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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
Racial Differences in Grip Strength
1700 words
Strength differences between the races are of big interest to me. Not only due to the evolutionary perspective, but also due to how it relates to health and disease. Hand grip strength (HGS) in men is a good predictor of: Parkinson’s disease (Roberts et al, 2015); lower cardiovascular health profile (Lawman et al, 2016); Alzheimer’s disease (Buchman et al, 2007) and other chronic diseases in men, not in women (Cheung et al, 2013). HGS also predicts diabetes and hypertension (Mainous 3rd et al, 2015), as well as death from all causes, cardiovascular disease (CVD) and cancer in men (Gale et al, 2006). Due to these associations, the study of HGS in men is well warranted. However, here too, we find racial differences and they just so happen to follow trends and corroborate with other data on the mortality of men with lower grip strength.
Araujo et al (2010) obtained data from the Boston Community Health/Bone (BACH/Bone) Survey which included 1,219 randomly selected black, white and ‘Hispanic’ men to assess lean mass, muscle strength, and physical function. Though out of this sample, 10 men didn’t have a DXA performed and 49 men missing data on lean mass, fat mass and Physical Activity for the Elderly (PASE), which left 1,157 men to be analyzed. These studies, however, leave a lot to be desired in how they measure strength (for the purposes that I’m interested in) but they will have to do, for now. Unlike the bench pressing study I wrote about yesterday in which calipers were used to assess body fat, in this study they measured body fat with the DXA scan to assess lean mass. That way, there won’t be any potential confounds, possibly skewing lean mass/fat comparisons. The age of the cohort ranged from 30 to 79 with a mean age of 48.
Table 1 shows the results of the DXA scan, anthropometric data and lean and fat mass. Blacks’ mean lean mass of 124 pounds (mean weight 193 pounds), ‘Hispanics” lean mass was 114 pounds (mean weight 179 pounds) and whites had a mean lean mass of 122 pounds (mean weight 196 pounds). Blacks had a mean grip strength of 89.826 pounds while ‘Hispanics’ had a mean grip strength of 82.698 pounds and whites had a mean grip strength of 88.528 pounds. Blacks had a higher lean mass index than whites by 5 percent, but had a composite physical function score 20 percent lower than whites.
White men had a 25 percent higher average composite physical functioning score, which, when indexed by lean mass and grip, white men had grips 10 percent stronger. White men also scored higher on physical function and lean mass. White men had lower levels of lean muscle mass than blacks and ‘Hispanics’ after controlling for confounding factors, yet whites were still stronger. Since lean mass is related to strength, blacks and ‘Hispanics’ should have had a stronger grip, yet they didn’t. Why?
The authors stated that the reason was unknown since they didn’t test for muscle quality or strength exerted for each unit of muscle. I have proven that whites, on average, are stronger than blacks. If the it were true that blacks were stronger, which is what you see upon first glance viewing table 1 of Araujo et al (2010), then the black population would have lower rates of morbidity and mortality due to higher levels of strength. The black population doesn’t have lower levels of morbidity or mortality. Therefore blacks are not stronger than whites.
Muscular strength is associated with mortality in men (Ruiz et al, 2008; Volaklis, Halle, and Meisenger, 2015), so if the strongest race of men has lower incidences of the above diseases mentioned above along with a higher life expectancy, then there is a good chance that muscular strength is a good predictor of disease within and between race and ethnicity as well. Muscular strength is inversely associated with death from all causes and cancer in men even after adjusting for cardiorespiratory factors. The findings from Ruiz et al (2008) are valid for young and old men (aged 20-82), as well as normal and overweight men.
There are clear associations between muscular strength/hand grip strength and mortality. These differences in mortality are also seen in the United States between race. In 2012, the death rate for all cancer combined was 24 percent higher in black men than in white men. Life expectancy is lower for blacks at 72.3 years compared to 76.7 years for white men (American Cancer Society, 2016). As shown above, men with lower levels of muscular strength have a higher risk of mortality.
As I have asserted in the past, blacks have differing muscle fiber typing (type II) on average when compared to whites (who have type I fibers). Type II muscle fibers are associated with a reduced Vo2 max, which has implications for the health of black Americans. Blacks have lower aerobic capacity along with a greater percentage of type II skeletal muscle fiber (Caesar and Hunter, 2015).
Slow twitch fibers fire through aerobic pathways. Fast twitch (Type II) fibers fire through anaerobic pathways and tire quicker than slow twitch. Each fiber fires off through different pathways, whether they be anaerobic or aerobic. The body uses two types of energy systems, aerobic or anaerobic, which then generate Adenosine Triphosphate, better known as ATP, which causes the muscles to contract or relax. Depending on the type of fibers an individual has dictates which pathway muscles use to contract which then, ultimately, dictate if there is high muscular endurance or if the fibers will fire off faster for more speed.
Differences in muscle fiber typing explain why whites had a stronger grip than non-whites in the BACH/Bone survey. Testing the fiber typings of the three ethnies would have found a higher percentage of type II fibers in blacks, which would account for the lower grip strength despite having higher levels of lean mass when compared to whites.
The apparent ‘paradox’ seen in Araujo et al (2010) is explained by basic physiology. However, in our politically correct society, such differences may be suppressed and thusly people won’t be able to receive the help they need. Race is an extremely useful marker in regards to medicine. By denying average racial differences in numerous anatomical/metabolic/physiologic traits, we deny people the right help they need. Common sense dictates that if such relationships are found, then further research must occur in order to find the cause and a possible solution to the problem.
This study by Araujo et al shows that we need to pay more attention to race when it comes to disease. By denying racial differences we are dooming people to a lower quality of life due to the implicit assumption that we are all the same on the inside (farrrrr from the truth). These average differences in metabolism, anatomy, and physiology do account for some of the variation in disease between race and ethnicity, so this warrants further research. If only we, as a country, can acknowledge racial differences and get people the correct help. Maybe one day we can stop assuming that all races are equal on the inside and when you notice a trend within a particular racial group you find out the cause and whether or not there is any way to ameliorate it.
Muscular strength adds to the protective effect of cardiorespiratory fitness and risk of death in men. That blacks have lower levels of strength than whites, have different muscle fiber typing than whites on average, a lower life expectancy than whites, and higher rates of cancer show that they do not have the physical strength that whites do. What really seals the deal is the fact that blacks have more type II muscle fibers (Caesar and Hunter, 2015). Muscular strength/grip strength is a great predictor of disease in men. Since blacks have lower grip strength yet higher levels of lean mass compared to whites, this show that the difference is due to muscle fiber typing, which, as I have covered in the past, are also associated with cardiometabolic disease and obesity.
Blacks have the highest rate of obesity in America. Looking at obesity rates in America, we see that 69 percent of black men are overweight or obese (remember that black Americans with more African ancestry are less likely to be obese), 71.4 percent of white men are overweight or obese, and 78.6 percent of ‘Hispanic’ men are overweight or obese (Ogden et al, 2016).
Blacks are not stronger than whites. I have compiled enough data to prove that fact. This adds further support for my contention.
References
American Cancer Society. Cancer Facts & Figures for African Americans 2016-2018. Atlanta: American Cancer Society, 2016.
Araujo, A. B., Chiu, G. R., Kupelian, V., Hall, S. A., Williams, R. E., Clark, R. V., & Mckinlay, J. B. (2010). Lean mass, muscle strength, and physical function in a diverse population of men: a population-based cross-sectional study. BMC Public Health,10(1). doi:10.1186/1471-2458-10-508
Buchman, A. S., Wilson, R. S., Boyle, P. A., Bienias, J. L., & Bennett, D. A. (2007). Grip Strength and the Risk of Incident Alzheimer’s Disease. Neuroepidemiology,29(1-2), 66-73. doi:10.1159/000109498
Ceaser, T., & Hunter, G. (2015). Black and White Race Differences in Aerobic Capacity, Muscle Fiber Type, and Their Influence on Metabolic Processes. Sports Medicine,45(5), 615-623. doi:10.1007/s40279-015-0318-7
Cheung, C., Nguyen, U. D., Au, E., Tan, K. C., & Kung, A. W. (2013). Association of handgrip strength with chronic diseases and multimorbidity. Age,35(3), 929-941. doi:10.1007/s11357-012-9385-y
Gale, C. R., Martyn, C. N., Cooper, C., & Sayer, A. A. (2006). Grip strength, body composition, and mortality. International Journal of Epidemiology,36(1), 228-235. doi:10.1093/ije/dyl224
Lawman, H. G., Troiano, R. P., Perna, F. M., Wang, C., Fryar, C. D., & Ogden, C. L. (2016). Associations of Relative Handgrip Strength and Cardiovascular Disease Biomarkers in U.S. Adults, 2011–2012. American Journal of Preventive Medicine,50(6), 677-683. doi:10.1016/j.amepre.2015.10.022
Mainous, A. G., Tanner, R. J., Anton, S. D., & Jo, A. (2015). Grip Strength as a Marker of Hypertension and Diabetes in Healthy Weight Adults. American Journal of Preventive Medicine,49(6), 850-858. doi:10.1016/j.amepre.2015.05.025
Ogden C. L., Carroll, M. D., Lawman, H. G., Fryar, C. D., Kruszon-Moran, D., Kit, B.K., & Flegal K. M. (2016). Trends in obesity prevalence among children and adolescents in the United States, 1988-1994 through 2013-2014. JAMA, 315(21), 2292-2299.
