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Possibly Retracting My Article on HBD and Baseball
700 words
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
1700 words
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 and Hunter (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
Female Mate Preference and Somatypes
1450 words
PumpkinPerson’s most recent article Are muscular guys genetically inferior? is a joke. He makes huge assumptions and attempts to this ‘social experiment’ as evidence that women find ‘nerds’ more attractive. The logic here is that since East Asians are the ‘most evolved’ race and (in his world) they have the least testosterone along with the highest intelligence, that this is some kind of apex of human evolution. However the conclusions he makes off of this one video are very erroneous and I will explain why.
PP writes:
They are simply genetically inferior because the muscular body type branched off the evolutionary tree pre-maturely.
…No idea what he’s talking about. No source that the ‘muscular body type branched off the evolutionary tree prematurely.’ This is just an assumption because Africans supposedly have higher testosterone than both Europeans and East Asians, except East Asians have the highest testosterone out of all of all three traditional races, not Africans.
After watching this video I feel like starving my muscles off (not that I recommend that).
Good luck with that.
I realize not everyone agrees with the progressive model of evolution, but real scientists do. For example, check out this phys.org article:
This article has nothing to do with progressive evolution at all. In fact, this article is basically a summary of Full House (Gould, 1996) in which Gould argues that since life began at the left wall of complexity—where no organism can get simpler—that a right-tail distribution of complexity was inevitable. I have covered this here. This is not evidence for progressive evolution. It is, in fact, the opposite. He’s never read Gould’s books so he wouldn’t know that.
Now, PP’s contention that women find nerds more attractive has no basis. When I think of a ‘nerd’, I think of a scrawny pencil-neck, buck teeth, person with thick-rimmed black glasses. This, obviously, isn’t true. If it were, then why do East Asians—Japan specifically—have the lowest birthrates? Of course, social factors have a lot to do with it—birthrates decline in developed countries (Nargund, 2009; Sinding, 2009), as well as genetic ones (Harris and Nielson, 2016). So, clearly, the more intelligent, more developed countries don’t have more children, which then, of course implies that either higher IQ people are less desirable from a reproductive point of view (plausible), or they forgo having children until around 28 years of age (Lange, Rinderu and Bushman, 2016). Whatever the case may be, those with higher IQs do not conceive as many children as those with lower IQs, signifying something about their fitness aspects.
Further, women, evolutionarily speaking, sexually selected men for high levels of testosterone, which leads to bigger muscles, more defined facial features, higher levels of aggression (good for protecting genetic interests) and so on. The fact that some people may think that nerds have better prospects than non-nerds, evolutionarily speaking, had no basis in reality and for one to believe as much, it has to be driven by ideology.
Dixson et al (2010) showed that women prefer men with the mesomorphic somatype and ‘average’ body type, then prefer ectomorphs (a skinnier body type) and finally endomorph (a heavier build) ranging from most attractive to least. This study shows that, at least when it comes to European females, they prefer mesomorphic somatypes, which, more often than not, one who is over 6 feet tall will have. Does that seem like a ‘nerd’ to you? I don’t think so. Someone who has the potential ability to control a room with his presence doesn’t seem like a nerd to me. These are the same people who are CEOs.
Journalist Malcolm Gladwell showed that on average, CEOs averaged just under 6 foot tall. Since the average American is 5 foot 9, the average CEO has a three-inch height advantage over the average man in America. However, when looking at those who are 6 feet tall and up, for average Joe the percentage is a paltry 3.9 percent while, in Gladwell’s sample, 30 percent were over 6’2″. So, Gladwell states, the lack of minorities and women in high positions has a plausible explanation: height. Men are, on average taller than women. Tall men earn more money than their shorter counterparts. Taller children also perform better on cognitive tests, taller men earn more money in Mexico, and taller children do better on learning tests in India (Lawson and Spears, 2016).
Women want taller men more than men want taller women (Stulp, Buunk, and Pollet, 2012). Tall men are also more likely to have a mesomorphic somatype. Those somatypes are seen as the most attractive. Does that seem like a nerd somatype to you? An athletic somatype? On the other hand, women aren’t attracted to short men (Nettle, 2002). East Asians—the so-called ‘most evolved race’—are the shortest race. Doesn’t look too good for them.
Furthermore, while East Asian men see themselves as attractive and dateable, they don’t believe society sees it that way. Forty-six percent of the sample said they could recall one instance where they hear someone state that they do not date Asian men, while eleven percent of Asian men have heard it at least six times. For Okcupid’s 2009 race/dating data, 18 percent of Asian women (3,381 yes) would date someone of their own background/skin color while 82 percent (17,227) wouldn’t! So much for the ‘most evolved’ race having dating prospects in their own race. East Asian men said yes to the question at a rate of 24 percent (7,965 yes) and no 76 percent of the time (25,358).
