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No, Black Women Do Not Have Higher Testosterone than White Women (And More On Hereditarian Claims on Racial Testosterone Differences)
It has been over a year since I wrote the article Black Women and Testosterone, and I really regret it. Yes, I did believe that black women had higher levels of testosterone than white women due to one flimsy study and another article on pregnant black women. I then wised up to the truth about testosterone and aggression/crime/race/sex and revised the articles (like I have done with r/K selection theory). However, after I revised my views on the supposed differences in testosterone between black men/white men and black women/white women, people still cite the article, disregarding the disclaimer at the top of the article. I quoted Mazur (2016), who writes (emphasis mine):
The pattern [high testosterone] is not seen among teenage boys or among females.
There is no indication of inordinately high T among young black women with low education.
Honor cultures are cast as male affairs, but with T data in hand for both sexes, it is worth exploring whether or not a similar pattern exists among women. Mean T was calculated as a function of age for the four combinations of race and education used in Table 1 but now for women. All plots show T declining with age, from about 35 ng/dL in the 20–29 age group to about 20 ng/dL among women 60 years and older. The four plots essentially overlap without discernible differences among them. Given the high skew of T among adult females, both raw and ln-transformed values were analyzed with similar results. There is no indication of inordinately high T among young black women with low education.
In the present study, at least, the sexes differ because the very high T seen among young black men with low education does not occur among young black women with low education.
This is very clear… Mazur (2016) analyzed the NHANES 2011-2012 data and this is what he found. I understand that most HBD bloggers do believe this, well, like a lot of their strong assertions (which I have rebutted myself), they’re wrong. They don’t get it. They do not understand the hormone.
The reason why I’m finally writing this (which is long overdue) is that I saw a referral from this website today: https://www.minds.com/RedPillTV who writes about the aforementioned black women and testosterone article:
It is known that blacks have the highest levels of testosterone out of the major races of humanity. However, what’s not known is that black women have higher rates than white women. The same evolutionary factors that make it possible for black men to have high testosterone make it possible for women as well.
…..No. It seems that people just scroll on by the disclaimer at the top that is bolded and italicized and just go to the (now defunct) article and attempt to prove their assertion that black women have higher testosterone than white women with an article that I have stated myself I no longer believe and have provided the rationale/data for the position. This shows that people have their own biases and no matter what the author writes about their views that have changed due to good arguments/data, they will still attempt to use the article to prove their assertion.
I’ve written at length that testosterone does not cause 1) aggression, 2) crime and 3) prostate cancer. People are scared of testosterone mostly due to the media fervor of any story that may have a hint of ‘toxic masculinity’. They (most alt-righters) are scared of it because of Lynn/Rushton/Templer/Kanazawa bullshit on the hormone. Richard Lynn doesn’t know what he’s talking about on testosterone. No, Europeans did not need lower levels of aggression in the cold; Africans didn’t need higher levels of aggression (relative to Europeans) to survive in the tropics. The theory that supposed differential testosterone differences between the races are “the physiological basis in males of the racial differences in sexual drive which form the core of the different r/K reproduction strategies documented by J.P. Rushton” (Lynn, 1990: 1203). The races, on average, do not differ in testosterone as I have extensively documented. So hereditarians like Lynn and others need to look for other reasons to explain blacks’ higher rate of sexual activity.
Rushton’s views on the testosterone and supposed r/K continuum have been summarily rebutted by me. These psychologists’ views on the hormone (that they don’t understand the production of nor do they understand the true reality of the differences between the races) are why people are afraid of testosterone. No, testosterone is not some ‘master switch’ as Rushton (1999) asserts. Rushton asserts that racial differences in temperament are mediated by the hormone testosterone. He further dives into this assertion stating “Testosterone level correlates with temperament, self-concept, aggression, altruism, crime, and sexuality, in women as well as in men (Harris, Rushton, Hampson, & Jackson, 1996). It may ‘correlate’ with aggression and crime, but as I have documented, they do not cause either.