Roberts, H. C., Syddall, H. E., Butchart, J. W., Stack, E. L., Cooper, C., & Sayer, A. A. (2015). The Association of Grip Strength With Severity and Duration of Parkinson’s. Neurorehabilitation and Neural Repair,29(9), 889-896. doi:10.1177/1545968315570324
Ruiz, J. R., Sui, X., Lobelo, F., Morrow, J. R., Jackson, A. W., Sjostrom, M., & Blair, S. N. (2008). Association between muscular strength and mortality in men: prospective cohort study. Bmj,337(Jul01 2). doi:10.1136/bmj.a439
Volaklis, K. A., Halle, M., & Meisinger, C. (2015). Muscular strength as a strong predictor of mortality: A narrative review. European Journal of Internal Medicine,26(5), 303-310. doi:10.1016/j.ejim.2015.04.013
The Testosterone and Fertility Conundrum: A Western Perspective
2750 words
Some people are scared of testosterone. This is no surprise, since a super-majority of people have no background in the human sciences. I’m sure plenty men know what it’s like to have low testosterone, just like some men know what it’s like to have higher T levels than average. What is the optimum level of testosterone? Why are some people scared of this hormone?
Rushton (1997) posited that r/K Selection Theory could be used to classify the races of Man on a spectrum, going from r-selection (having many children but showing little to no parental care) to K-selection (having fewer children but showing a lot of parental care). He stated that the traits of the races were also on the r/K spectrum, with the races having stark differences in morphology. Rushton’s application of r/K theory to humans isn’t completely wrong, though I do have some problems with some of his claims, such as his claims that the races differ in average penis size. He contends that testosterone is the cause for higher crime rates for black Americans and higher rates of prostate cancer in black Americans compared to white Americans.
However, in 2014, Richard et al showed that when controlling for age, blacks had 2.5 to 4.9 percent more testosterone than whites, on average. This cannot explain racial differences in prostate cancer. However, some people may emphatically claim that the races differ in average testosterone, with blacks having 13 percent higher free testosterone than whites on average. The citation that gets used the most to prove that blacks supposedly have higher testosterone than whites is Ross et al (1986), which is based on a sample of 100 people (50 black, 50 white). He claims that it’s when T levels are higher, so it’s a ‘better study’ even though the sample leaves a lot to be desired. A much more robust study showed that the difference was negligible, and not enough to account for the differential prostate cancer rates between the races.
Rohrmann et al (2007) show that there are no differences in circulating testosterone between blacks and whites in a nationally representative sample of American men. Mexicans had the highest levels. There were, however, B-W differences in estradiol production. They couldn’t confirm the other studies that stated that blacks had higher testosterone, possibly due to variations in age or using non-representative samples (that’s the culprit). Their nationally representative sample showed there was no difference in testosterone between blacks is whites, while the meta-analysis showed by Richard et al (2014) showed the difference was negligible at 2.5 to 4.9 percent higher rate of testosterone which doesn’t explain why blacks have a higher rate of acquiring prostate cancer.
The much more likely culprit for blacks having higher rates of prostate cancer, as I have written about before, are environmental factors. The two main factors are receiving less sunlight and diet. There is no evidence that higher levels of testosterone lead to prostate cancer (Michaud, Billups, and Partin, 2015). Contrary to those who say that higher levels of T cause prostate cancer, there is growing evidence that lower levels of T lead to prostate cancer (Park et al, 2015). Put simply, there is no evidence for testosterone’s supposed impact on the prostate (Stattin et al, 2013).
Differences in androgen/androgen receptors have been explained as a cause for racial differences in prostate cancer (Pettaway, 1999), however, these results haven’t been consistent (Stattin et al, 2003) and these differences in circulating androgen may possibly be explained by differences in obesity between the two populations (Gapstur et al, 2002; also see my posts on obesity and race).
Due to the ‘testosterone scare’, some people may believe that having low T is a ‘good thing’, something that’s preferred over being a high T savage. However, testosterone and the androgen receptor gene polymorphism are both associated with competitiveness and confidence in men (Eisenegger et al, 2016) and a reduced risk of cardiovascular disease in elderly men (Ohlsson et al, 2011). Obviously, lower testosterone is related to less overall confidence. People who have the thought in their head that testosterone is a ‘bad hormone’ will believe the negativity about it in the media and popular headlines.
Testosterone alone does not cause violence, but it does cause men to be socially dominant. Testosterone has been shown to increase in the aggressive phases of sports games and when shown artificial humans made to invoke physiologic responses, leading some researchers to argue that testosterone should be classified as a stress hormone. Testosterone does change based on watching one’s favorite soccer team winning or losing in a sample of 21 men (Bernhardt et al, 1998), lending some credence to the claim that testosterone is and should be classified as a stress hormone. Also of interest is that men who administered high levels of testosterone did not report higher levels of aggression (Batrinos, 2012).
I’ve heard some people literally say that having low testosterone is ‘a good thing’. People say this out of ignorance. There are a whole slew of problems associated with low testosterone, including but not limited to: insulin resistance in diabetic men (Grossmann et al, 2008); metabolic syndrome (Tsuijimura et al, 2013); muscle loss (Yuki et al, 2013); stroke and transient ischemic attack (a mini-stroke; Yeap et al, 2009); associated with elevated risk for dementia in older men (Carcaillon et al, 2014); myocardial infarction (heart attack) in diabetic men (Daka et al, 2015) etc. So it seems that the fear of testosterone from those in the anti-testosterone camp are largely blown out of proportion.
Testosterone is also a ‘food’ for the brain, with low levels being related to mental illness, sexual dysfunction, lower quality of life and cognitive impairment (Moffat et al, 2011) in both sexes (Ciocca et al, 2016). Noticed in both men in women with testosterone deficits were: cognitive impairment (reduction of working memory, episodic memory, processing speed, visual-spatial functioning and executive performance); a decrease in sexual activity; anxiety, schizophrenia, depression and stress; and alterations in cortical thickness in the brain. The fact that testosterone is so heavily important to the body’s central functioning is extremely clear. This is why it’s laughable that some people would be happy and brag about having low testosterone.
I recently came across a book called The Testosterone Hypothesis: How Hormones Regulate the Life Cycles of Civilization. Barzilai’s main premise is that the rise and fall of the West is mediated by the hormone testosterone, and due to lower testosterone levels this is one large reason for what is currently occurring in the West. The book has an extremely interesting premise. Barzilai’s hypothesis does line up with the declining levels of testosterone in America (Travison et al, 2007) though other research shows no decline in American testosterone levels from the years 88-91 to 99-04 (Nyante et al, 2007). Moreover, men who had higher level of n-6 in their blood then n-3 were far more likely to be infertile (Safarinejad et al, 2010) a marker of low testosterone (Sharpe, 2012). The ratio of n-6 to n-3 from the years 1935 to 1939 were 8.4 to 1, whereas from the years 1935 to 1985, the ratio increased to about 10 percent (Raper et al, 1992). The ratio of n-6 to n-3, on top of lowering sperm count (which is correlated with testosterone) also has negative effects on male and female cognitive ability (Lassek and Gaulin, 2011).
Barzilai’s research also corroborates Rushton’s (1986) theory of why there are lower birthrates for Europeans around the world. Rushton stated that this cycle has been noticed throughout history, with empires rising and falling due to differential birthrates between the ruling class and the ruled. Rushton also hypothesized that the cultures and gene pools associated with the Graeco-Roman empire were “evolutionary dead ends” (Rushton, 1986: 148). Knowing what we now know about the relationship between cognitive ability, testosterone, and fertility, we now have a plausible hypothesis for Rushton’s hypothesis and one of the (many) reasons why the Graeco-Roman empire collapsed. Rushton further hypothesized that the cause for lower fertility in European populations “may be partly mediated by a psychological process in which the desire to be in control of both oneself and one’s environment is taken to an extreme.” Of course there’s a good chance that this psychological process is mediated/influenced by testosterone.
Europe is the continent with the lowest fertility (ESHRE Capri Workshop Group, 2010). Testosterone has declined in Europe as a whole (Rivas et al, 2014), and this is a strong cause for the lower birthrates in Europe (along with genetic reasons) and in Finland (Perheentupa et al, 2013). The introduction of Westernized diets lowers testosterone, so this is no surprise that a reduction is seen in countries that begin to consume a Western diet. Another probable cause for lower testosterone/fertility in Europe at the moment is the large number of European men that died in WWI and WWII. Those that were more willing to fight died, meaning there was less of a chance he spread his genes. So, over time, this lead to the current cucking of Europe that we are now witnessing.
