Home » Posts tagged 'Race Differences'
Tag Archives: Race Differences
It has come to my attention that near the end of 2007, Nike boasted about releasing a running shoe that specifically targeted Native American communities. Nike developed the shoe to “to address the specific fit and width requirements for the Native American foot.” Since Native Americans have a high rate of obesity and diabetes (“diabesity”), then it seems that it would be a good thing to promote a shoe specifically for and to the population in question. But do such gestures translate to racist ideas or do they translate to a corporation wanting to be seen as promoting health (while their ultimate goal is profit)? Nike, specializing in athletic clothing, surely would be a good organization to spearhead such a movement, right? On what research is this initiative based on and does it hold water?
Through such outreach programs, Nike hopes to be seen to make social and community impacts when it comes to health. As Welch (2019: 12) notes, the N7 imitative hopes “to further promote sport and physical activity in Native American communities.” Such programs and specific items that would catch the eye of the consumers in question to heighten their physical activity and, subsequently, lessen their rates of fatal diseases, should be seen as a good thing, which would be irrespective of the feelings of the groups in question who see such outreach as racist.
The shoe was developed by a podiatrist named Rodney Stapp who served the Native community for his whole life (b. 1961, d. 2016). This was the first—and since then, only—time that Nike developed a shoe for a specific racial group. Was it a good idea? Was it racist? Even if it could be construed as racist, wouldn’t it be negated by targeting a group that has some of the highest rates of diabesity in America, therefore leading to a more active population and mitigation of the diseases in question? (See Broussard et al, 1991; Narayan, 1996; Acton et al, 2002). Since exercise seems to be necessary in managing diabetes and its symptoms (Colberg et al, 2010; Kirwan, Sacks, and Nieuwoudt, 2018; Borhade and Singh, 2020), then it seems that, irrespective of whether or not such gestures are racist, that such outreach and initiatives are a net good for the population in question.
Stapp was a big-name figure in the outreach to Native groups in Texas, and was the podiatrist that Nike consulted with in the development of their Nike Native American N7 shoe. Stapp was the one that contacted Nike to make such a shoe, since the patients that he serviced did not like the black and bulky shoes that were specially developed for diabetics—the efficacy of such shoes, though, have been debated in the literature (e.g., Brunner, 2015), while others have noted that diabetics have stated that the style and appearance of such diabetic shoes are the reasons why there is such low compliance in wearing them (Macfarlane and Jensen, 2003). In any case, wouldn’t marketing shoes toward specific demographics be a net-good, irrespective of the ultimate goals of the company if they would then promote healthier behaviors in the population in question?
Nike, though, has been criticized for the initiative, with Native right’s groups claiming that Nike is using Native plight for profit (Cole, 2008; Sanders, Phillips, and Alexander, 2018). It has been criticized by such groups since they have embroidered the shoe with feathers and sunsets, arrows, and different kinds of symbolism prevalent in Native cultures in the Americas. Here, I would not say that such things are racist on its face, it’s just a marketing ploy to sell more of their shoes. While it can be construed that such marketing is racist in a way, I think that the good such a program and shoe would do to reach at-risk populations outweighs any racist connotations that the shoes and the outreach program makes.
But most would have a problem with the claim that the shoe was developed specifically for “Native American feet”. Stapp claimed that “Indians tend to have a wider foot, but their heels are about average“, which would indicate slippage while running in a normal running shoe. Nike’s press release on the shoe says that “A strong emphasis was placed on providing a performance product that would cater to the specific needs of Native American foot shapes and help provide motivation to Native Americans predisposed to, or suffering from, health issues that can be improved by leading physically active lifestyles“, while also stating that “Research has engaged individuals from over 70 tribes as well as consulting podiatrists and members of Indian Health Services and the National Indian Health Board.“
(I am unable to find the research in question; hopefully someone can point me in the right direction so that I can find it.)
There is a history of such differences in the appendages between North and South Native Americans—where North Americans have longer and more slender feet than South Americans (e.g., Kate, 1918). Nike stated that the reason they developed the shoes were so that they could accommodate Native American’s wider feet, along with combating the diabesity epidemic that affects them. In 2015, though, Stapp stated that he believed the introduction of the shoe dropped amputations from 5-6 per year to 0-1 per year. If it is indeed true that the shoes were related in lowering the incidences of foot amputations in Native communities, then it would seem that the cause of that would be that they are moving more and getting more blood to their lower extremities which would then lead to lowered rates of amputation in these diabetic populations.
The claim that such shoes “racially profile” Natives is ridiculous. Stapp said that Nike asked him if there were differences in the feet of Native groups compared to others to which he answered “Yes.” Apparently, around the time of the marketing for the shoes, Nike was told that Native Americans had problems fitting into Nike’s ‘normal’ running shoes due to the width of their feet (being wider than average). Along with Natives supposedly having wider feet, since diabetes causes inflammation of tissue, which is concentrated in the feet—for instance, with diabetic foot ulcers (Pendsey, 2010; Schoen and Norman, 2014; Tuttolomondo, Maida, and Pinto, 2015; Amin and Doupis, 2016)—would seem that the call for such shoes to be develop would be a net-good for the population.
Though I can see how the claims that the shoe targeted at a specific racial group could be construed as racist, the net-good that a shoe does in getting to certain populations would outweigh the negative connotations that the racist accusation brings on Nike. Indeed, some of the developers of the shoe were Native, worked with Natives, and developed it to specifically target and help Natives manage a debilitating disease that leads to many negative health outcomes—like foot amputation and eventually death. So if exercise is conducive to managing diabetes and diabetic foot and the N7’s would then target certain populations with different average foot morphology, then it seems that the shoe has been a net-good for the population since, according to Stapp, seven years after the introduction of the shoe diabetic foot amputations went from 5-7 to 0-1 per year. While he may have had financial incentives to say that, I don’t think that it underscores the fact that Nike’s N7 program did not have positive benefits—even if they could be construed in a negative way (i.e., claims of racism).
The answer to the question “Should we market shoes to specific demographics” is “Yes.” It would be a good idea to, for example, make more demographic-specific shoes with specific embroideries in order to attempt to target certain at-risk populations that are more likely to acquire certain diseases on the basis of physical inactivity—like the Nike N7 program and Nike Native American N7 shoe attempt to do. It is for these reasons, then (irrespective of whether or not such morphologic claims of the feet of Natives are true) that the initiative in question is a good thing. The moral “should” question on whether or not we “should” market things—in this example, shoes—to certain demographics seems to rest on whether or not the marketing would have a positive effect on the lifestyles of the groups in question. If it does have positive effects, then we should market such programs toward at-risk populations, irrespective of claims that such marketing is racist toward certain groups.
Race, aggression, and prostate cancer are all linked, with some believing that race is the cause of higher testosterone which then causes aggression and higher rates of crime along with maladies such as prostate cancer. These claims have long been put to bed, with a wide range of large analyses.
The testosterone debate regarding prostate cancer has been raging for decades and we have made good strides in understanding the etiology of prostate cancer and how it manifests. The same holds true for aggression. But does testosterone hold the key to understanding aggression, prostate cancer and does race dictate group levels of the hormone which then would explain some of the disparities between groups and individuals of certain groups?
For decades it was believed that heightened levels of testosterone caused prostate cancer. Most of the theories to this day still hold that large amounts of androgens, like testosterone and it’s metabolic byproduct dihydrotestosterone, are the two many factors that drive the proliferation of cells and therefore, if a male is exposed to higher levels of testosterone throughout their lives then they are at a high risk of prostate cancer compared to a man with low testosterone levels, so the story goes.
In 1986 Ronald Ross set out to test a hypothesis: that black males were exposed to more testosterone in the womb and this then drove their higher rates of prostate cancer later in life. He reportedly discovered that blacks, after controlling for confounds, had 15 percent higher testosterone than whites which may be the cause of differential prostate cancer mortality between the two races (Ross et al, 1986) This is told in a 1997 editorial by Hugh McIntosh. First, the fact that black males were supposedly exposed to more testosterone in the womb is brought up. I am aware of one paper discussing higher levels of testosterone in black women compared to white women (Perry et al, 1996). Though, I’ve shown that black women don’t have high levels of testosterone, not higher than white women, anyway (see Mazur, 2016 for discussion). (Yes I changed my view on black women and testosterone, stop saying that they have high levels of testosterone it’s just not true. I see people still link to that article despite the long disclaimer at the top.)
Alvarado (2013) discusses Ross et al (1986), Ellis and Nyborg (1992) (which I also discussed here along with Ross et al) and other papers discussing the supposed higher testosterone of blacks when compared to whites and attempts to use a life history framework to explain higher incidences of prostate cancer in black males. He first notes that nutritional status influences testosterone production which should be no surprise to anyone. He brings up some points I agree with and some I do not. For instance, he states that differences in nutrition could explain differences in testosterone between Western and non-Western people (I agree), but that this has no effect within Western countries (which is incorrect as I’ll get to later).
He also states that ancestry isn’t related to prostate cancer, writing “In summation, ancestry does not adequately explain variation among ethnic groups with higher or lower testosterone levels, nor does it appear to explain variation among ethnic groups with high or low prostate cancer rates. This calls into question the efficacy of a disease model that is unable to predict either deleterious or protective effects.”
He then states that SES is negatively correlated with prostate cancer rates, and that numerous papers show that people with low SES have higher rates of prostate cancer mortality which makes sense, since people in a lower economic class would have less access to and a chance to get good medical care to identify problems such as prostate cancer, including prostate biopsies and checkups to identify the condition.
