2008; D’Orazio et al, 2010; Bradford, 2009). Skin cancer is a possible selective force in black pigmentation of the skin in early hominin evolution (Greaves, 2014). With these adaptations in skin color between genetically and geographically isolated populations, are changes in the brain, however small, really out of the question?

A better population to bring up in regards to geographic isolation having an effect on human evolution is the Tibetans. For instance, Tibetans have higher total lung capacities in comparison to the Han Chinese (Droma et al, 1991). There are even differences in lung capacity between Tibetans and Han Chinese who live at the same altitude (Yangzong et al, 2013), with the same thing noticed for peoples living in the Andean mountains (Beall, 2007). Tibetans evolved in a higher elevation than the Han Chinese who lived closer to sea level, so it makes sense that they would be selected for the ability to take deeper inhales They also have a larger chest circumference and greater capacity than the Han Chinese who live at lower altitudes (Gilbert-Kawai et al, 2014).

Admittedly, the acceptance of the usefulness of race in regards to human differences is a touchy subject. So much so, that social scientists do not take genetics into account in their models. However, researchers in the relevant fields accept the usefulness of race (Risch et al, 2002; Tang et al, 2005; Wade, 2014; Sesardic, 2010), so the fact that social scientists do not is to be ignored. Race is a social construct, yes. But no matter what we call these clusters, clines, demes, races, ethnies—whatever name you want to use to describe them—this does not change the fact that race is a useful category in biomedical research. Race is an issue when talking about bone marrow transplants, so by treating all populations as the same with no variation between them, people are pretty much saying that differences between people in a biomedical context do not exist, with there being other explanatory factors behind population differences, in this case, bone marrow transplants. Ignoring heritable human variation will lead to disparate health outcomes for all human populations with the assumption that all humans are the same. Is that what we want? Is that what race-deniers want?

So there are anatomical and physiological differences between human populations (Wagner and Hayward, 2000), with black Americans having a different morphology and lower fat-free body mass on average in comparison to white Americans. This, then, is one of the variables that dictates racial differences in sports, along with muscle fiber explaining a large portion of the variance, in my opinion. No one denies that blacks and whites differ at elite levels in baseballfootballswimming and jumping, and bodybuilding and strength sports. Though, accepting the fact that these morphological and anatomical differences between the races come down to evolution, one would then have to accept the fact that different races/ethnies differ in the brain, thusly destroying their egalitarian fantasy in their head of all genetically isolated human populations being the same in the brain. Wade (2014) writes on page 106:

“… brain genes do not lie in some special category exempt from natural selection. They are as much under evolutionary pressure as any other category of gene”

This is a hard pill to swallow for race-deniers, especially those who emphatically deny any type of selection pressure on the human brain within the past 10,000 to 100,000 years.

Winegard, Winegard, and Boutwell (2017) write:

Consider an analogy that might make this clear while simultaneously illuminating the explanatory importance of population differences. Most cars are designed from the same basic blueprint and consist of similar parts—an internal combustion engine, a gas tank, a chassis, tires, bearings, spark plugs, et cetera. Cars as distinct as a Honda Civic and a Subaru Outback are built from the same basic blueprint and comprised of the same parts; so, in this sense, there is a “universal car nature” (Newton 1999). However, precise, correlated changes in these parts can dramatically change the characteristics of a car.

Humans, like cars, are built from the same basic body plan. They all have livers, lungs, kidneys, brains, arms, and legs. And these structures are built from the same basic building blocks, tissues, which are built of proteins, which are built of amino acids, et cetera. However, small changes in the structures of these building blocks can lead to important and scientifically meaningful differences in function.

Put in this context, yes, there is a ‘universal human nature’, but the application of that human nature will differ depending on what a population has to do to survive in that climate/ecosystem. And, over time, populations will diverge away from each other, both physically and mentally. The authors also argue that societal differences between Eurasians (Europeans and East Asian) can be explained partly by genetic differences. Indeed, the races do differ on the Big Five Personality traits, with heritable components explaining 40 to 60 percent of the variation (Power and Pluess, 2015). So some of the cultural differences between European and East Asians must come down to some biological variation.