Testosterone is also hypothesized to have driven evolution (Howard, 2001). Testosterone is such an important part of human evolution and development, so much so that if we had a lower level of the hormone all throughout our evolution that we would be a different species today. Testosterone is needed for sexual functioning, good mental and brain health, fertility, cognitive ability, muscle mass retention in both young and old men, etc. Testosterone is one of the most important hormones for both men and women, and low levels for both sexes are detrimental to a high quality of life. The current data on testosterone and prostate cancer shows that higher levels of testosterone don’t contribute to prostate cancer. Testosterone, then, also isn’t a cause for the racial gap in prostate cancer because other environmental factors better explain it. If people really are happy about having lower testosterone, then I hope they have fun living a life with a low sex drive, lower cognition in old age, lower muscle mass and a higher chance of stroke and metabolic syndrome.
One of the most interesting things about testosterone is the possibility that it explains why civilizations rise and fall. There is anecdotal evidence from Rushton, as well as his theorizing that the higher classes in Rome didn’t breed which led to their downfall. We now know that lower fertility rates for men are associated with lower testosterone, so along with Barzilai’s thesis of testosterone causing the rise and fall of civilizations, Rushton’s theorizing of the cause of lower European fertility and the cause of the fall of the Graeco-Roman empire.
Testosterone is an extremely important hormone, one that drives human evolution and society formation since it’s associated with dominance and confidence. Low testosterone is looked at as ‘good’ because those with higher intelligence have lower levels of the hormone (indicated by lower confidence and having sex at a later age). I showed that the higher IQ East Asian men have a problem finding dates and being looked at as sexually attractive (even though they rated themselves as average). Along with lower East Asian fertility, specifically in Japan, does it seem to you like the high IQ people are more desired if they are having problems keeping their birthrates up? The fact of the matter is, lower levels of testosterone are correlated with lower levels of fertility. If men don’t have as much testosterone pumping through their veins, they will be less likely to have sex and thusly reproduce.
References
Batrinos, M. L. (2012). Testosterone and aggressive behavior in man. International Journal of Endocrinology & Metabolism,10(3), 563-568. doi:10.5812/ijem.3661
Bernhardt, P. C., Jr, J. M., Fielden, J. A., & Lutter, C. D. (1998). Testosterone changes during vicarious experiences of winning and losing among fans at sporting events. Physiology & Behavior,65(1), 59-62. doi:10.1016/s0031-9384(98)00147-4
Carcaillon, L., Brailly-Tabard, S., Ancelin, M., Tzourio, C., Foubert-Samier, A., Dartigues, J., . . . Scarabin, P. (2014). Low testosterone and the risk of dementia in elderly men: Impact of age and education. Alzheimer’s & Dementia,10(5). doi:10.1016/j.jalz.2013.06.006
Ciocca G, Limoncin E, Gravina GL, et al. Is testosterone a food for brain? Sex Med Rev 2016;4:15-25.
Daka, B., Langer, R. D., Larsson, C. A., Rosén, T., Jansson, P. A., Råstam, L., & Lindblad, U. (2015). Low concentrations of serum testosterone predict acute myocardial infarction in men with type 2 diabetes mellitus. BMC Endocrine Disorders,15(1). doi:10.1186/s12902-015-0034-1
Eisenegger, C., Kumsta, R., Naef, M., Gromoll, J., & Heinrichs, M. (2016). Testosterone and androgen receptor gene polymorphism are associated with confidence and competitiveness in men. Hormones and Behavior. doi:10.1016/j.yhbeh.2016.09.011
, , , , , . Serum androgen concentrations in young men: a longitudinal analysis of associations with age, obesity, and race—the CARDIA male hormone study. Cancer Epidemiol Biomarkers Prev 2002; 11: 1041–7
Grossmann, M., Thomas, M. C., Panagiotopoulos, S., Sharpe, K., Macisaac, R. J., Clarke, S., . . . Jerums, G. (2008). Low Testosterone Levels Are Common and Associated with Insulin Resistance in Men with Diabetes. The Journal of Clinical Endocrinology & Metabolism,93(5), 1834-1840. doi:10.1210/jc.2007-2177
Howard JM (2001): Androgens in human evolution. A new explanation of human evolution.
Lassek, W. D., & Gaulin, S. J. (2011). Sex Differences in the Relationship of Dietary Fatty Acids to Cognitive Measures in American Children. Frontiers in Evolutionary Neuroscience,3. doi:10.3389/fnevo.2011.00005
Michaud, J. E., Billups, K. L., & Partin, A. W. (2015). Testosterone and prostate cancer: an evidence-based review of pathogenesis and oncologic risk. Therapeutic Advances in Urology,7(6), 378-387. doi:10.1177/1756287215597633
Moffat, S. D., Zonderman, A. B., Metter, E. J., Blackman, M. R., Harman, S. M., & Resnick, S. M. (2002). Longitudinal Assessment of Serum Free Testosterone Concentration Predicts Memory Performance and Cognitive Status in Elderly Men. The Journal of Clinical Endocrinology & Metabolism,87(11), 5001-5007. doi:10.1210/jc.2002-020419
Nyante, S. J., Graubard, B. I., Li, Y., Mcquillan, G. M., Platz, E. A., Rohrmann, S., . . . Mcglynn, K. A. (2011). Trends in sex hormone concentrations in US males: 1988-1991 to 1999-2004. International Journal of Andrology,35(3), 456-466. doi:10.1111/j.1365-2605.2011.01230.x
Ohlsson C, Barrett-Connor E, Bhasin S, et al. High serum testosterone is associated with reduced risk of cardiovascular events in elderly men: the MrOS (Osteoporotic Fractures in Men) study in Sweden. J Am Coll Cardiol. 2011; 58(16):1674-1681.
Park, J., Cho, S. Y., Jeong, S., Lee, S. B., Son, H., & Jeong, H. (2015). Low testosterone level is an independent risk factor for high-grade prostate cancer detection at biopsy. BJU International,118(2), 230-235. doi:10.1111/bju.13206
Perheentupa, A., Makinen, J., Laatikainen, T., Vierula, M., Skakkebaek, N. E., Andersson, A., & Toppari, J. (2012). A cohort effect on serum testosterone levels in Finnish men. European Journal of Endocrinology,168(2), 227-233. doi:10.1530/eje-12-0288
Pettaway CA. Racial differences in the androgen/androgen receptor pathway in prostate cancer. J Natl Med Assoc 1999, 91: 653:650
Raper, N. R., Cronin, F. J., & Exler, J. (1992). Omega-3 fatty acid content of the US food supply. Journal of the American College of Nutrition,11(3), 304-308. doi:10.1080/07315724.1992.10718231
Richard, A., Rohrmann, S., Zhang, L., Eichholzer, M., Basaria, S., Selvin, E., . . . Platz, E. A. (2014). Racial variation in sex steroid hormone concentration in black and white men: a meta-analysis. Andrology,2(3), 428-435. doi:10.1111/j.2047-2927.2014.00206.x
Rivas AM, Mulkey Z, Lado-Abeal J, Yarbrough S. Diagnosing and managing low serum testosterone. Proc (Bayl Univ Med Cent) 2014;27:321-324
Rohrmann, S., Nelson, W. G., Rifai, N., Brown, T. R., Dobs, A., Kanarek, N., . . . Platz, E. A. (2007). Serum Estrogen, But Not Testosterone, Levels Differ between Black and White Men in a Nationally Representative Sample of Americans. The Journal of Clinical Endocrinology & Metabolism,92(7), 2519-2525. doi:10.1210/jc.2007-0028
Ross R, Bernstein L, Judd H, Hanisch R, Pike M, Henderson B. Serum testosterone levels in healthy young black and white men. J Natl Cancer Inst. 1986 Jan;76(1):45–48
Rushton, J. P. (1986). Gene-Culture Coevolution and Genetic Similarity Theory: Implications for Ideology, Ethnic Nepotism, and Geopolitics. Politics and the Life Sciences,4(02), 144-148. doi:10.1017/s0730938400004706
Rushton J P (1997). Race, Evolution, and Behavior. A Life History Perspective (Transaction, New Brunswick, London).
Safarinejad, M. R., Hosseini, S. Y., Dadkhah, F., & Asgari, M. A. (2010). Relationship of omega-3 and omega-6 fatty acids with semen characteristics, and anti-oxidant status of seminal plasma: A comparison between fertile and infertile men. Clinical Nutrition,29(1), 100-105. doi:10.1016/j.clnu.2009.07.008
Sharpe, R. M. (2012). Sperm counts and fertility in men: a rocky road ahead. EMBO reports,13(5), 398-403. doi:10.1038/embor.2012.50
Stattin, P., Lumme, S., Tenkanen, L., Alfthan, H., Jellum, E., Hallmans, G., . . . Hakama, M. (2003). High levels of circulating testosterone are not associated with increased prostate cancer risk: A pooled prospective study. International Journal of Cancer,108(3), 418-424. doi:10.1002/ijc.11572
Travison, T. G., Araujo, A. B., O’Donnell, A. B., Kupelian, V., & Mckinlay, J. B. (2007). A Population-Level Decline in Serum Testosterone Levels in American Men. The Journal of Clinical Endocrinology & Metabolism,92(1), 196-202. doi:10.1210/jc.2006-1375
Tsujimura, A., Miyagawa, Y., Takezawa, K., Okuda, H., Fukuhara, S., Kiuchi, H., . . . Nonomura, N. (2013). Is Low Testosterone Concentration a Risk Factor for Metabolic Syndrome in Healthy Middle-aged Men? Urology,82(4), 814-819. doi:10.1016/j.urology.2013.06.023
Yeap, B. B., Hyde, Z., Almeida, O. P., Norman, P. E., Chubb, S. A., Jamrozik, K., . . . Hankey, G. J. (2009). Lower Testosterone Levels Predict Incident Stroke and Transient Ischemic Attack in Older Men. Endocrine Reviews,30(4), 411-411. doi:10.1210/edrv.30.4.9994
Yuki, A., Otsuka, R., Kozakai, R., Kitamura, I., Okura, T., Ando, F., & Shimokata, H. (2013). Relationship between Low Free Testosterone Levels and Loss of Muscle Mass. Scientific Reports,3. doi:10.1038/srep01818
SAT and KFC
by Scott Jameson
700 words
For my first post on this blog, I thought I’d talk about something relevant to the mission of the blog: Political Correctness. I’m very grateful to RaceRealist for inviting me to hop on board here (although I should put out the categorical disclaimer that me posting here is not in and of itself an endorsement of any given thing he’s said over the years).