To further put this into perspective, white women would said yes to the question at a rate of 54 percent (154,595) and no at a rate of 46 percent (132,497) while white men said yes at a 40/60 yes/no rate (183,360/277,827 respectively). In total, 45 percent of whites would prefer to date someone of their skin color/ethnicity while 55 percent wouldn’t (337,955/410,324) while non-whites said yes to the question 20 percent of the time while they said no 80 percent of the time (56,080/222,484).
A 2014 follow-up found the same thing, however with Asian women showing some positive ratings toward Asian males (while all races of men didn’t find black women particularly attractive). However, Asian men were seen as the least attractive throughout the whole sample. Asian males are also seen as less attractive than males of other races (Fisman et al, 2008). In their sample, they found even after running regressions that Asian women found white, black, and ‘Hispanic’ men. They also show that even Asian men find white, black and ‘Hispanic’ females more attractive than Asian females.
In sum, PP’s contentions and reaches in his article are wrong. ‘Nerds’ (in the way I’m defining the word) are not more successful than the alpha CEOs who are over 6’2”. PP seems to have an aversion to testosterone (believes that it is the cause for racial differences in prostate cancer differences, but vitamin D deficiencies are a more likely culprit). East Asian men—the so-called ‘most evolved’ men of the ‘most evolved’ race do not fair well in terms of physical attractiveness, and this may be a reason why the Japanese birthrate is declining, with the average Japanese woman having only one child during her lifetime (Nomura and Koizumi, 2016). PP’s theory makes no sense, because women favor mesomorphic somatypes. Mesomorphs are more likely to be CEOs of 500 companies, more likely to be more cognitively adept and make more money than their shorter counterparts. Making evolutionary theories off of one (obviously fake) ‘social experiment’ is ridiculous. East Asian men, the so-called ‘most evolved man’ fall short in the dating game, due to being seen as less attractive.
References
Dixson, B. J., Dixson, A. F., Bishop, P. J., & Parish, A. (2009). Human Physique and Sexual Attractiveness in Men and Women: A New Zealand–U.S. Comparative Study. Archives of Sexual Behavior,39(3), 798-806. doi:10.1007/s10508-008-9441-y
Fisman, R. J., Iyengar, S. S., Kamenica, E., & Simonson, I. (2008) (n.d.). Racial Preferences in Dating: Evidence from a Speed Dating Experiment. SSRN Electronic Journal. doi:10.2139/ssrn.610589
Gould, S. J. (1996). Full house: The Spread of Excellence from Plato to Darwin. New York: Harmony Books.
Harris, K., & Nielsen, R. (2016). The Genetic Cost of Neanderthal Introgression. Genetics, 2016 doi:10.1101/030387
Lange, P. A., Rinderu, M. I., & Bushman, B. J. (2016). Aggression and Violence Around the World: A Model of CLimate, Aggression, and Self-control in Humans (CLASH). Behavioral and Brain Sciences, 1-63. doi:10.1017/s0140525x16000406
Nargund G. (2009) Declining birth rate in Developed Countries: A radical policy re-think is required. F.V & V in ObGyn. 2009;1:191-3
Nettle, D. (2002). Women’s height, reproductive success and the evolution of sexual dimorphism in modern humans. Proceedings of the Royal Society B: Biological Sciences,269(1503), 1919-1923. doi:10.1098/rspb.2002.2111
Nomura, K., & Koizumi, A. (2016). Strategy against aging society with declining birthrate in Japan. Industrial Health INDUSTRIAL HEALTH,54(6), 477-479. doi:10.2486/indhealth.54-477
Sinding S.(2009) Population, poverty and economic development. Phil. Trans. R. Soc. B 364.
Stulp, G., Buunk, A. P., & Pollet, T. V. (2013). Women want taller men more than men want shorter women. Personality and Individual Differences,54(8), 877-883. doi:10.1016/j.paid.2012.12.019
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, 2010, 2000; 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 baseball, football, swimming 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:
- Variation is the grist for the mill of natural selection and is ubiquitous within and among human populations.
- 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.
- 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.
- 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).
- 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).
- 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.
Racial Differences in Prostate Cancer: Part II
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I showed in part I, that the oft-cited reason for racial differences in prostate cancer acquisition and mortality are not due to higher levels of circulating testosterone when comparing blacks to whites (Richard et al, 2014). I posited (and provided sufficient evidence) that the disparity could come down to differences in vitamin D between the races. Black Americans are far removed from their ancestral environment, living in a cooler area. Their pigmentation reduces vitamin D production in the skin, since blacks need a lot more sunlight to synthesize the hormone than whites do, and the main culprit is the environment: not getting enough sunlight (Harris, 2006). I will provide further evidence for the theory.