One of the easiest ways to see the effects of cultural/environmental selective pressures in humans is to look at Ashkenazi Jews (Cochran et al, 2006). Due to Ashkenazi Jews being barred from numerous occupations, they were confined to a few cognitively demanding occupations. Over time, only the Jews that could handle these occupations would prosper, further selecting for higher intelligence due to the cognitive demands of the jobs they were able to acquire. Thus, Ashkenazi Jews who could handle the few occupations they were allowed to do would breed more and pass on variants for higher intelligence to their offspring, whereas those Jews who couldn’t handle the cognitive demands of the occupation were selected out of the gene pool. This is one situation in which natural selection worked swiftly, and is why Ashkenazi Jews are so overrepresented in the fields of academia today—along with nepotism.

Winegard, Winegard, and Boutwell (2017) lay out six basic principles for a new Darwinian paradigm, as follows:

  1. Variation is the grist for the mill of natural selection and is ubiquitous within and among human populations.
  2. Evolution by natural selection has not stopped acting on human traits and has significantly shaped at least some human traits in the past 50,000 years.
  3. Current hunter-gatherer groups might be slightly different from other modern human populations because of culture and evolution by natural selection acting to influence the relative presence, or absence, of trait-relevant alleles in those groups. Therefore, using extant hunter-gatherers as a template for a panhuman nature is problematic.
  4. It is probably more accurate to say that, while much of human nature is universal, there may have been selective tuning on various aspects of human nature as our species left Africa and settled various regions of the planet (Frost 2011).
  5. The human brain is subject to selective forces in the same way that other organ systems are. Natural selection does not discriminate between genes for the body and genes for the brain (Wade 2014).
  6. The concept of a Pleistocene-based environment of evolutionary adaptedness (EEA) is likely unhelpful (Zuk 2013). Individual traits should be explored phylogenetically and historically. Some human traits were sculpted in the Pleistocene (or before) and have remained substantially unaltered; some, however, have been further shaped in the past 10,000 years, and some probably quite recently (Clark 2007). It remains imperative to describe what selection pressures might have been actively shaping human nature moving forward from the Pleistocene epoch, and how those ecological pressures might have differed for different human populations.

No stone should be left unturned when attempting to explain population differences between geographically isolated peoples, and these six principles are a great start, which all social scientists should introduce into their models.

As I brought up earlier, Kanazawa’s (2004b) hypothesis doesn’t make sense in regards to what we know about the evolution of human psychology. Thus, any type of proposed evolutionary mismatch in regards to our societies do not make much sense. However, one mismatch that does need to be looked into is the negative mismatch we have with our modern-day Western diets. Agriculture was both a gift and a negative event in human history. Yes, without the advent of agriculture 10,000 years ago we would not have the societies we have today. However, on the other hand, we have higher rates of disease compared to our hunter-gatherer ancestors. This is one evolutionary mismatch that cannot and should not go ignored as it has devastating effects on our populations that consume a Western diet—which we did not evolve to eat.

Winegart, Winegart, and Boutwell (2017) then discuss how their new Darwinian paradigm could be used by researchers: 1) look for differences among human populations; 2) after population differences are found, causal analyses should be approached neutrally; 3) researchers should consider a broad range of data to consider whether or not the trait or traits in question are heritable; and 4) researchers should test the posited biological cause more indepth. Without understanding—and using—biological differences between human populations, the quality of life for some populations will be diminished, all for the false notion of ‘equality’ between human races.

There are huge barriers in place to studying human differences, however. Hayden (2013) documents differing taboos in genetics, with intelligence having a high taboo rating. Of course, we HBDers know that intelligence is a highly heritable trait, largely genetic in nature, and so studying these differences between human populations may lead to some uncomfortable truths for some people. On the 200th anniversary of Darwin’s On the Origin of Species, Ceci and Williams (2009) said that “the scientific truth must be pursued” and that researchers must study race and IQ, much to the chagrin of anti-hereditarians (Horgan, 2013). He does write something very troubling in regards to this research, and free speech in our country as a whole:

Some readers may wonder what I mean by “ban,” so let me spell it out. I envision a federal prohibition against speech or publications supporting racial theories of intelligence. All papers, books and other documents advocating such theories will be burned, deleted or otherwise destroyed. Those who continue espousing such theories either publicly or privately (as determined by monitoring of email, phone calls or other communications) will be detained indefinitely in Guantanamo until or unless a secret tribunal overseen by me says they have expressed sufficient remorse and can be released.