This is going to be something of an opinion essay about why denying reality is silly: because you still have to live in it. Most of my content is going to be more empirically driven, as you’re used to on this blog. Bear with me.
The SAT’s name change story is a classic case of “Political Correctness,” and is mirrored by KFC’s story of adapting to new nutritional standards. For those out of the loop: after the public realized how unhealthy fried foods are, Kentucky Fried Chicken changed its name to KFC. The point was to make the unhealthy nature of the food one conceptual extrapolation away from the name itself, in hopes that the public would not bother to recall what the “F” stood for.
SAT originally stood for “Scholastic Aptitude Test.” It was (and is) a test to determine how apt you are for scholarly endeavors. Put bluntly, it’s a somewhat sloppy IQ test oriented towards scholarly settings in particular. Of course, that name was too accurate, so it fell out of favor. The public does not want to live in a world wherein poor students are less apt than rich students and Black students are less apt than White students, and so the Scholastic Aptitude Test became the Scholastic Assessment Test. In order to be offended by that, you have to remember that what’s being assessed is aptitude and that nothing has changed. Like “KFC,” it was one conceptual extrapolation away from the reality at hand. Most people were probably too harebrained to see through that.
For some reason, they kept rolling with it. It became an alleged Reasoning Test, and then simply a series of letters that used to be an abbreviation: “the SAT,” no doubt an homage to The Colonel and the chicken he hawks. They’re both just a series of letters now – the unpleasant realities contained therein have been conceptually sterilized. Like the SAT, the nutritional content of the chicken hasn’t changed as much as the name has.
You may suspect that I’m simply flinging excrement in the general direction of The College Board, but there’s a point to what I’m saying here. What we call “Political Correctness” is a pervasive scrubbing of reality out of the consciousness of the public at large, especially the young. There was a time when people were allowed to say things like “I do not enjoy living around Blacks/Whites/Hispanics/whomever.” “Political Correctness” entered from stage left, and then Boomers had to say “bad schools” and “bad neighborhood” instead. Odds are, the Boomers understood the connotative meanings, at least at first. But if you asked millennials what those terms are, I’d bet on most of them actually being ignorant enough to think that the schools are themselves the problem. Nobody ever pointed out to these kids that almost all of the “bad schools” – the schools with low average test scores – are simply full of Hispanics (Mestizos) and African Americans who have low average test scores regardless of what school they’re in, and that the supermajority of all of the “good schools” aren’t. Anyone who doesn’t know this has been deliberately rendered ignorant of a reality that is important to their lives.
What we call “Political Correctness” is in fact the successful, systematic obfuscation of reality, and having reality perpetually hidden from you is dangerous. That is why we at this blog are NotPoliticallyCorrect. As long as I’m here, I can promise you my best attempt at discovering and conveying the truth in the NotPoliticallyCorrect fashion exemplified thus far by RaceRealist: bringing you interesting truths, obscure truths, and of course, controversial truths.
*****
I’m not the first to make the SAT-KFC comparison, by the way. After I wrote this article, I looked around for sources only to dredge this up.
Psychology, Anti-Hereditarianism, and HBD
3800 words
Abstract
The denial of human nature is extremely prevalent, most noticeably in our institutions of higher learning. To most academics, the fact that there could be population differences that are genetic in nature is troubling for many people. However, denying genetic/biological causes for racial differences is 1) intellectually dishonest; 2) will lead to negative health outcomes for populations due to the assumption that all human populations are the same; and 3) the ‘lie of equality’ will not allow all human populations to reach their ‘potential’ to be as good as they can be due to the fact that implicit assumption that all human populations are the same. Anti-hereditarians fully deny any and all genetic explanations for human differences, believing that human brain evolution somehow halted around 50-100 kya. Numerous studies show that race is a biological reality; it doesn’t matter what we call the clusters as those are the social constructs. The contention is that ‘all brains are the same color’ (Nisbett, 2007; for comment see my article Refuting Richard Nisbett), and that evolution in differing parts of the world for the past 50,000 years was not enough for any meaningful population differences between people. But to accept that means you must accept the fact that the brain is the only organ that is immune to natural selection. Does that make any sense? I will show that these differences do exist and should be studied, as free of any bias as possible, with every possible hypothesis being looked at and not discarded.
Evolution is true. It’s not ‘only a theory’ (as some anti-evolutionists contend). Anti-evolutionists do not understand the definition of the word ‘theory’. Richard Dawkins (2009) wrote that a theory is a scheme or system of ideas or statements held as an explanation or account of a group of facts or phenomena. This is in stark contrast to the layperson’s definition of the word theory, which means ‘just a guess’. Evolution is a fact. What biologists argue with each other about is the mechanisms behind evolution, for any quote-mining Creationists out there.
We know that evolution is a fact and it is the only game in town (Dawkins, 2009) to explain the wide diversity and variation we see on our planet. However, numerous scholars deny the effect of evolution on human behavior (most residing in the social sciences, but other prominent biologists have denied (or implied there were no differences between us and our ancestors) the effect of human evolution on behavior and cognition; Gould 1981, 1996, for a review of Gould 1996, see my article Complexity, Walls, 0.400 Hitting and Evolutionary “Progress” and Stephen Jay Gould and Anti-Hereditarianism; Mayr 1963; see Cochran and Harpending 2009). A prominent neuroscientist, who I have written about here, Herculano-Houzel, implied that Neanderthals and Antecessor may have been just as intelligent as we are due to a neuronal count in a similar range to ours (Herculano-Houzel 2013). This raises an interesting question (which I have tackled here and will return to in the future): did our recent hominin ancestors at least have the capacity for similar intellect to ours (Villa and Roebroeks, 2014; Herculano-Houzel and Kaas, 2011)? It is interesting that neuronal scaling rules hold for our extinct ancestors, and this question is most definitely worth looking into.
Whatever the case may be in regards to recent human evolution and our extinct hominin ancestors, human evolution has increased in the past 10,000 years (Cochran and Harpending, 2009; Wade, 2014). This is due to the dispersal of Anatomical Modern Humans (AMH) OoA around 70 kya; and with this geographical isolation, populations began to diverge with no interbreeding with each other. However, this is noticed most in ‘Native’ Americans, who show no gene flow with other populations due to being genetically isolated (Villena et al, 2000). Who’s to say that evolution stops at the neck, and no further evolution occurs on the brain? Is the brain itself exempt from the laws of natural selection? We know that there is no/hardly any gene flow between populations before the advent of modern-day technology and vehicles; we know that humans differ on morphological and anatomical traits, why are genetic differences out of the question, especially when genetic differences may explain, in part, some of the variation between populations?
We know that evolution is true, without a reasonable doubt. So why, do some researchers contend, is the human brain exempt from such selective pressures?
A theoretical article by Winegard, Winegard, and Boutwell (2017) was just released on January 17th. In the article, they argue that social scientists should integrate HBD into their models. Social scientists do not integrate genetics into their models, and the longer one studies social sciences, the more likely it is they will deny human nature, regardless of political leaning (Perry and Mace, 2010). This poses a problem. By completely ignoring a huge variable (possible genetic differences), this has the potential to harm people’s health, as race is a very informative marker when discussing diseases acquisition as well as whether certain drugs will work on two individuals of different races (Risch et al, 2002; Tang et al, 2005; Wade, 2014). People who deny the usefulness of race, even in a medical context, endanger the lives of individuals from different races/ethnies since they assume that all humans are the same inside, despite ‘superficial differences’ between populations.
The notion that all human populations—genetic isolation and evolution in differing ecosystems/climates/geographic locales be damned—is preposterous to anyone who has a true understanding of evolution. Why should man’s brain be the only organ on earth exempt from the forces of natural selection? Why do egalitarians assume that all humans are the same and have the same psychological faculties compared to other humans, despite the fact that rapid evolution has occurred within the human species within the last 10,000 years?