The etiology of prostate cancer is not known (ACA, 2016; Bashir, 2015). The cause for the disparity in racial differences in prostate cancer may possibly come down to circulating vitamin D levels, with sunlight playing a large role in the variance. Racial differences in prostate cancer were larger in areas with less sunshine (Taksler et al, 2013). However, it is not known whether getting more sunlight (though the problem would still be getting enough in places with low levels of sunlight) or supplementing with vitamin D will help close the gap. Vitamin D is relevant for lethal prostate cancer (Shui et al 2012), whereas Li et al (2007) showed that supplementing with higher rates of vitamin D, especially during the winter months, may be particularly beneficial to men with low levels of circulating vitamin D. A study on veterans showed that men who had prostate cancer AND the lowest levels of vitamin D were more likely to die than veterans who had higher levels of the hormone (Der et al, 2014). Murphy et al (2014) showed in a biopsy, that in black Americans, low levels of vitamin D were associated with increased the odds of prostate cancer acquisition during the biopsy.
Black Americans are significantly more likely than European Americans to suffer from and die from prostate cancer (Hardiman et al, 2016). A difference of over 8,000 genes were found to be expressed differently. Blacks also have higher rates of prostate tumors and higher grade tumors than do European men. The racial disparity in prostate cancer mirrors circulating levels of vitamin D in the blood between the races (Nelson et 2016). Prostate cells become less sensitive to vitamin D through loss of receptors or signaling molecules “that mediate vitamin D’s actions, or through changes in metabolic enzymes that synthesize or degrade vitamin D compounds” (Peehl and Feldman, 2013). Hardiman et al (2016) showed that there were over 3,000 genes that differed between blacks and whites. Due to the fact that blacks are living outside of their ancestral climes, this is a large mediator of the prostate cancer gap. Vitamin D deficiency can also explain a large variation of the black-white prostate cancer gap (Grant and Peiris 2011).
Along with direct measurement of circulating vitamin D in the bloodstream, we also have correlates. Hypertension is correlated with prostate cancer: blacks have higher rates of hypertension; obesity further exacerbates the problem. Blacks males are more likely to be obese (though barely, which is where the other environmental factors come in). Men suffering from two or more health problems linked to metabolic syndrome are more likely to get prostate cancer. Blacks are more likely to get metabolic syndrome.
Clearly, a large portion of the variation in prostate cancer acquisition and mortality can be attributed to environmental factors (vitamin D intake specifically). We can also look to East Asia and their increasing rates of prostate cancer as well (Chen et al, 2014; Zhu et al, 2014). There are no genetic changes in the past ten years to account for this, so the only culprit is diet. Our Americanized diets have been making it to East Asia recently and it’s having a negative effect on them. China’s obesity rate is dramatically increasing, along with their rates of prostate cancer acquisition. It seems that the Western diet could also play a part in racial differences in prostate cancer acquisition.
To be fair the non-significance of this result might be attributable to the small number (only four) of African nations in the analysis. A number of previous studies have actually found that people of African descent on average do have shorter CAG repeats than other peoples (Ackerman et al., 2012; Esteban et al., 2005; Kittles et al., 2001; Lange et al., 2008). However, whether this actually indicates anything about the life history strategy of different populations remains questionable. The two other androgen indicators for which African data was available follow a completely different pattern. For androgenic hair, Caucasians have the highest rate, followed by Asians, then Africans. For prostate cancer, Caucasians have the highest rate, followed by Asians and Africans, who do not significantly differ.
The difference comes down, mostly in my opinion, due to diet. You can see this by looking at rates of prostate cancer in populations that have adopted, or are current adopting our Western diet.
There is a good chance that environmental factors explain a large part of the variance in prostate cancer acquisition and mortality. I, of course, do not deny intrinsic genetic explanations or other hormonal imbalances, however this is the best explanation I’ve come across. The fact that sunlight dictates prostate cancer acquisition is a huge tell and should be further researched.
I used to be a proponent of the testosterone theory, however, Richard et al (2014) shows a 2.5 to 4.9 percent difference in free testosterone between blacks and whites, which they conclude, does not explain the disparity between the races. Hormones do matter, and hormones can and do vary individually and by group, which are mediated by diet. Once we find out which foods either hurt or help prostate cancer growth, then we can have better treatments for this disease for men of all races.
There are numerous ways in which prostate cancer can be mitigated, with diet obviously playing a large factor (Son, Aronson, and Litwin, 2005; Lin, 2015; Nelson, Demarzo, and Yegnasubramanian, 2014). Future studies researching the racial disparities in prostate cancer should take into account UV radiation from the sun, circulating vitamin D in the blood, and diet amongst a myriad of other variables (these three just stand out to me). Moreover, large-scalre cohorts should be undertaken to see what effects diet can have on the mortality of those suffering from prostate cancer, as possibly supplementing vitamin D to attempt to fight the disease
Are Caesarian Sections Affecting Human Evolution?