He finally discusses the challenge hypothesis and prostate cancer risk. He cites studies by Mazur and Booth (who I’ve cited in the past in numerous articles) as evidence that, as most know, black-majority areas have more crime which would then cause higher levels of testosterone production. He cites Mazur’s old papers showing that low-class men, no matter if they’re white or black, had heightened levels of testosterone and that college-educated men did not, which implies that the social environment can and does elevate testosterone levels and can keep them heightened. Alvarado concludes this section writing: “Among Westernized men who have energetic resources to support the metabolic costs associated with elevated testosterone, there is evidence that being exposed to a higher frequency of aggressive challenges can result in chronically elevated testosterone levels. If living in an aggressive social environment contributes to prostate cancer disparities, this has important implications for prevention and risk stratification.” He’s not really wrong but on what he is wrong I will discuss later on this section. It’s false that testosterone causes prostate cancer so some of this thesis is incorrect.
I rebutted Ross et al (1986) December of last year. The study was hugely flawed and, yet, still gets cited to this day including by Alvarado (2013) as the main point of his thesis. However, perhaps most importantly, the assay times were done ‘when it was convenient’ for the students which were between 10 am and 3 pm. To not get any wacky readings one most assay the individuals as close to 8:30 am as possible. Furthermore, they did not control for waist circumference which is another huge confound. Lastly, the sample was extremely small (50 blacks and 50 whites) and done on a nonrepresentative sample (college students). I don’t think anyone can honestly cite this paper as any evidence for blacks having higher levels of testosterone or testosterone causing prostate cancer because it just doesn’t do that. (Read Race, Testosterone and Prostate Cancer for more information.)
What may explain prostate cancer rates if not for differences in testosterone like has been hypothesized for decades? Well, as I have argued, diet explains a lot of the variation between races. The etiology of prostate cancer is not known (ACA, 2016) but we know that it’s not testosterone and that diet plays a large role in its acquisition. Due to their dark skin, they need more sunlight than do whites to synthesize the same amount of vitamin D, and low levels of vitamin D in blacks are strongly related to prostate cancer (Harris, 2006). Murphy et al (2014) even showed, through biopsies, that black American men had higher rates of prostate cancer if they had lower levels of vitamin D. Lower concentrations of vitamin D in blacks compared to whites due to dark pigmentation which causes reduced vitamin D photoproduction and may also account for “much of the unexplained survival disparity after consideration of such factors as SES, state at diagnosis and treatment” (Grant and Peiris, 2012).
As mentioned above, testosterone is assumed to be higher in certain races compared to others (based on flawed studies) which then supposedly exacerbates prostate cancer. However, as can be seen above, a lot of assumptions go into the testosterone-prostate cancer hypothesis which is just false. So if the assumptions are false about testosterone, mainly regarding racial differences in the hormone and then what the hormone actually does, then most of their claims can be disregarded.
Perhaps the biggest problem is that Ross et al is a 32-year-old paper (which still gets cited favorably despite its huge flaws) while our understanding of the hormone and its physiology has made considerable progress in that time frame. So it’s in fact not so weird to see papers like this that say “Prostate cancer appears to be unrelated related to endogenous testosterone levels” (Boyle et al, 2016). Other papers also show the same thing, that testosterone is not related to prostate cancer (Stattin et al, 2004; Michaud, Billups, and Partin, 2015). This kills a lot of theories and hypotheses, especially regarding racial differences in prostate cancer acquisition and mortality. So, what this shows is that even if blacks did have 15 percent higher serum testosterone than whites as Ross et al, Rushton, Lynn, Templer, et al believed then it wouldn’t cause higher levels of prostate cancer (nor aggression, which I’ll get into later).
How high is testosterone in black males compared to white males? People may attempt to cite papers like the 32-year-old paper by Ross et al, though as I’ve discussed numerous times the paper is highly flawed and should therefore not be cited. Either way, levels are not as high as people believe and meta-analyses and actual nationally representative samples (not convenience college samples) show low to no difference, and even the low difference wouldn’t explain any health disparities.
One of the best papers on this matter of racial differences in testosterone is Richard et al (2014). They meta-analyzed 15 studies and concluded that the “racial differences [range] from 2.5 to 4.9 percent” but “this modest difference is unlikely to explain racial differences in disease risk.” This shows that testosterone isn’t as high in blacks as is popularly misconceived, and that, as I will show below, it wouldn’t even cause higher rates of aggression and therefore criminal behavior. (Rohrmann et al 2007 show no difference in testosterone between black and white males in a nationally representative sample after controlling for lifestyle and anthropometric variables. Whereas Mazur, 2009 shows that blacks have higher levels of testosterone due to low marriage rates and lower levels of adiposity, while be found a .39 ng/ml difference between blacks and whites aged 20 to 60. Is this supposed to explain crime, aggression, and prostate cancer?)
However, as I’ve noted last year (and as Alvarado, 2013 did as well), young black males with low education have higher levels of testosterone which is not noticed in black males of the same age group but with more education (Mazur, 2016). Since blacks of a similar age group have lower levels of testosterone but are more highly educated then this is a clue that education drives aggression/testosterone/violent behavior and not that testosterone drives it.
Mazur (2016) also replicated Assari, Caldwell, and Zimmerman’s (2014) finding that “Our model in the male sample suggests that males with higher levels of education has lower aggressive behaviors. Among males, testosterone was not associated with aggressive behaviors.” I know this is hard for many to swallow that testosterone doesn’t lead to aggressive behavior in men, but I’ll cover that in the last and final section.
So it’s clear that the myth that Rushton, Lynn, Templer, Kanazawa, et al pushed regarding hormonal differences between the races are false. It’s also with noting, as I did in my response to Rushton on r/K selection theory, that the r/K model is literally predicated on 1) testosterone differences between races being real and in the direction that Rushton and Lynn want because they cite the highly flawed Ross et al (1986) and 2) testosterone does not cause higher levels of aggression (which I’ll show below) which then lead to higher rates of crime along with higher rates of incarceration.
A blogger who goes by the name of ethnicmuse did an analysis of numerous testosterone papers and he found:
Which, of course, goes against a ton of HBD theory, that is, if testosterone did what HBDers believed it does (it doesn’t). This is what it comes down to: blacks don’t have higher levels of testosterone than whites and testosterone doesn’t cause aggression nor prostate cancer so even if this relationship was in the direction that Rushton et al assert then it still wouldn’t cause any of the explanatory variables they discuss.
Last year Lee Ellis published a paper outlining his ENA theory (Ellis, 2017). I responded to the paper and pointed out what he got right and wrong. He discussed strength (blacks aren’t stronger than whites due to body type and physiology, but excel in other areas); circulating testosterone, umbilical cord testosterone exposure; bone density and crime; penis size, race, and crime (Rushton’s 1997 claims on penis size don’t ‘size up’ to the literature as I’ve shown two times); prostate-specific antigens, race, and prostate cancer; CAG repeats; intelligence and education and ‘intelligence’; and prenatal androgen exposure. His theory has large holes and doesn’t line up in some places, as he himself admits in his paper. He, as expected, cites Ross et al (1986) favorably in his analysis.
Testosterone can’t explain all of these differences, no matter if it’s prenatal androgen exposure or not, and a difference of 2.5 to 4.9 percent between blacks and whites regarding testosterone (Richard et al, 2014) won’t explain differences in crime, aggression, nor prostate cancer.
Other authors have attempted to also implicate testosterone as a major player in a wide range of evolutionary theories (Lynn, 1990; Rushton, 1997; Rushton, 1999; Hart, 2007; Rushton and Templer, 2012; Ellis, 2017). However, as can be seen by digging into this literature, these claims are not true and therefore we can discard the conclusions come to by the aforementioned authors since they’re based on false premises (testosterone being a cause for aggression, crime, and prostate cancer and r/K meaning anything to human races, it doesn’t)
Finally, to conclude this section, does testosterone explain racial differences in crime? No, racial differences in testosterone, however small, cannot be responsible for the crime gap between blacks and whites.
Testosterone and aggression
Testosterone and aggression, are they linked? Can testosterone tell us anything about individual differences in aggressive behavior? Surprisingly for most, the answer seems to be a resounding no. One example is the castration of males. Does it completely take away the urge to act aggressively? No, it does not. What is shown when sex offenders are castrated is that their levels of aggression decrease, but importantly, they do not decrease to 0. Robert Sapolsky writes on page 96 of his book Behave: The Biology of Humans at Our Best and Worst (2017) (pg 96):
… the more experience a male has being aggressive prior to castration, the more aggression continues afterward. In other words, the less his being aggressive in the future requires testosterone and the more it’s a function of social learning.
He also writes (pg 96-97):
On to the next issue that lessens the primacy of testosterone: What do individual levels of testosterone have to do with aggression? If one person higher testosterone levels than another, or higher levels this week than last, are they more likely to be aggressive?
Initially the answer seemed to be yes, as studies showed correlation between individual differences in testosterone levels and levels of aggression. In a typical study, higher testosterone levels would be observed in those male prisoners with higher rates of aggression. But being aggressive stimulates testosterone secretion; no wonder more aggressive individuals had higher levels. Such studies couldn’t disentangle chickens and eggs.
Thus, a better question is whether differences in testosterone levels among individuals predict who will be aggressive. And among birds, fish, mammals, and especially other primates, the answer is generally no. This has been studied extensively in humans, examining a variety of measures of aggression. And the answer is clear. To quote British endocrinologist John Archer in a definitive 2006 review, “There is a weak and inconsistent association between testosterone levels and aggression in [human] adults, and . . . administration of testosterone to volunteers typically does not increase aggression.” The brain doesn’t pay attention to testosterone levels within the normal range.