To see some of the most obvious ways to see natural selection in action in human populations, one should look to the Inuits (Fumagalli, 2015; Daanen and Lichtenbelt, 2016; NIH, 2015; Cardona et al, 2014; Tishkoff, 2015; Ford, McDowell, and Pierce, 2015; Galloway, Young, and Bjerregaard, 2012; Harper, 2015). Global warming is troubling to some researchers, with many researchers suggesting that global warming will have negative effects on the health and food security of the Inuit (Ford et al, 2014, 2016; Ford, 2012, 2009; Wesche, 2010; Furgal and Seguin, 2006; McClymont and Myers, 2012; Petrasek et al, 2015; Rosol, Powell-Hellyer, and Chan, 2016; Petrasek, 2014; WHO, 2003). I could go on and on citing journal articles for both claims, but you get the point already. The main point is this: we know the Inuit have evolved for their climate, and a (possible) climate change would then have a negative effect on their quality of life due to their adaptations to the cold weather climate. However, egalitarians still contend, with these examples and numerous others I could cite, that any and all differences within and between human populations can be explained by socio-cultural factors and not any genetic ones.
One of the best examples of genetic isolation in a geographic locale that is the complete opposite from the environment of evolutionary adaptedness (EEA; Kanazawa, 2004), the African savanna in which we evolved in. I did entertain the idea of the Savanna hypothesis, and while I do believe that it could explain a lot of the variance in IQ between countries (Kanazawa, 2007), his hypothesis doesn’t make sense with what we know about human evolution over the past 10,000 years.
The most obvious differences we can see between populations is differences in skin color. Skin color does not signify race, per se, but it is a good indicator. Skin color is an adaptation to UV radiation (Jablonski and Chaplin, 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.
Is General Intelligence Domain-Specific?
1600 words
Is the human brain ‘special’? Not according to Herculano-Houzel; our brains are just linearly scaled-up primate brains. We have the number of neurons predicted for a primate of our body size. But what does this have to do with general intelligence? Evolutionary psychologists also contend that the human brain is not ‘special’; that it is an evolved organ just like the rest of our body. Satoshi Kanazawa (2003) proposed the ‘Savanna Hypothesis‘ which states that more intelligent people are better able to deal with ‘evolutionary novel’ situations (situations that we didn’t have to deal with in our ancestral African environment, for example) whereas he purports that general intelligence does not affect an individuals’ ability to deal with evolutionarily familiar entities and situations. I don’t really have a stance on it yet, though I do find it extremely interesting, with it making (intuitive) sense.
Kanazawa (2010) suggests that general intelligence may both be an evolved adaptation and an ‘individual-difference variable’. Evolutionary psychologists contend that evolved psychological adaptations are for the ancestral environment which was evolved in, not in any modern-day environment. Kanazawa (2010) writes:
The human brain has difficulty comprehending and dealing with entities and situations that did not exist in the ancestral environment. Burnham and Johnson (2005, pp. 130–131) referred to the same observation as the evolutionary legacy hypothesis, whereas Hagen and Hammerstein (2006, pp. 341–343) called it the mismatch hypothesis.
From an evolutionary perspective, this does make sense. A perfect example is Eurasian societies vs. African ones. you can see the evolutionary novelty in Eurasian civilizations, while African societies are much closer (though obviously not fully) to our ancestral environment. Thusly, since the situations found in Africa are not evolutionarily novel, it does not take high levels of g to survive in, while Eurasian societies (which are evolutionarily novel) take much higher levels of g to live and survive in.
Kanazawa rightly states that most evolutionary psychologists and biologists contend that there have been no changes to the human brain in the last 10,000 years, in line with his Savanna Hypothesis. However, as I’m sure all readers of my blog know, there were sweeping changes in the last 10,000 years in the human genome due to the advent of agriculture, and, obviously, new alleles have appeared in our genome, however “it is not clear whether these new alleles have led to the emergence of new evolved psychological mechanisms in the last 10,000 years.”
General intelligence poses a problem for evo psych since evolutionary psychologists contend that “the human brain consists of domain-specific evolved psychological mechanisms” which evolved specifically to solve adaptive problems such as survival and fitness. Thusly, Kanazawa proposes in contrast to other evolutionary psychologists that general intelligence evolved as a domain-specific adaptation to deal with evolutionary novel problems. So, Kanazawa says, our ancestors didn’t really need to think inorder to solve recurring problems. However, he talks about three major evolutionarily novel situations that needed reasoning and higher intelligence to solve:
1. Lightning has struck a tree near the camp and set it on fire. The fire is now spreading to the dry underbrush. What should I do? How can I stop the spread of the fire? How can I and my family escape it? (Since lightning never strikes the same place twice, this is guaranteed to be a nonrecurrent problem.)
2. We are in the middle of the severest drought in a hundred years. Nuts and berries at our normal places of gathering, which are usually plentiful, are not growing at all, and animals are scarce as well. We are running out of food because none of our normal sources of food are working. What else can we eat? What else is safe to eat? How else can we procure food?
3. A flash flood has caused the river to swell to several times its normal width, and I am trapped on one side of it while my entire band is on the other side. It is imperative that I rejoin them soon. How can I cross the rapid river? Should I walk across it? Or should I construct some sort of buoyant vehicle to use to get across it? If so, what kind of material should I use? Wood? Stones?
These are great examples of ‘novel’ situations that may have arisen, in which our ancestors needed to ‘think outside of the box’ in order to survive. Situations such as this may be why general intelligence evolved as a domain-specific adaptation for ‘evolutionarily novel’ situations. Clearly, when such situations arose, our ancestors who could reason better at the time these unfamiliar events happened would survive and pass on their genes while the ones who could not die and got selected out of the gene pool. So general intelligence may have evolved to solve these new and unfamiliar problems that plagued out ancestors. What this suggests is that intelligent people are better than less intelligent people at solving problems only if they are evolutionarily novel. On the other hand, situations that are evolutionarily familiar to us do not take higher levels of g to solve.
For example, more intelligent individuals are no better than less intelligent individuals in finding and keeping mates, but they may be better at using computer dating services. Three recent studies, employing widely varied methods, have all shown that the average intelligence of a population appears to be a strong function of the evolutionary novelty of its environment (Ash & Gallup, 2007; D. H. Bailey & Geary, 2009; Kanazawa, 2008).
Who is more successful, on average, over another in modern society? I don’t even need to say it, the more intelligent person. However, if there was an evolutionarily familiar problem there would be no difference in figuring out how to solve the problem, because evolution has already ‘outfitted’ a way to deal with them, without logical reasoning.
Kanazawa then talks about evolutionary adaptations such as bipedalism (we all walk, but some of us are better runners than others); vision (we can all see, but some have better vision than others); and language (we all speak, but some people are more proficient in their language and learn it earlier than others). These are all adaptations, but there is extensive individual variation between them. Furthermore, the first evolved psychological mechanism to be discovered was cheater detection, to know if you got cheated while in a ‘social contract’ with another individual. Another evolved adaptation is theory of mind. People with Asperger’s syndrome, for instance, differ in the capacity of their theory of mind. Kanazawa asks:
If so, can such individual differences in the evolved psychological mechanism of theory of mind be heritable, since we already know that autism and Asperger’s syndrome may be heritable (A. Bailey et al., 1995; Folstein & Rutter, 1988)?
A very interesting question. Of course, since it’s #2017, we have made great strides in these fields and we know these two conditions to be highly heritable. Can the same be said for theory of mind? That is a question that I will return to in the future.
Kanazawa’s hypothesis does make a lot of sense, and there is empirical evidence to back his assertions. His hypothesis proposes that evolutionarily familair situations do noot take any higher levels of general intelligence to solve, whereas novel situations do. Think about that. Society is the ultimate evolutionary novelty. Who succeeds the most, on average, in society? The more intelligent.
Go outside. Look around you. Can you tell me which things were in our ancestral environment? Trees? Grass? Not really, as they aren’t the same exact kinds as we know from the savanna. The only thing that is constant is: men, women, boys and girls.
This can, however, be said in another way. Our current environment is an evolutionary mismatch. We are evolved for our past environments, and as we all know, evolution is non-teleological—meaning there is no direction. So we are not selected for possible future environments, as there is no knowledge for what the future holds due to contingencies of ‘just history’. Anything can happen in the future, we don’t have any knowledge of any future occurences. These can be said to be mismatches, or novelties, and those who are more intelligent reason more logically due to the fact that they are more adept at surviving evolutionary novel situations. Kanazawa’s theory provides a wealth of information and evidence to back his assertion that general intelligence is domain-specific.
This is yet another piece of evidence that our brain is not special. Why continue believing that our brain is special, even when there is evidence mounting against it? Our brains evolved and were selected for just like any other organ in our body, just like it was for every single organism on earth. Race-realists like to say “How can egalitarians believe that we stopped evolving at the neck for 50,000 years?” Well to those race-realists who contend that our brains are ‘special’, I say to them: “How can our brain be ‘special’ when it’s an evolved organ just like any other in our body and was subject to the same (or similar) evolutionary selective pressures?”
In sum, the brain has problems dealing with things that were not in its ancestral environment. However, those who are more intelligent will have an easier time dealing with evolutionarily novel situations in comparison to people with lower intelligence. Look at places in Africa where development is still low. They clearly don’t need high levels of g to survive, as it’s pretty close to the ancestral environment. Conversely, Eurasian societies are much more complex and thus, evolutionarily novel. This may be one reason that explains societal differences between these populations. It is an interesting question to consider, which I will return to in the future.