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Our brains are the most metabolically demanding organ we have, sapping 5-600 kcal per day (25 percent of our daily energy needs). Due to how cost-efficient the brain is, it only would have evolved if it gave us a bigger fitness advantage (which it obviously did). In the news a couple of days ago, it broke that C-sections may be affecting our evolution. But in all of the articles I read about it I didn’t see any one of them talking about how C-sections may affect human evolution in America between race. Clearly, if C-sections are having this effect on the country as a whole, there must be racial differences as well. Could this have an effect on brain size between race in America?
C-sections have increased in frequency since 1996. Clearly, if there is any selection it’s for more narrow-hipped women and bigger-brained babies. The regular use of C-sections has led to an evolutionary increase of fetopelvic disproportion rates by 10 to 20%. (Mitteroecker et al, 2016) Fetopelvic disproportion is the inability of a babe’s head to pass through the mother’s birth canal. This is because the head—and along with it the brain—is too big, leading to emergency C-sections. Mitteroecker et al (2016) also say (which slightly amused me):
Mitteroecker et al (2016) also say (which slightly amused me):
Neonatal size and maternal pelvic dimensions influence fitness (i.e., reproductive success) of the newborn and the mother in multiple ways. Undoubtedly, relative brain size had increased during human evolution in response to directional selection. Recently, it has also been suggested that the large human brain may be the result of runaway selection for the childcare of infants that are born prematurely because of their large brain (12). It is unclear whether any of this selection still persists after the slight decrease of brain size in the late Pleistocene. However, birth weight, which correlates with brain size at birth, is strongly positively associated with infant survival rate (13) and has also been reported to correlate negatively with the risk of multiple diseases (14). Reducing neonatal brain size by shortening gestation length seems to be equally disadvantageous: Delivery before term clearly increases the likelihood of impaired cognitive function in later life (15, 16).
Brain size is decreasing. Associate professor of anthropology at the University of Wisconsin John Hawks also states in his blog post, Selection for smaller brains in Holocene human evolution, where he says (contrary to Pumpkin Person’s assertion) that human brain size has gotten smaller in the past 10,000 years:
The available skeletal samples show a reduction in endocranial volume or vault dimensions in Europe, southern Africa, China, and Australia during the Holocene. This reduction cannot be explained as an allometric consequence of reductions of body mass or stature in these populations. The large population numbers in these Holocene populations, particularly in post-agricultural Europe and China, rule out genetic drift as an explanation for smaller endocranial volume. This is likely to be true of African and Australian populations also, although the demographic information is less secure. Therefore, smaller endocranial volume was correlated with higher fitness during the recent evolution of these populations. Several hypotheses may explain the reduction of brain size in Holocene populations, and further work will be necessary to uncover the developmental and functional consequences of smaller brains.
The reduction in brain size began around 28 kya and accelerated around 10 kya after the dawn of agriculture. The planet getting warmer also played a part in the decrease in brain size, which also allowed for the beginning of agriculture. Anyway, I’m sidetracking, I will return to this point in the future.
Large brains were also selected for since we needed to care for helpless babies. Natural selection for large brains led to more premature births which itself selected for even larger brains.
One-hundred years ago, a narrow-hipped mother who was pregnant with a big-headed baby would have died. Narrow-hipped women with big-headed babies can now survive, transmitting genes for both big brains and narrower pelvises. This is natural selection currently at work as we speak.
One thing that I obviously didn’t see in any article I’ve read on this matter is how will this affect racial differences in brain size? Which race has the most C-sections and will that select for bigger heads and smaller pelvises in that population?
Black women are substantially more likely to deliver by C-section than are white women (pg. 4). Though, one reason that C-sections occur is due to obesity. Black women are the most likely to be obese, which is part of the reason why they have more C-sections. If this trend continues, I could see a slight uptick in black brain size, as even smaller hips get selected for in black women, along with an increase in brain size. That’s one reason why Africans have smaller heads and brains than East Asians and Europeans: they have narrower hips which allows for better athleticism. Conversely, Europeans and East Asians have wider hips which allows for bigger-brained children but hampers athletic ability.
While on the topic of race and C-sections, Asian female-European Male couples have higher rates of C-sections. The obvious explanation is that the Asian woman’s pelvis is too narrow to birth bigger babies. In the study, Asian female-white male couples had babies that had a median weight of 8 pounds, while Asian-Asian couples had babies that had a median weight of 7.1 pounds and finally Asian male-white female couples’ babies had a median weight of 7.3 pounds. However, Asian female-white male couples had an increased rate of C-section deliveries, proving that a significant differences exist between sex of the parent (whether the father or mother is Asian or white influences birth weight) which leads to increased C-section rates due to the white father passing clearly influencing the birth weight more, thusly making it difficult for his Asian partner to birth the baby. There are 100 deaths per 100,000 live births per year in the U.S., a rate of .1 percent. Clearly, though the death rate is low, C-sections lead to maternal mortality and since Asian females are more likely to have a C-section when the father is white due to the baby being bigger, the mortality rate is slightly increased when this interracial pairing occurs.