Thus, aggression is typically more about social learning than about testosterone, differing levels of testosterone generally can’t explain why some individuals are more aggressive than others.
Sapolsky also has a 1997 book of essays on human biology titled The Trouble With Testosterone: And Other Essays On The Biology Of The Human Predicament and he has a really good essay on testosterone titled Will Boys Just Be Boys? where he writes (pg 113 to 114):
Okay, suppose you note a correlation between levels of aggression and levels of testosterone among these normal males. This could be because (a) testosterone elevates aggression; (b) aggression elevates testosterone secretion; (c) neither causes the other. There’s a huge bias to assume option a while b is the answer. Study after study has shown that when you examine testosterone when males are first placed together in the social group, testosterone levels predict nothing about who is going to be aggressive. The subsequent behavioral differences drive the hormonal changes, not the other way around.
Because of a strong bias among certain scientists, it has taken do forever to convince them of this point.
As I said, it takes a lot of work to cure people of that physics envy, and to see interindividual differences in testosterone levels don’t predict subsequent differences in aggressive behavior among individuals. Similarly, fluctuations in testosterone within one individual over time do not predict subsequent changes in the levels of aggression in the one individual—get a hiccup in testosterone secretion one afternoon and that’s not when the guy goes postal.
And on page 115 writes:
You need some testosterone around for normal levels of aggressive behavior—zero levels after castration and down it usually goes; quadruple it (the sort of range generated in weight lifters abusing anabolic steroids), and aggression typically increases. But anywhere from roughly 20 percent of normal to twice normal and it’s all the same; the brain can’t distinguish among this wide range of basically normal values.
Weird…almost as if there is a wide range of ‘normal’ that is ‘built in’ to our homeodynamic physiology…
So here’s the point: differences in testosterone between individuals tell us nothing about individual differences in aggressive behavior; castration and replacement seems to show that, however broadly, testosterone is related to aggression “But that turns out to not be true either, and the implications of this are lost on most people the first thirty times you tell them about it. Which is why you’d better tell them about it thirty-one times, because it’s the most important part of this piece” (Sapolsky, 1997: 115).
Later in the essay, Sapolsky discusses a discusses 5 monkeys that were given time to form a hierarchy of 1 through 5. Number 3 can ‘throw his weight’ around with 4 and 5 but treads carefully around 1 and 2. He then states to take the third-ranking monkey and inject him with a ton of testosterone, and that when you check the behavioral data that he’d then be participating in more aggressive actions than before which would imply that the exogenous testosterone causes participation in more aggressive behavior. But it’s way more nuanced than that.
So even though small fluctuations in the levels of the hormone don’t seem to matter much, testosterone still causes aggression. But that would be wrong. Check out number 3 more closely. Is he now raining aggression and terror on any and all in the group, frothing in an androgenic glaze of indiscriminate violence. Not at all. He’s still judiciously kowtowing to numbers 1 and 2 but has simply become a total bastard to number 4 and 5. This is critical: testosterone isn’t causing aggression, it’s exaggerating the aggression that’s already there.
The correlation between testosterone and aggression is between .08 and .14 (Book, Starzyk, and Quinsey, 2001; Archer, Graham-Kevan, and Davies, 2005; Book and Quinsey, 2005). Therefore, along with all of the other evidence provided in this article, it seems that testosterone and aggression have a weak positive correlation, which buttresses the point that aggression concurrent increases in testosterone.
Sapolsky then goes on to discuss the amygdala’s role in fear processing. The amygdala has its influence on aggressive behavior through the stria terminalis, which is a bunch of neuronal connections. How the amygdala influences aggression is simple: bursts of electrical excitation called action potentials go up and down the stria terminalis which changes the hypothalamus. You can then inject testosterone right into the brain and will it cause the same action potentials that surge down the stria terminalis? No, it does not turn on the pathway at all. This only occurs only if the amygdala is already sending aggression-provoking action potentials down the stria terminalis with testosterone increasing the rate of action potentials you’re shortening the rest time between them. So it doesn’t turn on this pathway, it exaggerates the preexisting pattern, which is to say, it’s exaggerating the response to environmental triggers of what caused the amygdala to get excited in the first place.
He ends this essay writing (pg 119):
Testosterone is never going to tell us much about the suburban teenager who, in his after-school chess club, has developed a particularly aggressive style with his bishops. And it certainly isn’t going to tell us much about the teenager in some inner-city hellhole who has taken to mugging people. “Testosterone equals aggression” is inadequate for those who would offer a simple solution to the violent male—just decrease levels of those pesky steroids. And “testosterone equals aggression” is certainly inadequate for those who would offer a simple excuse: Boys will be boys and certain things in nature are inevitable. Violence is more complex than a single hormone. This is endocrinology for the bleeding heart liberal—our behavioral biology is usually meaningless outside of the context of social factors and the environment in which it occurs.
Injecting individuals with supraphysiological doses of testosterone as high as 200 and 600 mg per week does not cause heightened anger or aggression (Tricker et al, 1996; O’Connor et, 2002). This, too, is a large blow for the testosterone-induces-aggression hypothesis. Because aggressive behavior heightens testosterone, testosterone doesn’t heighten aggressive behavior. (This is the causality that has been looked for, and here it is. The causality is not in the other direction.) This tells us that we need to be put into situations for our aggression to rise and along with it, testosterone. I don’t even see how people could think that testosterone could cause aggression. It’s obvious that the environmental trigger needs to be there first in order for the body’s physiology to begin testosterone production in order to prepare for the stimulus that caused the heightened testosterone production. Once the trigger occurs, then it can and does stay heightened, especially in areas where dominance contests would be more likely to occur, which would be low-income areas (Mazur, 2006, 2016).
Lastly, one thing that gets on my nerves that people point to to attempt to show that testosterone and its derivatives cause violence, aggression etc is the myth of “roid rage” which is when an individual objects himself with testosterone, anabolic steroids or another banned substance, and then the individual becomes more aggressive as a result of more free-flowing testosterone in their bloodstream.
The problem here is that people believe what they hear on the media about steroids and testosterone, and they’re largely not true. One large analysis was done to see the effects of steroids and other illicit drug use on behavior, and what was found was that after controlling for other substance use “Our results suggest that it was not lifetime steroid use per se, but rather co-occurrring polysubstance abuse that most parsimoniously explains the relatively strong association of steroid use and interpersonal violence” (Lundholm et al, 2015). So after controlling for other drugs used, men who use steroids do not go to prison and be convicted of violence after other polysubstance use was controlled for, implying that is what’s driving interpersonal violence, not the substance abuse of steroids.
Numerous myths about testosterone have been propagated over the decades, which are still believed in the new millennium despite numerous other studies and arguments to the contrary. As can be seen, the myths that people believe about testosterone are easily debunked. Numerous papers (with better methodology than Ross et al) attest to the fact that testosterone levels aren’t as high as was believed decades ago between the races. Diet can explain a lot of the variation, especially vitamin D intake. Injecting men with supraphysiological doses of testosterone does not heighten anger nor aggression. It does not even heighten prostate cancer severity.
Racial differences in testosterone are also not as high as people would like to believe, there is even an opposite relationship with Asians having higher levels and whites having lower (which wouldn’t, on average, imply femininity) testosterone levels. So as can be seen, the attempted r/K explanations from Rushton et al don’t work out here. They’re just outright wrong on testosterone, as I’ve been arguing for a long while on this blog.
Testosterone doesn’t cause aggression, aggression causes heightened testosterone. It can be seen from studies of men who have been castrated that the more crime they committed before castration, the more crime they will commit after which implies a large effect of social learning on violent behavior. Either way, the alarmist attitudes of people regarding testosterone, as I have argued, are not needed because they’re largely myths.
The microbiome is the number and types of different microorganisms and viruses in the human body. Racial differences are seen everywhere, most notably in the phenotype and morphology. Though, of course, there are unseen racial differences that then effect bodily processes of different races and ethnic groups. The microbiome is one such difference, which is highly heritable (Goodrich et al, 2014; Beaumont et al, 2016; Hall, Tolonen, and Xavier, 2017) (though they use the highly flawed twin method, so heritabilities are most likely substantially lower). They also show that certain genetic variants predispose individuals to microbial dysbiosis. However, diet, antibiotics and birth mode can also influence the diversity of microbiota in your biome (Conlon and Bird, 2015; Bokulich et al, 2017; Singh et al, 2017) and so while the heritability of the microbiome is important (which is probably inflated due to the twin method), diet can and does change the diversity of the biome.
It used to be thought that our bodies contained 90 percent bacteria and only 10 percent human cells (Collen, 2014), however that has been recently debunked and the ratio is 1.3 to 1, human to microbe (Sender, Fuchs, and Milo, 2016). (Collen’s book is still an outstanding introduction to this subject despite the title of her book being incorrect.) Though the 10:1 microbe/human cell dogma is debunked, in no way does that lessen the importance of the microbiome regarding health, disease and longevity.
Lloyd-Price, Abu-Ali, and Huttenhower (2016) review definitions for the ‘healthy human microbiome’ writing “several population-scale studies have documented the ranges and diversity of both taxonomic compositions and functional potentials normally observed in the microbiomes of healthy populations, along with possible driving factors such as geography, diet, and lifestyle.” Studies comparing the biomes of North and South America, Europe and Africa, Korea and Japan, and urban and rural communities in Russia and China have identified numerous different associations that are related to differences in the microbiome between continents that include (but are not limited to) diet, genetics, lifestyle, geography, and early life exposures though none of these factors have been shown to be directly causal regarding geographic microbiome diversity.