Expounding On My Theory for Racial Differences In Sports
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In the past, I’ve talked about why the races differ—at the extremes—(and the general population, but the extremes put the picture into focus) in terms of what sports they compete and do best in. These differences come down to morphology somatype, physiology. People readily admit racial differences in sports and—rightly say—that these differences are largely genetic in nature. Why is it easier for people to accept racial differences in sports and not accept other truisms, like racial IQ differences?
I’ve muscle fiber typing and how the variances in fiber typing dictate which race/ethny performs best at which sport. I’ve also further evidence that blacks have type II fibers (responsible for explosive power), which leads to a reduced Vo2 max. This lends yet more credence to my theory of racial differences in sports—black Americans (West African descendants) have the fiber typing that is associated with explosive power, less so with endurance activities. Since I’ve documented evidence on the differences in sports such as baseball, football, swimming and jumping, bodybuilding, and finally strength sports, tonight I will talk about the evolutionary reasons for muscle fiber and somatype differences that will have us better understand the evolutionary conditions in which these traits evolved and why they got selected for.
Most WSM winners are from Nordic countries or have Nordic ancestry. There’s a higher amount of slow twitch fibers in Nordics and East Asians (and Kenyans) which is more conducive to strength and less conducive to ‘explosive’ sports. West Africans and their descendants dominate in sprinting competitions. Yea yea yea white guy won in 1960. So they will be less likely to be in strength comps and more likely to win BBing and physique comps. This is what we see.
Only three African countries have placed in the top ten in the WSM (Kenya, Namibia, and Nigeria, however, one competitor from Namibia I was able to find has European ancestry). Here is a video of a Nigerian Strongest Man competition (notice how his chest isn’t up and his hips rise before the bar reaches his knees, horrible form). Fadesere Oluwatofunmi is Nigeria’s Strongest Man, competing in the prestigious Arnold Classic, representing Nigeria. However, men such as Fadesere Olutaofunmi are outliers.
Now for a brief primer on muscle fibers and which pathways they fire through. Understanding this aspect of the human body is paramount to understanding how and why the races differ in elite competition.
Life history and muscle fiber typing
Slow twitch fibers fire through aerobic pathways. Breaking down fats and proteins takes longer through aerobic respiration. Moreover, in cold temperatures, the body switches from burning fat to burning carbohydrates for energy, which will be broken down slower due to the aerobic perspiration. Slow twitch (Type I) fibers fire through aerobic pathways and don’t tire nearly as quickly as type II fibers. Also, CHO reserves will be used more in cold weather. The body’s ability to use oxygen decreases in cold weather as well, so having slow twitch fibers is ideal (think about evolution thousands of years ago). Type I fibers fire off slower so they’ll be able to be more active for a longer period of time (studies have shown that Africans with Type II fibers hit a ‘wall’ after 40 seconds of explosive activity, which is why there are so few West-African descended marathon runners, powerlifters, Strongmen, etc). Those who possess these traits will have a higher chance to survive in these environments. Those with slow twitch fibers also have to use more oxygen. They have larger blood vessels, more mitochondria and higher concentrations of myoglobin which gives the muscles its reddish color.
Each fiber fires off through different pathways, whether they be anaerobic or aerobic. The body uses two types of energy systems, aerobic or anaerobic, which then generate Adenosine Triphosphate, better known as ATP, which causes the muscles to contract or relax. Depending on the type of fibers an individual has dictates which pathway muscles use to contract which then, ultimately, dictate if there is high muscular endurance or if the fibers will fire off faster for more speed.
Type I fibers lead to more strength and muscular endurance as they are slow to fire off, while Type II fibers fire quicker and tire faster. Slow twitch fibers use oxygen more efficiently, while fast twitch fibers do not burn oxygen to create energy. Slow twitch muscles delay firing which is why the endurance is so high in individuals with these fibers whereas for those with fast twitch fibers have their muscles fire more explosively. Slow twitch fibers don’t tire as easily while fast twitch fibers tire quickly. This is why West Africans and their descendants dominate in sprinting and other competitions where fast twitch muscle fibers dominate in comparison to slow twitch.
Paleolithic Europeans who had more stamina spread more of their genes to the next generation as their genotype was conducive to reproductive success in Ice Age Europe. Conversely in Africa, those who could get away from predators and could hunt prey more efficiently survived. Over time, frequencies of genes related to what needed to be done to survive in those environments increased, along with the frequencies of muscle fibers in the races.
Racial differences in anatomy and physiology
Along with muscle fiber differences, blacks and whites also have differences in fat-free body mass, bone density, distribution of subcutaneous fat, length of limbs relative to the trunk, and body protein contents (Wagner and Heyward, 2000). These differences are noticed and talked about in the scientific literature, even in University biology and anatomy textbooks. However, in terms of University textbooks, authors who recognize the concept of race do so in spite of what other authors write (Hallinan, 1994). Furthermore, Strkalj and Solyali (2010) analyzed 18 English textbooks on anatomy and concluded that discussion of race was ‘superficial’ and the content ‘outdated’, i.e., using the ‘Mongoloid, Caucasoid, Negroid terminology (I still do out of habit). They conclude that most mentions of race are either not mentioned in anatomy textbooks or are only ‘superficially accounted for in textbooks’. Clearly, though they are outdated, some textbooks do talk about human biological diversity, though the information needs to be updated (especially now). The center of mass in blacks is 3 percent higher than in whites, meaning whites have a 1.5 percent speed advantage in swimming while blacks have a 1.5 percent speed difference in sprinting. East Asians that are the same height as whites are even more favored in swimming, however, they are shorter on average so that’s why they do not set world records (Bejan, Jones, and Charles, 2010).
For another hand grip strength (HGP) test, see Leong et al (2016). Most studies on HGS are done on Caucasian populations with little data for non-Caucasoid populations. They found that HGS values were higher for North America and Europe, intermediate in China, South America and the Middle East, and the lowest in South Asia, Southeast Asia, and Africa. These are, most likely, average Joes and not elite BBers or strength trainers. This is one of the best papers I’ve come across on this matter (though I would kill to have a nice study done on the three classical races and their performance on the Big 3 lifts: squat, bench press and deadlift; I’m positive it would be Asian/white and blacks as the tail end).
Among other physical differences is brain size and hip width. Blacks have narrower hips than whites who have narrower hips than Asians (Rushton, 1997: 163). Bigger-brained babes are more than likely born to women who have wider hips. If you think about athletic competition, one with wide hips will get decimated by one with narrower hips as he will be better able to move. People with big crania, in turn, have the hip structure to birth big brains. This causes further division between racial groupings in sports competition.
Some people may dispute a genetic causation and attribute the success of, say, Kenyan marathoners (the Kalenjin people) and attribute the effects to the immediate environment (not ancestral), training and willpower (see here for discussion). This Kenyan subpopulation also has the morphology conducive to success in marathons (tall and lengthy), as well as type II muscle fibers (which is why Kenya placed in the WSM).
I would also like to see a study of men in their prime (age 21 to 24) from European, Africans, and East Asian backgrounds with a high n (for a study like this it’d be 20 to 30 participants for each race), with good controls. You’d see, in my opinion, East Asians slightly nudge out whites who destroy blacks. The opposite would occur in sports that use type II fibers. West Africans also have the gene variant ACTN3 which is associated with explosive sports.
For a better (less ethical study) we can use a thought experiment.
We take two babes fresh out of the womb (one European, the other West African) and keep them locked in a metabolic chamber for their whole entire lives. We keep them in the chamber until they die and monitor them, feeding them the same exact diet and giving them the same amount of attention. They start training at age 15. Who will be stronger in their prime (the European man)? Who will have more explosive power (the West African man)? A simple thought experiment can have one thinking about intrinsic racial differences in things the average American watches in their everyday lives. The subject of racial differences in sports is a non-taboo subject, however, the subject of racial differences in intelligence is a big no-no.
Think about that for a second. People obviously accept racial differences in sports, yet they have some kind of emotional attachment to the blank slate narrative. We don’t hear that you can nurture athletic success. We do, however, hear that ‘we can succeed at anything we put out minds to’. That’s not in dispute; that’s a fact. But it’s twisted in a way that genetics and ancestry has no bearing on it, when it explains a lot of the variance. People accept racial differences when they’re cheering on their favorite football team or basketball team. For instance, NFL announcer Gus Johnson said during a broadcast of a Titans and Jaguars game “He’s [Chris Johnson] got gettin’ away from the cops speed!”
Pro-sports announcers, as well as college recruiters, know what the average person doesn’t who is not exposed to these differences daily for decades on end. People in these types of professions, especially collegiate sports recruiters, must get the low-down on average racial differences and then use what they know to make their choices on who to draft for their team.
For more (anecdotal) evidence, you can look up the race/ethnicity of the winners in competitions where peoples from all over the world compete in. More West African descendants place higher in physique, BBing comps, etc; more Caucasians and East Asians (and Kenyans) place higher in strength comps. A white man has won the WSM every year since its inception. West African descended blacks dominate BBing and physique comps. Eurasians (and Kenyans) dominate in marathon running.