C-sections are causing natural selection, favoring for bigger heads and narrower hips. This helped us, evolutionarily speaking, as human bipedalism is promoted by a narrow pelvis. C-sections could possibly select for bigger-brained African Americans. Though brain size has decreased in the past 10,000 years, our brain size will slightly increase over time due to this selection pressure. Asian women and white male couples have C-sections more often. Pretty good case against race-mixing, if I don’t say so myself.
Race Is a Social Construct of a Biological Reality
2050 words
Race: social construct or biological reality? Why can’t it be both? When the Left (let’s use Liberal Creationists, LC for short) says that “race is a social construct”, what do they mean? They mean, obviously, that race is not a biological reality and that most ‘racists’ assume that race is only what we can physically see—the phenotype. However, genotypic differences give rise to phenotypic differences between humans. We can then say, with 100 percent certainty, that even ‘small genotypic differences’ can make ‘big differences in phenotype’ between two almost genetically similar organisms.
The thing that LCs don’t understand is that race is a ‘social construct’, but not in the way that they believe. They believe that since what we call ‘white’ and ‘black’ are genetically different depending on which geographic location you look at, that race must be something constructed by the mind based on the ‘small genotypic differences’ which lead to the ‘large differences in phenotype’. This couldn’t be further from the truth.
See, what we call the ‘races’ are arbitrary. Instead of ‘white’ we can say ‘hulina’, instead of ‘black’ we can say ‘lorux’ (two random ‘words’ I made up on the fly). What we call these biological realities is arbitrary, replacing the common usages of ‘white’ and ‘black’ WILL NOT change biology. This is what they don’t understand. They are correct that ‘race is a social construct’, but the ‘social constructions’ that we have chosen describe genotypic differences between geographically isolated populations. What we call races, ethnies, or anything for that matter, is arbitrary as the genetic underpinnings we are describing will not change if we call them another (arbitrary) name.
We have this article from The New York Times (which I have already responded to) which says:
Race is not biological. It is a social construct. There is no gene or cluster of genes common to all blacks or all whites. Were race “real” in the genetic sense, racialclassifications for individuals would remain constant across boundaries. Yet, a person who could be categorized as black in the United States might be considered white in Brazil or colored in South Africa.
This goes back to my point about using different ‘constructs’ for these biological realities (though mixed is a better ‘construct’ to use than ‘white’ or ‘black’. ‘Colored’ is a good term as that denotes a white/black mix). Call someone ‘black’ in America and he’ll be ‘white’ in Brazil or ‘colored’ in South Africa. OK? And? Does this change any type of underlying biology that is being described? I do admit that using the term ‘mixed’ is better than the ‘straight terms’ of ‘white’ and ‘black’, however, these ‘constructed terms’ are shockingly correct in describing the biological underpinnings of ‘race’.
I define ‘race’ as a genetically isolated breeding population. Sure, we can still conceive children between racial groups, that, however, doesn’t change any underlying biologic underpinnings. That should be obvious, though.
You have people like Richard Lewontin, of ‘Lewontin’s Fallacy’ fame who say that “because there is more variation within racial groups that the smaller variation between racial groups is insignificant, stating:
“Since such racial classification is now seen to be of virtually no genetic or taxonomic significance either, no justification can be offered for its continuance.”
There IS a genetic significance, and there IS taxonomic significance, to quote Dawkins:
It is genuinely true that, if you measure the total variation in the human species and then partition it into a between-race component and a within-race component, the between-race component is a very small fraction of the total. Most of the variation among humans can be found within races as well as between them. Only a small admixture of extra variation distinguishes races from each other. That is all correct. What is not correct is the inferene that race is therefore a meaningless concept. This point has been clearly made by the distinguished Cambridge geneticist A.W.F. Edwards in a recent paper “Human genetic diversity: Lewontin’s fallacy.” R.C. Lewontin is an equally distinguished Cambridge (Mass.) geneticist, known for the strength of his political convictions and his weakness for dragging them into science at every possibile opportunity. Lewontin’s view of race has become near-universal orthodoxy in scientific circles.
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We can all happily agree that human racial classification is of no social value and is positively destructive of social and human relations. That is one reason why I object to ticking boxes on forms and why I object to positive discrimination in job selection. But that doesn’t mean that race is of “virtually no genetic or taxonomic significance.” This is Edwards’s point, and he reasons as follows. However small the racial partition of total variation may be, if such racial characteristics as there are highly correlated with other racial characteristics, they are by definition informative, and therefore of taxonomic significance.