Gupta, Paul, and Dutta (2017) question the case of a universal definition of a ‘healthy microbiome’ since it varies by geographic ancestry. Of course, ancestry and geographic location influence culture which influences diet which influences microbiome diversity between populations. This, of course, makes sense. why have a universal healthy microbiome with a reference man that doesn’t reflect the diversity of both the individual and group differences in the microbiome? This will better help different populations with different microbiomes lose weight and better manage diseases in certain populations.
The microbiome of athletes also differs, too. Athletes had enhanced microbiome diversity when compared to non-athletes (Clarke et al, 2016). In a further follow-up study, it was found that microbial diversity correlated with both protein consumption and creatine kinase levels in the body (Clarke et al, 2017) are proxies for exercise, and since they’re all associations, causality remains to be untangled. Nevertheless, these papers are good evidence that both lifestyle and diet leads to changes in the microbiome.
Fortenberry (2013: 165) notes that American racial and ethnic classifications are “social and political in origin and represent little meaningful biologic basis of between-group racial/ ethnic diversity“. It is also known that eating habits, differing lifestyles and metabolic levels also influence the diversity of the microbiome in the three ‘races’* studied (Chen et al, 2016), while deep sequencing of oral microbiota has the ability to classify “African Americans with a 100% sensitivity and 74% specificity and Caucasians with a 50% sensitivity and 91% specificity” (Mason et al, 2014). The infant microbiome, furthermore, is influenced by maternal diet and breastfeeding as well as the infant’s diet (Stearns et al, 2017). This is why differences in race/ethnicity call into question the term of ‘healthy human microbiota’ (Gupta, Paul, and Dutta, 2017). These differences in the microbiome also lead to increased risk for colorectal cancer in black Americans (Goyal et al, 2016; Kinross, 2017).
Further, the healthy vagina “contains one of the most remarkably structured microbial ecosystems, with at least five reproducible community types, or “community state types” (Lloyd-Price, Abu-Ali, and Huttenhower 2016). The diversity of the microbiome in the vagina also varies by race. It was found that 80 percent of Asian women and 90 percent of white women harbored a microbiota species named Lactobacillus, whereas only about 60 percent of ‘Hispanics’ and blacks harbored this species. The pH level, too, varied by race with blacks and ‘Hispanics’ averaging 4.7 and 5.0 and Asians and whites averaging 4.4 and 4.2. So, clearly, since Asians and whites have similar vaginal pH levels, then it is no surprise that they have similar levels of vaginal Lactobacillus, whereas blacks and ‘Hispanics’, with similar pH levels have similar vaginal levels of Lactobacillus.
White subjects also have more diverse species of microbiota than non-white subjects while also having a different microbiota structure (Chen et al, 2015). Caucasian ethnicity/race was also shown to have a lower overall microbiome diversity, but higher Bacteroidetes scores, while white babes also had lower scores of Proteobacteria than black Americans (Sordillo et al, 2017). This comes down to both diet and genetic factors (though causation remains to be untangled).
Differences in the skin microbiome also exist between the US population and South Americans (Blaser et al, 2013). They showed that Venezuelan Indians had a significantly different skin biome when compared to US populations from Colorado and New York, having more Propionibacterium than US residents. Regarding the skin microbiota in the Chinese, Leung, Wilkins, and Lee (2015) write “skin microbiomes within an individual is more similar than that of different co-habiting individuals, which is in turn more similar than individuals living in different households.” Skin microbiota also becomes similar in cohabitating couples (Ross, Doxey, and Neufeld, 2017) and even cohabitating family members and their dogs (Song et al, 2013; Cusco et al, 2017; Torres et al, 2017).
Differences between the East and West exist regarding chronic liver disease, which may come down to diet which may influence the microbiota and along with it, chronic liver disease. (Nakamoto and Schabl, 2016). The interplay between diet, the microbiome and disease is critical if we want to understand racial/ethnic differentials in disease acquisition/mortality, because the microbiome influences so many diseases (Cho and Blaser, 2012; Guinane and Cotter, 2013; Bull and Plummer, 2014; Shoemark and Allen, 2015; Zhang et al, 2015; Shreiner, Kao, and Young, 2016; Young, 2017).
The human microbiome has been called our ‘second genome’ (Zhu, Wang, and Li, 2010; Grice and Seger, 2012) with others calling it an ‘organ’ (Baquero and Nombela, 2012; Clarke et al, 2014; Brown and Hazen, 2015). This ‘organ’, our ‘second genome’ can also influence gene expression (Masotti, 2012; Maurice, Haiser, and Turnbaugh, 2013; Byrd and Seger, 2015) which could also have implications for racial differences in disease acquisition and mortality. This is why the study of the microbiome is so important; since the microbiome can up- and down-regulate gene expression—effectively, turning genes ‘on’ and ‘off’—then understanding the intricacies that influence the microbiome diversity along with the diet that one consumes will help us better understand racial differences in disease acquisition. Diet is a huge factor not only regarding obesity and diabetes differences within and between populations, but a ‘healthy microbiome’ also staves off obesity. This is important. The fact that the diversity of microbiota in our gut can effectively up- and down-regulate genes shows that we can, in effect, influence some of this ourselves by changing our diets, which would then, theoretically, lower disease acquisition and mortality once certain microbiome/diet/disease associations are untangled and shown to be causative.
Finally, the Hadza have some of the best-studied microbiota, and since they still largely live a hunter-gatherer lifestyle, this is an important look at what the diversity of microbiota may have looked like in our hunter-gatherer ancestors (Samuel et al, 2017). The fact that they noticed such diverse changes in the microbiome—some species effectively disappearing during the dry season and reappearing during the wet season—is good proof that what drives these changes in the diversity of the microbiota in the Hadza are seasonal changes in diet which are driven by the wet and dry seasons.
Gut microbiota may also influence our mood and behavior, and it would be interesting to see which types of microbiota differ between populations and how they would be associated with certain behaviors. The microbes are a part of the unconscious system which regulates behavior, which may have causal effects regarding cognition, behavioral patterns, and social interaction and stress management; this too makes up our ‘collective unconscious’ (Dinan et al, 2015). It is clear that the microbes in our gut influence our behavior, and it even may be possible to ‘shape our second genome’ (Foster, 2013). Endocrine and neurocrine pathways may also be involved in gut-microbiota-to-brain-signaling, which can then alter the composition of the microbiome and along with it behavior (Mayer, Tillisch, and Gupta, 2015). Gut microbiota also plays a role in the acquisition of eating disorders, and identifying the specific microbiotal profiles linked to eating disorders, why it occurs and what happens while the microbiome is out of whack is important in understanding our behavior, because the gut microbiome also influences our behavior to a great degree.
The debate on whether or not racial/ethnic differences in microbiome diversity differs due to ‘nature’ or ‘nurture’ (a false dichotomy in the view of developmental systems theory) remains to be settled (Gupta, Paul, and Dutta, 2017). However, like with all traits/variations in traits, it is due to a complex interaction of the developmental system in question along with how it interacts with its environment. Understanding these complex disease/gene/environment/microbiotal pathways will be a challenge, as will untangling direct causation and what role diet plays regarding the disease/microbiota/dysbiosis factor. As we better understand our ‘second genome’, our ‘other organ’, and individual differences in the genome and how those genomic differences interact with different environments, we will then be able to give better care to both races/ethnies along with individuals. Just like with race and medicine—although there is good correlative data—we should not jump to quick conclusions based on these studies on disease, diet, and microbiotal diversity.
The study of ethnic/racial/geographic/cultural/SES differences in the diversity of the microbiome and how it influences disease, behaviors and gene expression will be interesting to follow in the next couple of years. I think that there will be considerable ‘genetic’ (i.e., differences out of the womb; I am aware that untangling ‘genetic’ and ‘environmental’ in utero factors is hard, next to impossible) differences between populations regarding newborn children, and I am sure that even the microbiota will be found to influence our food choices in the seas of our obesogenic environments. The fact that our microbiota is changeable with diet means that, in effect, we can have small control over certain parts of our gene expression which may then have consequences for future generations of our offspring. Nevertheless, things such as that remain to be uncovered but I bet more interesting things never dreamed of will be found as we look into the hows and whys of both individual and populational differences in the microbiome.
It’s well-known that blacks have narrower hips than whites (Rushton, 1997; Handa et al, 2008). These pelvic differences then account for part of the variation in elite sporting events such as sprinting and jumping (Entine, 2000). These pelvic differences are the result of climatic variation and sexual selection.
The evolution of the pelvis is due to bipedalism. We are bipeds because of our S-shaped spine, which helps us to cope with differing loads. The human pelvis had to evolve in two ways—to make birthing babies easier and to become more efficient for bipedal walking. Termed the ‘obstetric dilemma’, it has implications for osteoarthritis in both men and women (Hogervorst, Heinse, and de Vos, 2009). Having a more efficient bipedal gait meant the body could allocate energy to other parts of the body—mainly our growing brains/neuronal count. Over time, the brain grew while the pelvis had to shrink for more efficient bipedalism. The pelvis also got narrower in our evolution, being wider in Australopithicenes, while becoming more narrow when erectus appeared—which is the first instance of a humanlike pelvis in the fossil record—which increased how far we could travel as well as reduce our energy expenditure (Lieberman, et al, 2006). Further discussion can be found in my article Man the Athlete.