All of this talk of racial differences in sports (which largely has to do with whites vs. blacks, though Asians are included in my overall analysis), I’ve hardly cited anything on East Asians directly. In regards to sports that take extreme dexterity or flexibility (and high reaction), East Asians shine. They shine in diving, ping-pong, skating and gymnastics events. They usually have long torsos and small limbs. I theorize that this was an evolutionary adaptation for the East Asians, as shorter people have less surface area to keep warm. Taller people would have died out quicker than one who’s smaller and can cover up and get warmer faster. They also have quicker reaction times (Rushton and Jensen, 2005) and it has been hypothesized that this is why they dominate in ping pong.
Conclusion
We don’t need any tests to show that there are racial differences in sports; the test is the competition itself. On average, A white will be stronger than an Asian who will be stronger than a black. Conversely, a Kenyan will be a better marathoner than a West African, European or Asian. West Africans will be more likely to beat all three groups in a sprint. These differences come down to morphology, but they start inside the muscles with the muscle fibers. Some anatomy textbooks acknowledge the existence of race, however, they have old and outdated information. It’s a good thing that anatomy textbooks talk about racial differences in physiology and anatomy, now we need to start doing heavy research into racial differences in the brain. The races evolved their fiber typing depending on what they had to do to survive along with their immediate environment, i.e., high elevation like the Kalenjin people.
The evolution of differing muscle fiber types in different races is easily explainable: Europeans have slow twitch fibers. In cold temperatures, the body switches from burning fat to burning carbs for energy. Furthermore, the average person would need to have a higher lung capacity and not tire out during long hunts on megafauna. Over time, selection occurred on the individuals with more type I fibers. Conversely, West Africans and their descendants have the ACTN3 gene, which is associated with elite human athletic performance (Yang et al, 2003). Africans who could get away from predators survived and passed on the genes and fiber typing for elite athletic performance.
In sum, the races differ in terms of entrants to elite athletic competition. These differences are largely genetic in nature. Evolutionary processes explain racial differences in sports. These same selection processes that explain racial differences in elite sports competitions also explain racial differences in intelligence. I await the day that we can freely speak about racial differences in intelligence just like we speak about racial differences in sports. Denying human variation makes no sense, especially in today’s world where we have state of the art testing.
Why Are Men Attracted To Low Waist-to-Hip Ratios?
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Why are men attracted to low waist-to-hip ratios (WHR)? Like with a lot of our preferences, there is an evolutionary reason why men are attracted to low WHR. I came across a paper the other day by M.D. William Lassek, “Assistant Professor of Epidemiology and Research Associate in the department of Anthropology at the University of California, Santa Barbara” and co-author P.h.D. Steven Gaulin, Professor of Anthropology with specific research interests in “evolutionary psychology, cognitive adaptations, the human voice, sexual selection, evolution of sex differences, lipid metabolism and brain evolution.” This paper fascinates me because it talks about the evolution of human intelligence through a lens of nutrition and micronutrients, something that I’m well-read on due to my career. First, I will discuss the benefits of fish oil and the main reason for taking them: omega-3 fatty acids and DHA. Then I will discuss the WHR/intelligence theory.
Fish Oils, DPA/EPA, and Omega-3 Fatty Acids
Misinformation about fish oils is rampant, specifically in the HBD-sphere, specifically with Steve Sailer’s article HBD and Diet Advice. The study he cites (with no reference) I assume is this study by Yano et al (1978) in which they found that Japanese men who ate more carbohydrates had less of a chance to die of cardiovascular heart disease (CHD). He says that the first generation ate mostly rice and no fat while the second generation “ate cheeseburgers and had higher rates of coronary disease than their parents.” He then says that these diet recommendations (low-fat, high-carb) were put onto all populations with no proven efficacy for all ethnies/racial groups. These diet recommendations began around two decades before the 80s, however.
He then quotes an article by the NYT science write, Carl Zimmer, talking about how the Inuit study has “added a new twist to the omega-3 fatty acid story”. Now, I read papers on nutrition every day due to my career, I don’t know what kind of literature they read on the subject, but fish oil, more specifically DPA/EPA and omega-3s are hugely important for optimal brain growth, health, and function.
Controlled studies clearly show that omega-3 consumption had a positive influence on n-3 (fatty acid) intake. N-3 has also been recognized as a modulator of inflammation as well as the fact that omega-3 fatty acids down-regulate genes involved in chronic inflammation, which show that n-3 is may be good for atherosclerosis.
An increase in omega-3 consumption leads to decreased damage from heart attacks.
Omega-3 may also reduce damage after a stroke.
Dietary epidemiology has also shown a link between n-3 and mental disorders such as Alzheimers and depression. N-3 intake is also linked to intelligence, vision and mood. Infants who don’t get enough n-3 prenatally are at risk for developing vision and nerve problems. Other studies have shown n-3’s effects on tumors, in particular, breast, colon and prostate cancer.
Omega-3’s are also great for muscle growth. Omega-3 intake in obese individuals along with exercise show a speed up in fat-loss for that individual.
Where do these people get their information from? Not only are omega-3’s good for damage reduction after a stroke and a heart attack, they’re also good for muscle growth, breast, colon and prostate tumor reduction, infants deficient in omega-3 prenatally are at risk for developing nerve and vision problems. Increase in omega-3 consumption is also linked to increases in cognition, reduces chronic inflammation and is linked to lower instances of depression.
Clearly, fish oils have a place in everyone’s diet, not only Inuits’.
This also reminds me of The Alternative Hypothesis’s argument that there are differing CHO metabolisms based on geographic origin (not true, to the best of my knowledge).
WHR and Intelligence
Most of the theories of the increase in brain size and intelligence have to do with climate, in one way or another, along with sexual selection. Though recently, I’ve been rethinking my position on cold winters having that big of an effect on intelligence due to some new information I’ve come across. The paper titled Waist-hip ratio and cognitive ability: is gluteofemoral fat a privileged store of neurodevelopmental resources? by Lassek and Gaudin (2008) posits a very sensible theory about the evolution of human intelligence: mainly that men prefer hour-glass figures due to an evolutionary adaptation.
Why may this be the case? One of the most important reasons I can think of is that women with high WHR have a higher chance of rate of death. The Nurses Health Study followed 44,000 women for 16 years and found that women who had waists bigger than 35 inches had a two times higher risk of dying from heart disease when compared to women with the lowest waist size of less than 28 inches. Clearly, men prefer women with low WHR since they will live longer, conceive more children and be around longer to take care of said children. So while a low WHR is not correlated with fertility per se, it is correlated with longevity, so the woman can have more children to spread more of her genes.
Lassek and Gaulin also bring up the ‘thrifty gene hypothesis’, which states that these genes evolved in populations that experienced nutritional stress, i.e., famines. I’ve read a lot of books on nutrition and human evolution (I highly recommend The Story of the Human Body: Evolution, Health, and Disease) over the years and most of them discredit the idea of the thrifty gene hypothesis. However, recent research has shown the existence of these ‘thrifty genes’ in populations such as the Samoans and ‘Native’ Americans. It’s simple, really. Stop eating carbohydrates and the problems will fade away. (Hunter-gatherers don’t have these disease rates that we do in the West; it’s clear that the only difference is our diet and lifestyle. I will cover this in a future post titled “Diseases of Civilization”.)
Lassek and Gaulin pursued the hypothesis that gluteofemoral fat (fat stored in the thighs and buttocks) was the cause for the difference in the availability of neurodevelopmental nutrients available to a fetus. If correct, this could show why men prefer women with a low WHR and could show why we underwent such rapid brain growth: due to the availability of neurodevelopmental nutrients in the mother’s fat stores. Gluteofemoral body fat is the main source of long-chain polyunsaturated fatty acids (LPUFA) for children, along with another pertinent nutrient for fetal development: DHA. Lassek and Gaulin also state that 10 to 20 percent of the fat stored by a young woman during puberty is gluteofemoral fat, obviously priming her for childbearing. Even with caloric restriction, the gluteofemoral fat is not tapped utilized until late pregnancy/lactation when the baby needs nutrients such as DPA/EPA and omega-3s.
Further, 10 to 20 percent of the dry weight of the brain is made up of LCPUFA, which shows how important this one nutrient is for proper brain development in-vitro as well as the first few years of life. Lassek and Gaulin state:
A recent meta-analysis estimates that a child’s IQ increases by 0.13 point for every 100-mg increase in daily maternal prenatal intake of DHA (Cohen, Bellinger, Connor, & Shaywitz, 2005), and a recent study in England shows a similar positive relationship between a mother’s prenatal consumption of seafood (high in DHA) and her child’s verbal IQ (Hibbeln et al., 2007).