Whether he’s joking or not, that’s besides the point. The point is, is that these topics are extremely sensitive to the lay public, and with these articles being printed in popular publications, the reader will get an extremely biased look into the debate and their mind will already be made up for them. This is the definition of intellectual dishonesty, attempting to sway a lay-readers’ opinion on a subject they are ignorant of with an appeal to emotion. Shouldn’t all things be studied scientifically, without any ideological biases?

Speaking about the ethics of putting this information out to the general public, Winegard, Winegard, and Boutwell (2017) write:

If researchers do not responsibly study and discuss population differences, then they leave an abyss that is likely to be filled by the most extreme and hateful writings on population differences. So, although it is understandable to have concerns about the dangers of speaking and writing frankly about potential population differences, it is also important to understand the likely dangers of not doing so. It is not possible to hide the reality of human variation from the world, not possible to propagate a noble lie about human equality, and the attempt to do so leaves a vacancy for extremists to fill.

This is my favorite quote in the whole paper. It is NOT possible to hide the reality of HBD from the world; anyone with eyes can see that humans do differ. Attempting to continue the feel-good liberal lie of human equality will lead to devastating effects in all countries/populations due to the implicit assumption that all human groups are the same in their cognitive and mental faculties.

The denial of genetic human differences, could, as brought up earlier in this article, lead to negative effects in regards to health outcomes between populations. Black Americans have higher rates of hypertension than white Americans (Fuchs, 2011; Ferdinand, 2007; Ortega, Sedki, and Nayer, 2015; Nesbitt, 2009; Wright et al, 2005). To overlook possible genetic differences as a causal factor in regards to racial differences will mean the deaths of many people since people truly believe that people are the same and that all differences come down to the environment. This, however, is not true and believing so is extremely dangerous to the health of all populations in the world.

Epigenetic signatures of ethnicity may be biomarkers for shared cultural experiences. Seventy-six percent of the genetic alteration between Mexicans and Puerto Ricans in this study was due to DNA methylation—which is an epigenetic mechanism used by cells to control gene expression. Therefore, 24 percent of the effect is due to an unknown factor, probably regarding environmental, social, and cultural differences between the two ethnies (Galanter et al, 2017). This is but one of many effects that culture can have on the genome, leading to differences between two populations, and is good evidence for the contention that the different races/ethnies evolved different psychological mechanisms due to genetic isolation in different environments.

We must now ask the question: what if the hereditarian hypothesis is true (Gottfredson, 2005)? If the hereditarian hypothesis is true, Gottfredson argues, special consideration should be given to those found to have a lower IQ, with better training and schooling that specifically target those individuals at risk to be less able due to their lower intelligence. This is one way the hereditarian hypothesis can help race relations in the country: people will (hopefully) accept intrinsic differences between the races. What Gottfredson argues in her paper will hopefully then pacify anti-hereditarians, as less able people of all races/ethnicities will still get the extra help they need in regards to finding work and getting schooling/training/jobs that accommodate their intelligence.

Conclusion

People accept genetic causes for racial differences in sports, yet emphatically deny that human races/ethnies differ in the brain. The denial of human nature—racially and ethnically—is the next hurdle for us to jump over. Once we accept that these differences in populations can, in part, be explained by genetic factors, we can then look to other avenues to see how and why these differences exist between populations occur and if anything can be done to ameliorate them. However, ironically, anti-hereditarians do not realize that their policies and philosophy is actively hindering their goals, and by accepting biological causes—if only to see them researched and held against other explanations—will lead to further inequality, while they scratch their heads without realizing that the cause is the one variable that they have discarded: genetics. Still, however, I see this won’t happen in the future and the same non-answers will be given in response to findings on how the human races differ psychologically (Gottfredson, 2012). The races do differ in biologically meaningful ways, and denying or disregarding the truth will not make these differences disappear. Social scientists must take these differences into account in their models, and seriously entertain them like any other hypothesis, or else they will never fully understand human nature.