Strike out. Lewontin, like his colleague Gould and other ideological brother in Marxism Diamond all deny race, first and foremost, for ideological reasons, not scientific ones. Though, this doesn’t mean their arguments should be discarded. On the contrary. They should be deconstructed and shown how and why they are wrong.
In 2002, Risch, et al published a paper that confirms the existence of five racial categories (not three [as is commonly though] as ‘Natives’ cluster on their own due to genetic isolation and Melanesians and Australoids are NOT NEGROID; saying so makes race a true ‘social construct’. Sorry PP), writing:
The African branch included three sub-Saharan populations, CAR pygmies, Zaire pygmies, and the Lisongo; the Caucasian branch included Northern Europeans and Northern Italians; the Pacific Islander branch included Melanesians, New Guineans and Australians; the East Asian branch included Chinese, Japanese and Cambodians; and the Native American branch included Mayans from Mexico and the Surui and Karitiana from the Amazon basin. The identical diagram has since been derived by others, using a similar or greater number of microsatellite markers and individuals [8,9]. More recently, a survey of 3,899 SNPs in 313 genes based on US populations (Caucasians, African-Americans, Asians and Hispanics) once again provided distinct and non-overlapping clustering of the Caucasian, African-American and Asian samples [12]: “The results confirmed the integrity of the self-described ancestry of these individuals”. Hispanics, who represent a recently admixed group between Native American, Caucasian and African, did not form a distinct subgroup, but clustered variously with the other groups. A previous cluster analysis based on a much smaller number of SNPs led to a similar conclusion: “A tree relating 144 individuals from 12 human groups of Africa, Asia, Europe and Oceania, inferred from an average of 75 DNA polymorphisms/individual, is remarkable in that most individuals cluster with other members of their regional group” [13]. Effectively, these population genetic studies have recapitulated the classical definition of races based on continental ancestry – namely African, Caucasian (Europe and Middle East), Asian, Pacific Islander (for example, Australian, New Guinean and Melanesian), and Native American.
Pretty damn good for a ‘social construct’, right? Unless the computer somehow consciously knows the result we want and then allocates the clusters according to our desires, but I doubt it. These studies show, definitively, that race as we know it is a biological reality.
They then state in the conclusion:
As we enter this new millennium with an advancing arsenal of molecular genetic tools and strategies, the view of genes as immutable is too simplistic. Every race and even ethnic group within the races has its own collection of clinical priorities based on differing prevalence of diseases. It is a reflection of the diversity of our species – genetic, cultural and sociological. Taking advantage of this diversity in the scientific study of disease to gain understanding helps all of those afflicted. We need to value our diversity rather than fear it. Ignoring our differences, even if with the best of intentions, will ultimately lead to the disservice of those who are in the minority.
One of the best conclusions one can write after an article as ‘controversial’ as that one. We need to embrace our diversity, not destroy it. We need to study it and see how and why we are so diverse, not ruin the diversity making it impossible to study. This also has implications for disease acquisition as well as whether or not one responds to certain drugs (blacks and the drug Bidil, for instance). These inherent differences between races/ethnies need to be studied so we can get everyone the best care they need based on their genetic makeup, without pretending that it doesn’t exist. Pretending that these differences don’t exist does not make them go away.
If race were ‘fake’ and ‘socially constructed’, would there be a success rate of 99.86 percent between self-identified race/ethnicity and genetic structure? Tang et al (2005) write:
We have analyzed genetic data for 326 microsatellite markers that were typed uniformly in a large multiethnic population-based sample of individuals as part of a study of the genetics of hypertension (Family Blood Pressure Program). Subjects identified themselves as belonging to one of four major racial/ethnic groups (white, African American, East Asian, and Hispanic) and were recruited from 15 different geographic locales within the United States and Taiwan. Genetic cluster analysis of the microsatellite markers produced four major clusters, which showed near-perfect correspondence with the four self-reported race/ethnicity categories. Of 3,636 subjects of varying race/ethnicity, only 5 (0.14%) showed genetic cluster membership different from their self-identified race/ethnicity. On the other hand, we detected only modest genetic differentiation between different current geographic locales within each race/ethnicity group. Thus, ancient geographic ancestry, which is highly correlated with self-identified race/ethnicity—as opposed to current residence—is the major determinant of genetic structure in the U.S. population. Implications of this genetic structure for case-control association studies are discussed.
These ‘social constructs’ have some pretty damn good predictive power to guess geographic ancestry (race) 99.86 percent of the time. But isn’t it weird that this so-called ‘social construct’ fits neatly into 4 categories (‘Hispanic’ is not a race, but I assume it would cluster between ‘Natives’ and Europeans, showing that fourth cluster. There hasn’t been enough time for ‘Hispanics’ to cluster into a distinct race, so they cluster in between ‘Natives’ and Europeans)?