So we began evolving a narrower pelvis in comparison to our ancestors because it was more efficient for heat dissipation. Smaller trunks are more efficient for heat dissipation (Lieberman, 2015), whereas wider trunks are more efficient for thermoregulation in colder climes (Weaver and Hublin, 2008; Weaver, 2009; Gruss and Schmidt, 2015). Now, simply applying this logic to Eurasians and Africans (I am grouping East Asians and Europeans together since they were a single breeding population up until about 23,000-6,500ya), we can see one reason why that population has wider pelves than Africans.
When anatomically modern humans (AMH) left Africa between 50-100kya, human skeletal morphology was just like modern-day Africans’ today. When Man migrated into northerly climes, however, a wider pelvis was needed to retain heat in colder climes (Gruss and Schmidt, 2015). So, along with a wider pelvis evolving due to climatic demands on the body, as we migrated north the human brain expanded due to the climate of the area, along with expanding the pelvis to better thermoregulate (which a bigger brain also does in northerly climes). I did argue two months back (and added to Skoyles’ (1999) theory) that brain size increased for expertise capacity and not IQ since Arctic people needed more tools, as well as tools that were more complex, in comparison to peoples who evolved in a hotter climate. So selection then occurred for larger brains and pelvis due to the demand for thermoregulation and bigger brains—which then led to earlier births and more helpless babes, which higher levels of intelligence were then needed to care for them (Piantadosi and Kidd, 2016). The helplessness of infants predicts the intelligence of adults in the primate genera (Piantadosi and Kidd, 2016), so I will assume that this holds within primate species as well (I am not able to locate a citation that this doesn’t hold within the primate genera; if I am in error, please provide a citation). Since African children are born earlier and more mature than Eurasian children who are born slightly later and more helpless/less developed, this is one reason why Eurasians have higher levels of intelligence than Africans (which is independent of any direct effects of climate I may add!).
So since Eurasians needed a larger brains to make more tools in the Arctic/colder climes, their brains needed to expand in size for increased expertise capacity, which would then have further selected for wider pelves in Eurasian women. Climatic variation caused the wider hips/bigger brains in Eurasians, which then allowed the evolution of larger brains in comparison to those who remained in Africa.
Finally, the obstetric dilemma has been recently called into question; there is evidence that a wider pelvis does not increase locomotor costs in humans (Warrener et al, 2015), a treadmill tracked their gait, as well as the motion of their pelvis. This study is used as evidence that the obstetric dilemma is wrong—they argue that there is no trade-off between narrower hips in men and wider hips in women. However, as the authors point out, all subjects in the study walked/ran at the same speed. Let’s say that the speed was heightened; do you think the women/men with wider pelves would have had the same locomotor costs as the men/women with narrower pelves? The answer is, obviously, no.
The pelvis of all of the races of Man has evolved the way they are due to environmental/climatic demands. A wider pelvis is better for thermoregulation in colder climates, while a narrower pelvis/body is more efficient for heat loss (Gruss and Schmidt, 2015).
Thus, we can look at the evolution of brain size/pelvic size in a few ways: 1) The amount of tools/complexity of the tools in the area that led to a need for an increase in brain size for more ‘chunks’ (Gobet and Simon, 1998), which then—along with colder climates—selected for larger brains and a wider body/pelvis which made birthing babes with large heads/brains easier along with helping to conserve heat due to the wider body (Gruss and Schmidt, 2015); 2) Since people in higher altitudes needed a high amount of expertise to survive, further selection for bigger brains, wider pelves occurred because of this; 3) Africans have smaller pelves in comparison to Eurasians because they evolved in hotter climes and didn’t have the amount of tools that peoples in more northerly climes did—which also increased brain size; 4) putting this all together, we can say that because Africans live in hotter climates, they need narrow pelves in order to lose body heat; Eurasians, after they migrated into more northerly climes, needed a wider body/pelvis in order to retain heat. When Man migrated north, he needed the ability to become an expert in, say, tool-making and thus needed a bigger brain for more informational chunks (Simon and Gobet, 1998; Skoyles, 1999). Due to this, Eurasians have wider pelves since they needed larger brains for a higher expertise capacity (Skoyles, 1999).
When Man migrated north, he needed the ability to become an expert in, say, tool-making and thus needed a bigger brain for more informational chunks (Simon and Gobet, 1998; Skoyles, 1999). Due to this, Eurasians have wider pelves than Africans; so they can birth larger-brained children. The width of the female pelvis, too, was shaped by sexual selection (Lassek and Gaulin, 2009). Therefore, the evolution of the modern pelvis in human populations comes down to climatic variation, which, in turn, affects how large of a brain the babe is able to have. Climate constrains brain size in either ‘direction’, big or small. We don’t even need to look at the variation within modern Homo sapiens to see the pattern in pelvic size we do today; because the pelvic differences noted among Man definitely were in effect millions of years ago, with hominids in colder climates having wider pelves while hominids in warmer climates had narrower pelves.
Along with everything above, the evolution of the human pelvis has a few implications for the human races today. Some recent studies have shown that there is no obstetric dilemma at all, with birth complications being caused by babies with higher weights than in our ancestral past, due to environmental mismatches causing higher-weight babies (Warrener et al, 2015; Betti, 2017), which was also beneficial for the evolution of our large brains (Cunnane and Crawford, 2003) with the largest amount of cortical neurons in the animal kingdom. However, marked differences in locomotion would be seen in people who had wide pelves compared to narrow pelves; which is what we see in elite running competitions: the elite runners have narrower pelves. So wider pelves don’t impede normal bipedal walking, but it does impede being able to efficiently run, as evidenced in participants of elite sprinting and marathon competitions. Looking at champion athletes and studying their locomotion (along with other traits as I’ve covered here) you can see that those with narrower pelves win more competitions than those with wider pelves (and happen to have different muscle fiber competition, fat distribution/percent, and morphology).
Racial differences in the pelvis explain the reasons behind why a certain race dominates in certain elite competitions; it largely comes down to skeletal morphology. These skeletal differences have evolutionary underpinnings, with the same pelvic differences seen in hominins that evolved in colder/warmer climates in the past. These pelvic differences (along with body fat percentage/distribution, musculoskeletal morphology, muscle fiber type, lean mass percentage, lower Vo2 max, poorer running economy, a larger Q-angle [4.6 degrees greater than men], etc) are why women are less efficient runners. People with wider hips are more likely to have be endomorphic while people with narrower hips are more likely to be ecto and meso. Not surprisingly, people from northerly climes consistently win WSM competitions whereas East and West Africans dominate bodybuilding and sprinting/marathons due to having a narrower pelvis and other advantageous morphological traits that lead to success in the sport. Nevertheless, pelvic differences between the races largely come down to differences in climate, which was also seen in ancient hominins. These pelvic differences further lead to racial differences in elite sporting competition.
Betti, L. (2017). Human Variation in Pelvic Shape and the Effects of Climate and Past Population History. The Anatomical Record,300(4), 687-697. doi:10.1002/ar.23542
Cunnane, S. C., & Crawford, M. A. (2003). Survival of the fattest: fat babies were the key to evolution of the large human brain. Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology,136(1), 17-26. doi:10.1016/s1095-6433(03)00048-5
Dr. John R. Skoyles (1999) HUMAN EVOLUTION EXPANDED BRAINS TO INCREASE EXPERTISE CAPACITY, NOT IQ. Psycoloquy: 10(002) brain expertise
Entine, J. (2000). Taboo: why Black athletes dominate sports and why we are afraid to talk about it. New York: PublicAffairs.
Gobet, F., & Simon, H. A. (1998). Expert Chess Memory: Revisiting the Chunking Hypothesis. Memory,6(3), 225-255. doi:10.1080/741942359
Gruss, L. T., & Schmitt, D. (2015). The evolution of the human pelvis: changing adaptations to bipedalism, obstetrics and thermoregulation. Philosophical Transactions of the Royal Society B: Biological Sciences,370(1663), 20140063-20140063. doi:10.1098/rstb.2014.0063
Hogervorst, T., Heinse W.B., & de Vos J., (2009) Evolution of the hip and pelvis. Acta Orthopaedica, 80:sup336, 1-39, DOI: 10.1080/17453690610046620
Lieberman, D. E., Raichlen, D. A., Pontzer, H., Bramble, D. M., & Cutright-Smith, E. (2006). The human gluteus maximus and its role in running. Journal of Experimental Biology,209(11), 2143-2155. doi:10.1242/jeb.02255
Lieberman, D. E. (2015). Human Locomotion and Heat Loss: An Evolutionary Perspective. Comprehensive Physiology, 99-117. doi:10.1002/cphy.c140011
Piantadosi, S. T., & Kidd, C. (2016). Extraordinary intelligence and the care of infants. Proceedings of the National Academy of Sciences,113(25), 6874-6879. doi:10.1073/pnas.1506752113
Rushton J P (1997). Race, Evolution, and Behavior. A Life History Perspective (Transaction, New Brunswick, London).
Handa, V. L., Lockhart, M. E., Fielding, J. R., Bradley, C. S., Brubakery, L., Cundiffy, G. W., … Richter, H. E. (2008). Racial Differences in Pelvic Anatomy by Magnetic Resonance Imaging. Obstetrics and Gynecology, 111(4), 914–920.
Warrener, A. G., Lewton, K. L., Pontzer, H., & Lieberman, D. E. (2015). A Wider Pelvis Does Not Increase Locomotor Cost in Humans, with Implications for the Evolution of Childbirth. PLoS ONE, 10(3), e0118903.