Is General Intelligence Domain-Specific?

1600 words

Is the human brain ‘special’? Not according to Herculano-Houzel; our brains are just linearly scaled-up primate brains. We have the number of neurons predicted for a primate of our body size. But what does this have to do with general intelligence? Evolutionary psychologists also contend that the human brain is not ‘special’; that it is an evolved organ just like the rest of our body. Satoshi Kanazawa (2003) proposed the ‘Savanna Hypothesis‘ which states that more intelligent people are better able to deal with ‘evolutionary novel’ situations (situations that we didn’t have to deal with in our ancestral African environment, for example) whereas he purports that general intelligence does not affect an individuals’ ability to deal with evolutionarily familiar entities and situations. I don’t really have a stance on it yet, though I do find it extremely interesting, with it making (intuitive) sense.

Kanazawa (2010) suggests that general intelligence may both be an evolved adaptation and an ‘individual-difference variable’. Evolutionary psychologists contend that evolved psychological adaptations are for the ancestral environment which was evolved in, not in any modern-day environment. Kanazawa (2010) writes:

The human brain has difficulty comprehending and dealing with entities and situations that did not exist in the ancestral environment. Burnham and Johnson (2005, pp. 130–131) referred to the same observation as the evolutionary legacy hypothesis, whereas Hagen and Hammerstein (2006, pp. 341–343) called it the mismatch hypothesis.

From an evolutionary perspective, this does make sense. A perfect example is Eurasian societies vs. African ones. you can see the evolutionary novelty in Eurasian civilizations, while African societies are much closer (though obviously not fully) to our ancestral environment. Thusly, since the situations found in Africa are not evolutionarily novel, it does not take high levels of to survive in, while Eurasian societies (which are evolutionarily novel) take much higher levels of to live and survive in.

Kanazawa rightly states that most evolutionary psychologists and biologists contend that there have been no changes to the human brain in the last 10,000 years, in line with his Savanna Hypothesis. However, as I’m sure all readers of my blog know, there were sweeping changes in the last 10,000 years in the human genome due to the advent of agriculture, and, obviously, new alleles have appeared in our genome, however “it is not clear whether these new alleles have led to the emergence of new evolved psychological mechanisms in the last 10,000 years.”

General intelligence poses a problem for evo psych since evolutionary psychologists contend that “the human brain consists of domain-specific evolved psychological mechanisms” which evolved specifically to solve adaptive problems such as survival and fitness. Thusly, Kanazawa proposes in contrast to other evolutionary psychologists that general intelligence evolved as a domain-specific adaptation to deal with evolutionary novel problems. So, Kanazawa says, our ancestors didn’t really need to think inorder to solve recurring problems. However, he talks about three major evolutionarily novel situations that needed reasoning and higher intelligence to solve:

1. Lightning has struck a tree near the camp and set it on fire. The fire is now spreading to the dry underbrush. What should I do? How can I stop the spread of the fire? How can I and my family escape it? (Since lightning never strikes the same place twice, this is guaranteed to be a nonrecurrent problem.)

2. We are in the middle of the severest drought in a hundred years. Nuts and berries at our normal places of gathering, which are usually plentiful, are not growing at all, and animals are scarce as well. We are running out of food because none of our normal sources of food are working. What else can we eat? What else is safe to eat? How else can we procure food?

3. A flash flood has caused the river to swell to several times its normal width, and I am trapped on one side of it while my entire band is on the other side. It is imperative that I rejoin them soon. How can I cross the rapid river? Should I walk across it? Or should I construct some sort of buoyant vehicle to use to get across it? If so, what kind of material should I use? Wood? Stones?