If race is a ‘social construct’ as LCs would want you to believe, how do we have these clusters showing this variation? Because they’re genetically similar others. We can then start to wonder about things such as genetic similarity theory and ethnic genetic interests, as they then become a direct result of these genetically similar individuals. Yes we humans are 99.9 percent identical, but what matters is not how genetically distant humans are when being compared with one another, what matters is gene expression. We share over 90 percent of the same genes with dogs, cats, mice, and other great apes. Must mean we are almost all the same and any genetic differences ‘are meaningless’, then!
Think of it this way. People in the same family differ both genotypically and phenotypically. Hereditary traits get passed down through the generations and they stay in that family. If you broaden that to ethnic and the bigger racial groups, you can then see how genetically isolated human populations (key phrase here) do differ, on average, in hereditary traits.
We see racial in sports from swimming, baseball, football, bodybuilding, sprinting, and Strongman. We (somewhat) openly discuss racial differences being the cause for this, yet discussing racial differences in intelligence is taboo.
Liberal Creationists and their denial of race in the modern genomics age is absurd. It’s like people who deny evolution because they don’t understand basic evolutionary theory. Liberal Creationists, too, don’t understand basic evolutionary theory. Race-denialism, when the facts are right in front of you showing how these so-called ‘social constructs’ exist and outright denying them, is very telling. Ideology is the name of the game, not science.
It doesn’t matter how many people believe race doesn’t exist, the underlying realities are still there. LCs can say talk all about changing definitions of race in other countries and the past few hundred years, but this doesn’t address the fact that what we call ‘race’ and ‘ethnicity’ have real biological underpinnings. What we call ‘race’ and ‘ethnicity’ is meaningless. ‘Race’ is a social construct, but a ‘social construct’ of a biological reality. Even if we changed, or even eliminated the words from use, actual genetic differences between races will not go away.
The “Blank Slate”
1700 words
I see a lot of people talking about how there’s not such thing as certain behavior for different races and how we basically, without saying these words, are “blank slates”. People recognize physical differences between races, but not behavioral and cognitive ones? If you say to someone that peoples descended from West Africa have a certain gene, which 70 percent of them have, that give them fast twitch muscle fibers, which fire quickly but tire faster which allows them to win the 100 meter dash and reign over it in the Olympics, no one will call you a racist. A white man has won the World’s Strongest man every year from present day since 1974. Whites and Asians have slow twitch muscle fibers which allow them to be better in strength sports than African descended peoples. Here are the differences between the 2.
Type I fibers are different than type IIb fibers for many reasons. You can think of them as opposites. Type I is for long endurance activities while type IIb is for short fast bursts. Type I fibers are highly oxidative and are not likely to hypertrophy as much. Type IIb fibers are highly gycolytic and tend to hypertrophy more than type I fibers. Type I fibers are also known as red fibers due to their abundant supply of blood. Type IIb fibers have little blood causing them to be white in appearance. source
With that being said, why do people accept physical differences, such as those listed above, and not cognitive and behavioral differences? Why do people believe that “we are all the same” and that we are “blank slates” that are to be molded by our environment when that’s simply not true?
We get lied to from a very early age that we are all the same and that the differences between us only come down to environment, meaning the environment you’re raised in and grow up in, and not talking about the real reason, which is the type of environment that your ancestors evolved in for tens of thousands of years. They deny it because it goes against their liberal narrative of egalitarianism, which is basically a religion to the left. But, if that’s the case, then why do they push forward literal racist programs, such as Affirmative Action, if we are all the same and malleable to our environments? Why not put blacks and other “misfortuned” groups into high SES homes where they can get the correct environment they need to be successful and get high IQ, so they can be successful as IQ is one of the best descriptors for success and outcomes in life? It’s been tried already. It didn’t work.
In 1976, a study was conducted called the Minnesota Transracial Adoption study where they took children of different races who were adopted into different families and tested their IQs at age 7 and again at age 17. A follow-up study was published in 1992. What was found, was that IQs of transracially adopted children didn’t differ at all from children raised by their biological parents in the same area.
According to Dr. David Duke in his book My Awakening: A Path to Racial Understanding, he says that the authors waited about 4 years to publish these findings. They were most likely scared of the backlash they were going to get when they released these findings, which, to be frank, is ridiculous. Why should we walk on egg shells when we have a good study that shows these differences? As said in the study, blacks raised in white families hardly did any better than blacks raised in black families. If the differences supposedly were environmental in the way they say it is, how come blacks raised in rich white families didn’t reach the IQ of whites if “IQ is malleable by the immediate environment”? Because the differences are genetic.
The heritability of IQ is between .75 (as said by the APA) and .90. I like to say .85. So if the heritability is that high, then only a few points of the B-W IQ gap can be explained by environment, with the lion’s share being attributed to genetics.