Weaver, T. D., & Hublin, J. (2009). Neandertal birth canal shape and the evolution of human childbirth. Proceedings of the National Academy of Sciences,106(20), 8151-8156. doi:10.1073/pnas.0812554106
Weaver, T. D. (2009). The meaning of Neandertal skeletal morphology. Proceedings of the National Academy of Sciences,106(38), 16028-16033. doi:10.1073/pnas.0903864106
Numerous academics have been looked at as pariahs for uttering this word. This word has a pretty long history offending people. The word I’m talking about is natural. This “N” word—especially today—is extremely divisive in today’s society. If you say that something is ‘natural‘, are you taking away any accomplishments that one has done, all because it’s ‘natural‘?
Take what I’ve been writing about for the past three weeks: athletics. If you say that one is a “natural” at athletic competition, are you taking away the hard work it took for that specific athlete to accomplish his goal? No way. You’re acknowledging that that specific individual has something special that sets him apart from the average person. That’s not to say that hard work, determination, and confidence don’t matter; on the contrary. They DO matter. However, like I said with the Kalenjin Kenyan distance runners (who do have anatomical/physiologic advantages in regards to sprinting): you can take someone with elite genetics who has done elite training and put him up against someone who has subpar genetics (in terms of the athletic event) with elite training—the same training as the athlete with elite genetics—and the athlete with elite genetics/muscle fibers/physiology will constantly blow away the individual who is less genetically gifted.
People readily admit that certain races excel at certain physical activities whereas other races don’t fare as well. As I’ve extensively covered (and provided more than enough evidence/arguments for), the races differ in the number of muscle fibers which cause higher rates of obesity in blacks; this causes strength differences which then correlate with mortality. Finally, somatype is extremely important when speaking about athletics. Blacks have a mesomorphic somatype, which, along with their fiber typing and physiologic differences on average compared to whites, cause blacks to dominate most sporting events. However, when you say that certain races are “naturally more intelligent than others“, people all of a sudden have a bone to pick.
This “N” word when it comes to athletics is perfectly fine to use in our vocabulary, yet when we begin talking about intelligence differences—between races and individuals—all of a sudden we think that everyone is the same and that all brains are made the same. We believe that, although humans evolved genetically isolated for thousands of years and have incurred anatomic/physiologic differences, that one organ—the brain—is somehow exempt from the forces of natural selection. I can think of no traits that WON’T get selected for/against, and so I can think of no reason why the brain wouldn’t be under different selective pressures in Siberia/Northern Europe/the Americas/Africa/PNG/Australia.
However, as far as I can tell, we have not found any alleles that differ between populations. It was proposed in 2005 that the genes ASPM and Microcephalin influenced brain growth (Evans et al, 2005; Mekel-Brobov et al, 2005). However, two years later, Rushton, Vernon and Ann Bons (2007) showed that there was no evidence that Microcephalin and ASPM were associated with general mental ability (GMA), head circumference or altruism. Peter Frost cites Woodley et al, (2014) showing that the correlation between microcephalin and IQ is .79, whereas the correlation with ASPM and IQ was .254. Woodley et al (2014) also show there is a correlation between Disability Adjusted Life Years (DALY) and Microcephalin. The reasoning is that Microcephalin may improve the body’s immune response to viral infections, enabling humans to live in larger societies and thus get selected for higher IQ. Since the allele seems to give better disease resistance, then, over time, selection for higher intelligence can be selected for since fewer people are dying from disease due to increased resistance.
Nevertheless, the debate is still out on this allele. However, the data does look good in that we may have found certain polymorphisms that differ between populations which may explain some racial differences in intelligence. (For more information on IQ alleles, see Race and IQ: the Case for Genes).
Now, we are beginning to have some good evidence pile up showing that there are population differences in these alleles, and that they do predict intelligence. Racial differences in intelligence aren’t accepted by mainstream science and the public at large (obviously) like physiologic/anatomic differences are between human populations. Populations are split for thousands of years. They evolve different anatomy/physiology based on the environment. So, then, why wouldn’t psychological differences appear between the races of Man, when other, physical changes occurred from the OoA migration? It literally makes no sense.
People readily admit that athleticism is largely “natural“, yet when someone says that differences in intelligence are largely due to genes they get shouted down and called a ‘racist’, as if that adds anything to the dialogue. People readily admit that individuals/races are “naturally” leaner/stronger/faster/have quicker reflexes. But if one just even hints at thinking about “natural” differences between populations when it comes to general mental ability, they will be shouted down and their careers will be ruined.
Why? Why are people so scared of the “N” word? Because people want to believe that what they do or do not accomplish comes down to them as an individual and only them. They don’t want to think about the complex interaction between genes x environment and how that shapes an individual’s life path. They only think about environment, and not any possible genetic factors. Certain people—mostly social science majors—deny that evolution had ANY impact on human behavior. The “N” word, especially in today’s society, is a completely divisive word. State that you hold hereditarian views (in terms of mental ability) in regards to differences between populations and athletic events and no one will bat an eye.
“Didn’t you see Usain Bolt blow away the competition and set a new world record in the 100m dash at 9.58 seconds?!”
“He’s naturally good, he was born a gifted athlete.”
No one will bat an eye if you say this. This is where the tables will be flipped if you say:
“Don’t you know that differences in intelligence are largely genetic in nature and no matter how much you ‘train the brain’ you’ll stay at that intelligence level?”
“Man, that’s racist. That shouldn’t be looked at. We are all the same and equal. Except when it comes to certain athletic events, then we are not equal and some populations have natural predispositions that help them win. Evolution stopped at the neck 100kya; the only parts of the body under selective pressure over the past 100kya is below the neck!”
People who say this need to explain exactly what shields the brain from selection pressures. Man originated in Africa, the descendants of the soon-to-be coalesced races spent tens of thousands of years in differing environments. You need to do different things to survive in different environments. Just as the races differ physically, they differ mentally as well. Evolution did not stop at the neck. Significant changes in the brain have occurred in the past 10,000 years. There was a trade-off with agriculture, in that it was responsible for the population explosion which was responsible for mutations that affect intelligence and thus get selected for.
The “N” word is not a scary word. It is, in fact, it’s just common sense. People need to realize that by accepting genetic explanations for black domination in sports, that they would then, logically, have to accept racial differences in intelligence. It makes no sense to accept evolutionary theories (even if you don’t know it) in regards to athletics and not accept the same evolutionary theories for racial differences in the brain. There are real differences between populations, in both anatomy/physiology and our mental faculties and brain organization. If you accept one, you have to accept the other.
Strength differences between the races are of big interest to me. Not only due to the evolutionary perspective, but also due to how it relates to health and disease. Hand grip strength (HGS) in men is a good predictor of: Parkinson’s disease (Roberts et al, 2015); lower cardiovascular health profile (Lawman et al, 2016); Alzheimer’s disease (Buchman et al, 2007) and other chronic diseases in men, not in women (Cheung et al, 2013). HGS also predicts diabetes and hypertension (Mainous 3rd et al, 2015), as well as death from all causes, cardiovascular disease (CVD) and cancer in men (Gale et al, 2006). Due to these associations, the study of HGS in men is well warranted. However, here too, we find racial differences and they just so happen to follow trends and corroborate with other data on the mortality of men with lower grip strength.
Araujo et al (2010) obtained data from the Boston Community Health/Bone (BACH/Bone) Survey which included 1,219 randomly selected black, white and ‘Hispanic’ men to assess lean mass, muscle strength, and physical function. Though out of this sample, 10 men didn’t have a DXA performed and 49 men missing data on lean mass, fat mass and Physical Activity for the Elderly (PASE), which left 1,157 men to be analyzed. These studies, however, leave a lot to be desired in how they measure strength (for the purposes that I’m interested in) but they will have to do, for now. Unlike the bench pressing study I wrote about yesterday in which calipers were used to assess body fat, in this study they measured body fat with the DXA scan to assess lean mass. That way, there won’t be any potential confounds, possibly skewing lean mass/fat comparisons. The age of the cohort ranged from 30 to 79 with a mean age of 48.
Table 1 shows the results of the DXA scan, anthropometric data and lean and fat mass. Blacks’ mean lean mass of 124 pounds (mean weight 193 pounds), ‘Hispanics” lean mass was 114 pounds (mean weight 179 pounds) and whites had a mean lean mass of 122 pounds (mean weight 196 pounds). Blacks had a mean grip strength of 89.826 pounds while ‘Hispanics’ had a mean grip strength of 82.698 pounds and whites had a mean grip strength of 88.528 pounds. Blacks had a higher lean mass index than whites by 5 percent, but had a composite physical function score 20 percent lower than whites.
White men had a 25 percent higher average composite physical functioning score, which, when indexed by lean mass and grip, white men had grips 10 percent stronger. White men also scored higher on physical function and lean mass. White men had lower levels of lean muscle mass than blacks and ‘Hispanics’ after controlling for confounding factors, yet whites were still stronger. Since lean mass is related to strength, blacks and ‘Hispanics’ should have had a stronger grip, yet they didn’t. Why?
The authors stated that the reason was unknown since they didn’t test for muscle quality or strength exerted for each unit of muscle. I have proven that whites, on average, are stronger than blacks. If the it were true that blacks were stronger, which is what you see upon first glance viewing table 1 of Araujo et al (2010), then the black population would have lower rates of morbidity and mortality due to higher levels of strength. The black population doesn’t have lower levels of morbidity or mortality. Therefore blacks are not stronger than whites.
Muscular strength is associated with mortality in men (Ruiz et al, 2008; Volaklis, Halle, and Meisenger, 2015), so if the strongest race of men has lower incidences of the above diseases mentioned above along with a higher life expectancy, then there is a good chance that muscular strength is a good predictor of disease within and between race and ethnicity as well. Muscular strength is inversely associated with death from all causes and cancer in men even after adjusting for cardiorespiratory factors. The findings from Ruiz et al (2008) are valid for young and old men (aged 20-82), as well as normal and overweight men.