These are great examples of ‘novel’ situations that may have arisen, in which our ancestors needed to ‘think outside of the box’ in order to survive. Situations such as this may be why general intelligence evolved as a domain-specific adaptation for ‘evolutionarily novel’ situations. Clearly, when such situations arose, our ancestors who could reason better at the time these unfamiliar events happened would survive and pass on their genes while the ones who could not die and got selected out of the gene pool. So general intelligence may have evolved to solve these new and unfamiliar problems that plagued out ancestors. What this suggests is that intelligent people are better than less intelligent people at solving problems only if they are evolutionarily novel. On the other hand, situations that are evolutionarily familiar to us do not take higher levels of to solve.

For example, more intelligent individuals are no better than less intelligent individuals in finding and keeping mates, but they may be better at using computer dating services. Three recent studies, employing widely varied methods, have all shown that the average intelligence of a population appears to be a strong function of the evolutionary novelty of its environment (Ash & Gallup, 2007; D. H. Bailey & Geary, 2009; Kanazawa, 2008).

Who is more successful, on average, over another in modern society? I don’t even need to say it, the more intelligent person. However, if there was an evolutionarily familiar problem there would be no difference in figuring out how to solve the problem, because evolution has already ‘outfitted’ a way to deal with them, without logical reasoning.

Kanazawa then talks about evolutionary adaptations such as bipedalism (we all walk, but some of us are better runners than others); vision (we can all see, but some have better vision than others); and language (we all speak, but some people are more proficient in their language and learn it earlier than others). These are all adaptations, but there is extensive individual variation between them. Furthermore, the first evolved psychological mechanism to be discovered was cheater detection, to know if you got cheated while in a ‘social contract’ with another individual. Another evolved adaptation is theory of mind. People with Asperger’s syndrome, for instance, differ in the capacity of their theory of mind. Kanazawa asks:

If so, can such individual differences in the evolved psychological mechanism of theory of mind be heritable, since we already know that autism and Asperger’s syndrome may be heritable (A. Bailey et al., 1995; Folstein & Rutter, 1988)?

A very interesting question. Of course, since it’s #2017, we have made great strides in these fields and we know these two conditions to be highly heritable. Can the same be said for theory of mind? That is a question that I will return to in the future.

Kanazawa’s hypothesis does make a lot of sense, and there is empirical evidence to back his assertions. His hypothesis proposes that evolutionarily familair situations do noot take any higher levels of general intelligence to solve, whereas novel situations do. Think about that. Society is the ultimate evolutionary novelty. Who succeeds the most, on average, in society? The more intelligent.

Go outside. Look around you. Can you tell me which things were in our ancestral environment? Trees? Grass? Not really, as they aren’t the same exact kinds as we know from the savanna. The only thing that is constant is: men, women, boys and girls.

This can, however, be said in another way. Our current environment is an evolutionary mismatch. We are evolved for our past environments, and as we all know, evolution is non-teleological—meaning there is no direction. So we are not selected for possible future environments, as there is no knowledge for what the future holds due to contingencies of ‘just history’. Anything can happen in the future, we don’t have any knowledge of any future occurences. These can be said to be mismatches, or novelties, and those who are more intelligent reason more logically due to the fact that they are more adept at surviving evolutionary novel situations. Kanazawa’s theory provides a wealth of information and evidence to back his assertion that general intelligence is domain-specific.

This is yet another piece of evidence that our brain is not special. Why continue believing that our brain is special, even when there is evidence mounting against it? Our brains evolved and were selected for just like any other organ in our body, just like it was for every single organism on earth. Race-realists like to say “How can egalitarians believe that we stopped evolving at the neck for 50,000 years?” Well to those race-realists who contend that our brains are ‘special’, I say to them: “How can our brain be ‘special’ when it’s an evolved organ just like any other in our body and was subject to the same (or similar) evolutionary selective pressures?”

In sum, the brain has problems dealing with things that were not in its ancestral environment. However, those who are more intelligent will have an easier time dealing with evolutionarily novel situations in comparison to people with lower intelligence. Look at places in Africa where development is still low. They clearly don’t need high levels of to survive, as it’s pretty close to the ancestral environment. Conversely, Eurasian societies are much more complex and thus, evolutionarily novel. This may be one reason that explains societal differences between these populations. It is an interesting question to consider, which I will return to in the future.