People may try to point to lead lowering IQ, well, for that to be the case they would have to test the IQ of all racial groups and then test the levels of lead in each subject, which have not been done yet. That throws that out the window.
People may also tout other studies, such as the Eyferth study, which supposedly says a “100 percent environmental cause” for the B-W IQ gap, which is preposterous. First, the mothers were white, which according to the MTRA, white women and black fathers have generally higher IQ children. This is attributed to prenatal factors. One of the single best predictors of IQ is the mother’s IQ. The soldiers in the study were also pre-screened for IQ, which is another flaw in the study. Three percent of white applicants failed compared to 30 percent of black applicants. They also didn’t retest the children again at age adulthood, as did the MTAS.
Another one people like to use is the Tizard study which studies young black, white and mixed-race children in a nursery setting. They were given tests to determine cognitive abilities. The white and black children both had IQs at 102.6 and 106.3 respectively. They also did not test again at adulthood.
Another is the Moore study, which tested 23 black adopted children and 23 black children adopted by middle-class black families. Their findings indicated that blacks adopted to black families scored at 104 compared to the blacks adopted by white families who scored at 117. People may point to this and say “Well, they didn’t differ in their environment and not their genes, so therefore the B-W IQ gap is 100 percent environmental.” Ridiculous. As with the other 2 studies, they were not tested again at adulthood. To say that any of these 3 studies mentioned above prove a 100 percent environmental cause is intellectually dishonest.
Egalitarians love pointing to these studies saying that blacks grow up in bad neighborhoods and don’t get the same things that whites growing up in poor neighborhoods do. Again, ridiculous. It’s just pure wishful thinking by egalitarians to point to these studies to say that there the gap is 100 percent environmental. As I said earlier, it technically is, but not in the way egalitarians think it is. They think we stopped evolving at the neck and that everyone is the same both cognitively and behaviorally which is ridiculous.
There is also what’s known as the “Flynn Effect” (should be the Lynn-Flynn Effect) in which IQ gains have consistently occurred over the decades egalitarians use this data to say that IQ tests test something not genetic in nature
Let’s say Flynn is right. The average black now is as intelligent as the average white in 1945. That’s supposed to show that the race difference in IQ is environmentally caused because there hasn’t been that much genetic change in the white population and the IQ has allegedly gone up 15 points. So, you can have a 15 point difference created by just an environmental change, no one knows why. Some think better nutrition or malnourished brain, etc. That’s also a fallacy. Just because a change in one group over time is due to an environmental change, doesn’t mean, or even make it probable, that a difference between 2 groups at the same time is due to an environmental change. The Flynn Effect make’s that highly unlikely and here’s why.
The Flynn Effect, assuming it’s real, has been acting completely uniformly in every population. Any country you ask, the rate of increase is 3 per decade. That means it’s an environmental factor that affects whites and blacks the same way as well as the whole world. And as a result of this uniform environmental factor, you have a difference in IQ that’s being preserved. That would suggest that the response on the parts of blacks and whites is due to some non-environment factors, a genetic factor, which is making the difference in IQ remain constant as the Flynn Effect goes into effect.
What makes it even more unlikely, in the last 60 years, their environments have become very similar since segregation. These differences don’t exist now, they go to the same schools by court order, same TV shows, same movies, basically same environment for both, and yet, that increasing similarity in the environment, the Flynn Effect, the IQ gap has remained intact. Which means whatever counts for the gap is genetic and not environmental. The more and more similar the environment, the less and less of the difference can be due to the environment and the more and more it must be due to genes. So this 15 point gap surviving these changes in the environment, seems more and more likely to be genetic in origin.
So because this ‘Effect’ is the same across all populations and the gap didn’t close, that means it’s genetic. If the gap persisted even when IQs were rising 3 points per year, the B-W gap has still persisted, proving that it’s genetic.
That is why the Flynn Effect is irrelevant. This “Effect”, has been a slight upward trend in IQ, around 3 points per decade, which, in my opinion, has to do with the advent of better nutrition and an industrialized society. The rise in IQ started around 1880, almost perfectly coinciding with the industrial revolution in America. Along with a more industrialized society, it’s possible to give most citizens in the country good enough nutrition to where they are not iodine deficient (adding iodine to our salt boosted Americans IQs), as well as being deficient in zinc, iron, protein and certain B vitamins which the effects of not getting enough leads to the brain not growing to its full potential, which in turn leads to a lower IQ.
It’s also worth noting that the Flynn Effect is, mostly just better nutrition. Rushton also stated that the Flynn Effect wasn’t on the g factor.
In conclusion, the “blank slate” hypothesis is complete rubbish. We need the truth to come out and come out soon as it has serious implications on policy and the direction that our country is headed due to programs like affirmative action and the like. They need to be ended now.
NotPoliticallyCorrect 