There are clear associations between muscular strength/hand grip strength and mortality. These differences in mortality are also seen in the United States between race. In 2012, the death rate for all cancer combined was 24 percent higher in black men than in white men. Life expectancy is lower for blacks at 72.3 years compared to 76.7 years for white men (American Cancer Society, 2016). As shown above, men with lower levels of muscular strength have a higher risk of mortality.
As I have asserted in the past, blacks have differing muscle fiber typing (type II) on average when compared to whites (who have type I fibers). Type II muscle fibers are associated with a reduced Vo2 max, which has implications for the health of black Americans. Blacks have lower aerobic capacity along with a greater percentage of type II skeletal muscle fiber (Caesar and Hunter, 2015).
Slow twitch fibers fire through aerobic pathways. Fast twitch (Type II) fibers fire through anaerobic pathways and tire quicker than slow twitch. Each fiber fires off through different pathways, whether they be anaerobic or aerobic. The body uses two types of energy systems, aerobic or anaerobic, which then generate Adenosine Triphosphate, better known as ATP, which causes the muscles to contract or relax. Depending on the type of fibers an individual has dictates which pathway muscles use to contract which then, ultimately, dictate if there is high muscular endurance or if the fibers will fire off faster for more speed.
Differences in muscle fiber typing explain why whites had a stronger grip than non-whites in the BACH/Bone survey. Testing the fiber typings of the three ethnies would have found a higher percentage of type II fibers in blacks, which would account for the lower grip strength despite having higher levels of lean mass when compared to whites.
The apparent ‘paradox’ seen in Araujo et al (2010) is explained by basic physiology. However, in our politically correct society, such differences may be suppressed and thusly people won’t be able to receive the help they need. Race is an extremely useful marker in regards to medicine. By denying average racial differences in numerous anatomical/metabolic/physiologic traits, we deny people the right help they need. Common sense dictates that if such relationships are found, then further research must occur in order to find the cause and a possible solution to the problem.
This study by Araujo et al shows that we need to pay more attention to race when it comes to disease. By denying racial differences we are dooming people to a lower quality of life due to the implicit assumption that we are all the same on the inside (farrrrr from the truth). These average differences in metabolism, anatomy, and physiology do account for some of the variation in disease between race and ethnicity, so this warrants further research. If only we, as a country, can acknowledge racial differences and get people the correct help. Maybe one day we can stop assuming that all races are equal on the inside and when you notice a trend within a particular racial group you find out the cause and whether or not there is any way to ameliorate it.
Muscular strength adds to the protective effect of cardiorespiratory fitness and risk of death in men. That blacks have lower levels of strength than whites, have different muscle fiber typing than whites on average, a lower life expectancy than whites, and higher rates of cancer show that they do not have the physical strength that whites do. What really seals the deal is the fact that blacks have more type II muscle fibers (Caesar and Hunter, 2015). Muscular strength/grip strength is a great predictor of disease in men. Since blacks have lower grip strength yet higher levels of lean mass compared to whites, this show that the difference is due to muscle fiber typing, which, as I have covered in the past, are also associated with cardiometabolic disease and obesity.
Blacks have the highest rate of obesity in America. Looking at obesity rates in America, we see that 69 percent of black men are overweight or obese (remember that black Americans with more African ancestry are less likely to be obese), 71.4 percent of white men are overweight or obese, and 78.6 percent of ‘Hispanic’ men are overweight or obese (Ogden et al, 2016).
Blacks are not stronger than whites. I have compiled enough data to prove that fact. This adds further support for my contention.
American Cancer Society. Cancer Facts & Figures for African Americans 2016-2018. Atlanta: American Cancer Society, 2016.
Araujo, A. B., Chiu, G. R., Kupelian, V., Hall, S. A., Williams, R. E., Clark, R. V., & Mckinlay, J. B. (2010). Lean mass, muscle strength, and physical function in a diverse population of men: a population-based cross-sectional study. BMC Public Health,10(1). doi:10.1186/1471-2458-10-508
Buchman, A. S., Wilson, R. S., Boyle, P. A., Bienias, J. L., & Bennett, D. A. (2007). Grip Strength and the Risk of Incident Alzheimer’s Disease. Neuroepidemiology,29(1-2), 66-73. doi:10.1159/000109498
Ceaser, T., & Hunter, G. (2015). Black and White Race Differences in Aerobic Capacity, Muscle Fiber Type, and Their Influence on Metabolic Processes. Sports Medicine,45(5), 615-623. doi:10.1007/s40279-015-0318-7
Cheung, C., Nguyen, U. D., Au, E., Tan, K. C., & Kung, A. W. (2013). Association of handgrip strength with chronic diseases and multimorbidity. Age,35(3), 929-941. doi:10.1007/s11357-012-9385-y
Gale, C. R., Martyn, C. N., Cooper, C., & Sayer, A. A. (2006). Grip strength, body composition, and mortality. International Journal of Epidemiology,36(1), 228-235. doi:10.1093/ije/dyl224
Lawman, H. G., Troiano, R. P., Perna, F. M., Wang, C., Fryar, C. D., & Ogden, C. L. (2016). Associations of Relative Handgrip Strength and Cardiovascular Disease Biomarkers in U.S. Adults, 2011–2012. American Journal of Preventive Medicine,50(6), 677-683. doi:10.1016/j.amepre.2015.10.022
Mainous, A. G., Tanner, R. J., Anton, S. D., & Jo, A. (2015). Grip Strength as a Marker of Hypertension and Diabetes in Healthy Weight Adults. American Journal of Preventive Medicine,49(6), 850-858. doi:10.1016/j.amepre.2015.05.025
Ogden C. L., Carroll, M. D., Lawman, H. G., Fryar, C. D., Kruszon-Moran, D., Kit, B.K., & Flegal K. M. (2016). Trends in obesity prevalence among children and adolescents in the United States, 1988-1994 through 2013-2014. JAMA, 315(21), 2292-2299.
Roberts, H. C., Syddall, H. E., Butchart, J. W., Stack, E. L., Cooper, C., & Sayer, A. A. (2015). The Association of Grip Strength With Severity and Duration of Parkinson’s. Neurorehabilitation and Neural Repair,29(9), 889-896. doi:10.1177/1545968315570324
Ruiz, J. R., Sui, X., Lobelo, F., Morrow, J. R., Jackson, A. W., Sjostrom, M., & Blair, S. N. (2008). Association between muscular strength and mortality in men: prospective cohort study. Bmj,337(Jul01 2). doi:10.1136/bmj.a439
Volaklis, K. A., Halle, M., & Meisinger, C. (2015). Muscular strength as a strong predictor of mortality: A narrative review. European Journal of Internal Medicine,26(5), 303-310. doi:10.1016/j.ejim.2015.04.013
I just came across this video on YouTube published yesterday called “White people are not 100% human (Race differences) (I.Q debunked)“, with, of course, outrageous claims (the usual from Afrocentrists). I already left a comment proving his nonsense incorrect, but I thought I’d further expound on it here.
His first ‘evidence’ that whites aren’t 100 percent human is showing some individuals who are born with tails. Outliers are meaningless, of course. The cause of the human tail is due to the unsuccessful inhibition of the Wnt3-a gene. When this gene isn’t successful in signaling the cell death of the tail in early embryonic development, a person is then born with a small vestigial tail. This doesn’t prove anything.
His next assertion is that since “94 percent of whites test positive for Rh blood type” and that “as a result, they are born with a tail”, then whites must have interbred with rhesus monkeys in the past. This is ridiculous. This blood type was named in error. The book Blood Groups and Red Cell Antigens sums it up nicely:
The Rh blood group is one of the most complex blood groups known in humans. From its discovery 60 years ago where it was named (in error) after the Rhesus monkey, it has become second in importance only to the ABO blood group in the field of transfusion medicine. It has remained of primary importance in obstetrics, being the main cause of hemolytic disease of the newborn (HDN).
It was wrongly thought that the agglutinating antibodies produced in the mother’s serum in response to her husbands RBCs were the same specificity as antibodies produced in various animals’ serum in response to RBCs from the Rhesus monkey. In error, the paternal antigen was named the Rhesus factor. By the time it was discovered that the mother’s antibodies were produced against a different antigen, the rhesus blood group terminology was being widely used. Therefore, instead of changing the name, it was abbreviated to the Rh blood group.
As you can see, this is another ridiculous and easily debunked claim. One only needs to do a bit of non-biased reading into something to get the truth, which some people are not capable of.
What he says next, I don’t really have a problem with. He just shows articles stating that Neanderthals had big brains to control their bodies and that they had a larger, elongated visual cortex. However, there is archeological evidence that our cognitive superiority over Neanderthals is a myth (Villa and Roebroeks, 2014). What he shows in this section is the truest thing he’ll say, though.
Then he shows how African immigrants to America have a higher educational achievement than whites and immigrant East Asians. However, it’s clear he’s not heard of super-selection. The people with the means to leave will, and, most likely, those with the means are the more intelligent ones in the group. We also can’t forget about ‘preferential treatment’, AKA Affirmative Action.
The concept of ‘multiple intelligences’ is then brought up. The originator of the theory, Howard Gardner, rejects general intelligence, dismisses factor analysis, doesn’t defend his theory with quantitative data, instead, drawing on anthropology to zoology findings for his claims, being completely devoid of any psychometric or quantitative data (Herrnstein and Murray, 1994: 18). The Alternative Hypothesis also has a thorough debunking of this claim.