Along with what I cited above about these nutrients and their effects on our bodies while we’re in our adolescence and even adulthood, this is yet another huge reason WHY we should be consuming more fish oils, not only for the future intelligence of our offspring, but for our own brain health as a whole. Lassek and Gaulin state on pg. 3:
Each cycle of pregnancy and lactation draws down the gluteofemoral fat store deposited in early life; in many poorly nourished populations, this fat is not replaced, and women become progressively thinner with each pregnancy, which is termed “maternal depletion” (Lassek & Gaulin, 2006). We have recently shown that even well-nourished American women experience a relative loss of gluteofemoral fat with parity (Lassek & Gaulin, 2006). In parallel, parity is inversely related to the amount of DHA in the blood of mothers and neonates (Al, van Houwelingen, & Hornstra, 1997).
That critical fatty acids are depleted with parity is also consistent with studies showing that cognitive functioning is impaired with parity. IQ is negatively correlated with birth order (Downey, 2001), and twins have decreased DHA (McFadyen, Farquharson, & Cockburn, 2001) and compromised neurodevelopment compared to singletons (Ronalds, De Stavola, & Leon, 2005). The mother’s brain also typically decreases in size during pregnancy (Oatridge et al., 2002).
This also could explain why first born children are more intelligent than their siblings: because they have first dibs on the neurodevelopmental nutrients from the gluteofemoral fat, which aids in their brain growth and intelligence. What also lends credence to the theory is how the mother’s brain size typically decreases during pregnancy, due to the neurodevelopmental nutrients going to the child. (I also can’t help but wonder if this has any effect on Chinese IQ, since they had a nice increase in intelligence due to the Flynn Effect from 1982 to 2012. I will cover that in the future.)
“This hypothesis,” the authors write, “thus unites two derived (evolutionarily novel) features of Homo sapiens: sexually dimorphic fat distributions and large brains. On this view, a low WHR signals the availability of critical brain-building resources and should therefore have consequences for cognitive performance.”
The authors put forth three predictions for their study: 1) that a woman’s WHR should be negatively correlated with the cognitive ability of her offspring, 2) a woman’s WHR should be negatively correlated with her own intelligence since a woman passes on DPA as well as her own genes for low WHR to female offspring and 3) “cognitive development should be impaired in women whose first birth occurred early as well as in her future offspring, but lower WHRs, which indicate large stores of LCPUFA should be significantly protective for both” the mother and the child.
Lassek and Gaulin used data from the NHANES (National Health and Nutrition Examination Survey) III which included over 16,000 females with a mean age of 29.9 years. Measurements were taken on waist and hip circumference, WHR, BMI, and body fat as measured from bioelectrical impedance.*
For 752 “nulligravidas” (medical term for a woman who has never been pregnant), WHR explained 23 percent of the variance in total body fat estimated from the bioelectrical impedance (ugh, such a horrible measure). Moreover, “controlling for age and race/ethnicity” showed an increase of “0.01 in WHR increases total body fat by .83 kg” (1.82 pounds in freedom units). They also discovered that WHR explains 28 percent of the variance in BMI, with an increase of .47 kg per square meter, increasing the WHR by 0.01. BMI also explained 89 percent of the variance in body fat (garbage ‘body fat measuring instrument’ aside) with an increase of 1 kg per square meter increasing fat by 1.8 kg (close to 4 pounds in freedom units), but when added to the regression model, WHR made no additional contribution.
Lassek and Gaulin’s first hypothesis was corroborated when they found that the mother’s WHR was negatively correlated with the child’s intelligence on 4 cognitive tests. WHR accounted for 2.7 percent of the variation in test scores, “with a decrease of 0.01 in the mother’s current WHR increasing the child’s mean cognitive score by 0.061 points”. In the first subsample, they controlled for mother’s age, parental education, family income and race/ethnicity. Even when these variables were controlled for, WHR was still negatively correlated with the cognitive score. When these variables were controlled for, a decrease of 0.01 in WHR increased the average score by 0.024 points.
Their second hypothesis was also confirmed: that women with lower WHR would be more intelligent than women with higher WHRs. In girls aged 14-16, the WHR accounted for 3.6 percent of the variance in the average of the four cognitive tests. Also discovered was that in women aged 18 to 49, WHR accounted for 7 percent of the variance in years of education and 6 percent of the variance in two tests of cognitive ability. Even when controlling for age, parity, family income, age at first birth, and race/ethnicity, the negative correlation was still seen in 14 to 16-year-old girls.
There is also competition neurodevelopmental resources between mother and child. As I showed earlier in this article, a woman’s brain size decreases during pregnancy. This decrease in brain size during pregnancy is due to the babe getting more of the neurodevelopmental nutrients for brain growth from the mother. Clearly, as the mother’s stores of brain-growing nutrients become depleted, so does her brain size as te nutrients from her stored fat goes to developing the fetuses’ brain.
Lassek and Gaulin confirmed their hypothesis that a woman with a lower WHR would be more intelligent as well as have more intelligent children. WHR predicts the cognitive ability of the offspring while BMI does not. However, controlling for family income and parental education decreases the effect of WHR on the child’s intelligence, the effect still remains giving strong support to the hypothesis that women with low WHR pass on genes for low WHR as well as nutrients needed for neurodevelopment. Further, controlling for parental cognitive ability may mask the effects of the WHR. It’s well known that the mother’s intelligence is the best predictor for her offspring’s intelligence, which is due to the mother and grandmother passing on genes that augment the effect of LCPUFAs, along with the genes for lower WHR.
Women with a lower WHR were found to be more intelligent, and a lower WHR helps to protect cognitive resources (neurodevelopmental nutrients) for the mother and child. The mother’s body has a dilemma, though: it has to store nutrients for the mother’s own cognition; store resources for future pregnancies; and provide nutrients for their growing fetus. Obviously, especially in young mothers, this poses a problem as there is a conflict for what the brain should do with the nutrients the mother ingests. Children born to teenaged mothers have lower cognitive test scores, but, they are protected from this fate if the mother has a low WHR. This shows, definitively, that young mothers who are still growing will show no negative effects on their growth when pregnant if they have a low WHR which signals they have a large amount of LCPUFAs and other essential neurodevelopmental nutrients for the baby’s brain growth.
LCPUFAs are scarce in human diets. Thusly, an evolutionary preference for low WHR evolved for men so their children can have optimal nutrients while growing in the mother’s womb. The study confirmed that large brains, and along with it higher intelligence, and sexually dimorphic fat distribution have a strong link. Clearly, if a mother doesn’t have adequate levels of LCPUFAs, neurodevelopment will be impeded since the babe will not be getting the optimal nutrients for brain growth. Moreover, diets low in omega-3s should have consequences for intelligence and brain size of a baby, since when a baby is in the womb that is the most important time for it to get optimal brain nutrients. Is there any type of environment we can make ourselves and lifestyle choices we can take for ourselves, spouses and children to foster higher intelligence in them? I will cover that in the future.
Men love hour-glass figures, a low WHR. As I’ve shown in this article, there is an evolutionary reason for this. Men were asked to rate women who had surgery to move fat to their buttocks. Body weight stayed the same, but the fat was redistributed. It was found in brain scans of the men that the same parts of the brain related to reward lit up, including regions associated with drugs and alcohol. (more information here)
Conclusion
I’ve long known of the tons of positive benefits of omega-3 fatty acids and fish oil on human brain development. Fish oils and the nutrients in them are imperative for a healthy and growing brain. Without it, brain development will suffer. As a man, I can say firsthand that a low WHR is the most attractive. Now I understand the evolutionary reason behind it: fostering high intelligence due to the mothers lower-body fat stores. Omega-3s and LCPUFA are extremely important for optimal fetal brain growth. Moreover, the current American diet is low in omega-3s, while high in omega-6s. There is evidence of high omega-6 intake being related to obesity, metabolic syndromes, a progressive increase in body fat over the generations. The omega-6 and -3 ratios in the body also play a role in obesity, with a lower omega-3 ratio and higher omega-6 ratio being related to obesity. This is due to adipogenesis, browning of the fat tissue, lipid homeostasis, and systemic inflammation. Clearly, as shown in this article, it’s imperative to have a balance of omega-3 and omega-6 fatty acids. This could also have to do with the hyperactivity of the cannabinoid system (which we all know what that’s involved with: eating more) and that could also be a cause for obesity with out-of-whack omega-6 to -3 fatty acid levels in the body. That’s for another day, though.
The totality of evidence is clear. If you want healthy children, choose a mate with a low WHR. She and her offspring will be more likely to be more intelligent. Clearly, if you’re reading this, you’re interested in intelligence as well as having the best possible life and life outcomes for your children. Well, choose a woman with a low WHR and you’ll be more likely to have more intelligent children!
* I have one problem with this study. They assessed body fat with bioelectrical impedance. The machine sends a light electrical current through the body and measures the degree of resistance to the flow of the current, which body fat can then be estimated. Problems with measuring body fat this way are as follows: it depends on how hydrated you are, whether you exercised that day, when you last ate, even whether your feet are calloused. Most importantly, they vary depending on the machine as well. Two differing machines will give two differing estimates. This is my only problem with the study. I would like if, in a follow-up study, they would use the DXA scan or hydrostatic weighing. These two techniques would be much better than using bioelectrical impedance, as the variables that prevent bioelectrical impedance from being a good way to measure body fat don’t exist with the DXA scan or hydrostatic weighing.
(Also see Eternal Curves by the Lassek and Gaulin and their book Why Women Need Fat for more information.)