He then makes the claim that hereditarians assume that environment/experience play no factor in performance on IQ tests/life success. We know that both the individual heritability is 80/20 genetics and environment, with the black-white gap being the same (Rushton and Jensen 2005: 279). Another easily refuted claim.
The term ‘inferior’ is brought up due to whites’ supposed ‘inferiority’, though we know that terms such as those have no basis in evolutionary biology.
He claims that a black man named Jesse Russel invented the cell phone, when in reality a white man named Martin Cooper did. He claims that Lewis Latimer invented the filament lightbulb, when a man named Joseph Swan obtained the patent in the UK in 1860. Of course, individual outliers are meaningless to group success, as they don’t reflect the group average as a whole, so these discussions are meaningless.
He finally claims that the “black Moors civilized Europe”. Europeans didn’t need to “be civilized”, I guess people don’t understand that empires/kingdoms rise and fall and go through highs and lows. That doesn’t stop people from pushing a narrative, though. Further, the Moors were not black. People love attempting to create their own fantasy history in which their biases are a reality.
I don’t know why people have to make these idiotic and easily refuted videos. Lies that push people further from the truth of racial differences, genetics, and history as a whole. Biases such as these just cloud people’s minds to the truth, and when the truth is shown to them, refuting their biases and twisting of history, genetics, and IQ, they then look at it as an attack on what they deem to be true despite all of the conflicting, non-biased evidence shown to them. Afrocentric loons need to be refuted, lest people believe their lies, misconceptions and twistings of history.
The black-white prostate cancer gap: genetic? Environmental? Both? Over the years, countless studies have been carried out—mostly on testosterone—to find the cause of the disparity between American blacks and whites. Numerous research has shown that black Americans’ test is substantially higher than white Americans (Ross et al, 1986; Winters et al, 2001; etc). However, studies with larger samples showed this was not the case. In a sample of 3,654 whites and 585 black Vietnam veterans shows there is a 3 percent difference favoring blacks (Ellis and Nyborg, 1992). The gold standard—a meta-analysis on 14 relevant studies (which I will discuss tonight) shows that the difference in (free) testosterone is nowhere near what Ross et al (1986) say, but was substantially lower at 2.5 to 4.9 percent (Richard et al, 2014). The meta-analysis, which was done due to the conflicting figures in each study showed that the gap in testosterone.
Obviously these people weren’t genotyped for racial ancestry, so the authors included studies that only included racial descriptors:
If races/ethnicities included in the study were referred to as ‘black’, ‘African-American’, ‘non-Hispanic black’, ‘white’, ‘non-Hispanic white’ or ‘Caucasian’. We did not include men of Hispanic or Asian origin.
Since we know that self-identified race is an almost perfect predictor of genetic ancestry, and the meta-analysis included studies that used the only the descriptors for race/ethnicity then the fact that this is done on American sample shows that testosterone is not as high as commonly thought in blacks when compared to whites (13 percent higher free testosterone).
In this sphere, one of the most common things said is that testosterone is one of the biggest causes of the black-white crime gap. High levels of testosterone ARE linked to higher crime rates, and blacks commit the most crimes, therefore blacks MUST have substantially higher levels of testosterone to account for the difference, right? Wrong. As I’ve shown above, Richard et al (2014) show that even after controlling for age, the difference in free testosterone was 2.5 to 4.9 percent. Black American males have an annual death rate from prostate cancer 2.4 times higher than whites (Taksler, Keating, and Cutler, 2012). If testosterone—one of the main possible culprits—does not explain the higher rate of prostate cancer mortality in American blacks in comparison to whites, what does?
Diet/environment and smaller genetic effects. People who have lower income cannot afford high-quality food, so they, therefore, have to buy low-quality, high carb, highly processed foods which lead to nutrient deficiencies. Drewnowski and Specter (2004) showed that 1) the highest rates of obesity are found in populations with the lowest incomes and education (correlated with IQ); 2) an inverse relationship between energy density and energy cost; 3) sweets and fats have higher energy density and are more palatable; and 4) poverty and food insecurity are associated with lower food expenditures, lower fruit and vegetable intake, and lower-quality diet. All of these data points show that those who are poor are more likely to be obese due to more energy-dense food being cheaper and fats and sugars being more palatable.
One important nutrient that people are often deficient in is vitamin D. Due to the name, people assume it’s a vitamin. It’s really not. It’s a steroid hormone. Vitamin D promotes calcium absorption, maintains normal calcium and phosphate levels, promotes bone and cell growth, and reduces imflamation. Black Americans have numerous ailments that are associated with low vitamin D intake.
Black Americans have a lower intake of vitamin D in comparison to white Americans. This is due to low dietary intake of vitamin D and less sun exposure. Dark skin pigmentation reduces vitamin D production in the skin, as dark skin requires more sunlight in order to produce vitamin D. Rickets is a common a common problem for blacks as when the mother is pregnant, she doesn’t get sufficient vitamin D so when the baby is born, it is deficient.
One variable that Dr. Joseph Mercola brings up is that black women don’t breastfeed as much as white women (though the gap is beginning to close a bit) causing rickets (as well as the lack of availability of vitamin D for the baby due to darker skin needing more sunlight to acquire adequate vitamin D).
Pretty much a great case for why race and geography should inform vitamin D intake. This is pivotal for our understanding for racial/ethnic differences in disease acquisition, why these differences occur and what can be done to prevent them.
Elevated levels of testosterone in black men comparison to white men are supposed to explain the higher rate of mortality in black men compared to white men. Except Richard et al (2014) showed that the testosterone gap wasn’t as high as previously thought (at 2.4 to 5.9 percent higher). The deficiency in vitamin D explains this phenomenon. Low vitamin D is linked to aggressive prostate cancer. This is the cause for the disparity, not higher rates of testosterone.
Numerous factors prevented Colonial America from becoming a united empire. The main reason was that it was not a homogeneous nation. Looking back at history united empires were racially homogeneous. IQ differences both within and between races also play a factor. When a country is homogenous, all (or most) of the people living within the boundaries of the country all have the same interests, which is not seen when a land is non-homogeneous.
The first and most important factor preventing America from becoming a united empire was that America was not a racially homogenous land. All of the races currently in the country at the time had their own motivations and how they wanted to get them done. When countries are not racially homogenous, they don’t have the same goals and thusly cannot work together for common goals. The African slaves wouldn’t work together with Europeans as the Europeans held them as slaves. The Natives in the country had their own goals as well (such as protecting their land), and would not work together either.
The Colonial settlers did conduct trade with the ‘Natives’, however, we had quite a few wars with them and the great Andrew Jackson isn’t looked at too highly amongst ‘Native Americans’. However, this is just what occurs when a land is so racially/ethnically divided. When a country is homogeneous, there is less of a chance for wars and strife to break out (that is, if they’re not as inbred as Arab Muslims are).
Contrary to popular belief, a paltry amount of slaves came to America, around 2 to 3 percent (with the rest going to the Carribean and Latin America) of slaves from West Africa were transported to what is now America. However, with the ‘Natives’ also being in what is now America, when Europeans settled America there were now three ethnies in one land who all had their own separate ethnic genetic interests. This small amount of slaves had large negative effects on the QoL of the American citizens at the time. The African slaves rebelled a lot; these rebellions killed a lot of people, both black and white. This also
Another reason for this was that between the North and South, there was a difference between the ethnic demographics of the area. The South had more slaves while the North had less. Another factor was, for instance with regards to Chesapeake and New England, they both had differing amounts of men and women, and the biggest factor was that both regions had differing amounts of slaves. With two such distinct areas of the country both with peoples from differing parts of the world, this is yet another reason why Colonial America would not become a united empire.
Lastly, the ethnic demographic differences between the North and the South prevented America from realizing its true potential. The North had a much more complex economy with farming, trading ship building, and related matters. The differences from both regions of the country greatly contributed to why the new country never became a superpower.
The Southern part of the Colonies was more Scots-Irish, while the Northern ones, like the New England territories, were more English. Along with these ethnic differences (they will have differing ideas of ethnic interests), there were also differences in death rates (in the South, the average age of death was 43, due in part to the amount of slaves). Moreover, in the North the male/female ratio was 3 males for 2 females where in the South it was 6 males to every one female.
I could also see IQ differences playing a factor here. Scots-Irish are less intelligent today; and if you look at their current descendants in Appalachia today, they’re what is called ‘white trash’. The English had a much better environment, encouraged family life, and they also developed their own hierarchy. Looking at America in the American South and New England, we can see these intelligence differences still exist today. I wouldn’t doubt that these IQ differences DO go back to Colonial America, and if so, it is a great explanation for economic as well as life differences between the two different parts of the Colony with peoples from different countries.
The reasons Colonial America never became a superpower are numerous, however, the main reason is that it was not racially/ethnically homogenous. When a land is homogeneous, the people can work towards a common goal and feel safer. The differences in lifestyle and economy between the North and the South were also two other contributing factors. Intelligence differences played a huge factor in life outcomes and how each part of the country conducted day-to-day life. Other things such as inequalities between classes can be (somewhat) ameliorated, however, if a country is not racially/ethnically homogeneous, they will never become a world power as too much in-country strife will ensue. The story of why Colonial America never became a United Empire is imperative to show that races and ethnies have differing ways of life and when they live together in the same area, ethnic strife occurs. The main difference, I believe, that there was no united empire was due to the huge intelligence differences both between races and within them. As we can see today, intelligence differences both within and between countries and peoples are a huge reason for the readily apparent differences between them.