The aggression/testosterone correlation is only .08 (Archer, Graham-Kevan, and Davies, 2005). Furthermore, the diurnal variation in testosterone does not directly correlate to when testosterone levels are highest in the day (at 8 am and drop thereafter), with adults peaking in crime at 10 pm and kids at 3 pm, with rises at 8 pm and 12 pm (not surprisingly, kids go in to school around 8 am, go to recess at 12 and leave at 3).
If you’ve read as much Rushton as I have, you’ll notice that he begins to sound like a broken record when talking about certain things. One of the most telling is Rushton’s repeated assertions that blacks average 3-19 percent higher testosterone than whites. The 3 percent number comes from Ellis and Nyborg (1992) and the 19 percent number comes from Ross et al (1986) (which Rushton should know that after adjustments for confounding, it decreased to 13 percent). These are the only studies that hereditarians ever cite for these claims that blacks average higher testosterone than whites. That seems a bit fishy to me. Cite a 30-year-old study along with a 25-year-old study (with such huge variation from Rushton and those who cite him for this matter—3-19 percent!!) as ‘proof’ that blacks average such higher levels of testosterone in comparison to whites.
Ross et al (1986) is one of the most important studies to rebut for this hereditarian claim that testosterone causes all of these maladies in black American populations. Ross et al (1986) propose that higher levels of the hormone lead to the higher rates of prostate cancer in black American populations. However, meta-analyses do not show this (Zagars et al, 1998; Sridhar et al, 2010).
Rushton et al’s assertions—largely—lie on this supposed testosterone difference between the races and how it supposedly leads to higher rates of crime, prostate cancer, aggression, and violence. However, the truth of the matter is, this is all just hereditarian bullshit. Larger analyses—as I have extensively documented—do not show this trend. And even accepting the claim that blacks have, say, 19 percent higher levels of testosterone than whites, it still would not explain the supposed prostate cancer rates between the races (Stattin et al, 2003; Michaud, Billups, and Partin, 2015). Even if blacks had 19 percent higher testosterone than whites, it would not explain higher levels of crime nor aggression due to such a hilariously low correlation of .08 (Archer, Graham-Kevan, and Davies, 2005).
Finally, I have a few words for Michael Hart and his (albeit sparse) claims on testosterone in his 2007 book Understanding Human History.
Hart (2007) writes:
(Many of these differences in sexual behavior may be a consequence of the fact that
blacks, on average, have higher levels of testosterone than whites.7) (pg. 127)
And….. footnote number 7 is…. surprisingly (not): 7) Ross, R., et al. (1986). Not going to waste my time on this one, again. I’ve pointed out numerous flaws in the study. (I will eventually review the whole thing.)
It seems unlikely, though, that the higher testosterone level in blacks — which is largely genetic in origin — has no effect on their sexual behavior (pg. 128; emphasis mine)
This is bullshit. People see the moderately high heritability of testosterone (.60; Harris, Vernon, and Boomsma, 1998) and jump right to the “It’s genetics!!!” canard without even understanding its production in the body (it is a cholesterol-based hormone which is indirectly controlled by DNA, there are no ‘genes for’ testosterone). Here are the steps: 1) DNA codes for mRNA; 2) mRNA codes for the synthesis of an enzyme in the cytoplasm; 3) luteinizing hormone stimulates the production of another messenger in the cell when testosterone is needed; 4) this second messenger activates the enzyme; 5) the enzyme then converts cholesterol to testosterone
I have documented numerous lines of evidence showing that testosterone is extremely sensitive to environmental factors (Mazur and Booth, 1998; Mazur, 2016), and due to the homeodynamic physiology we have acquired due to ever-changing environments (Richardson, 2017), this allows our hormones to up- or down-regulate depending on what occurs in the environment. The quote from Hart is bullshit; he doesn’t know what he’s talking about.
For females in Siberia, the disadvantages of failing to find a man who would
provide for her and her children during their childhood were much greater than they were in tropical climates, and females who were not careful to do so were much less likely to pass on their genes. Furthermore, because females in harsh climates were so demanding on this point, males who seemed unlikely to provide the needed assistance found it hard to find mates. In other words, there was a marked sexual selection against such males. Such selection could result, for example, in the peoples living in northerly climates gradually evolving lower levels of testosterone than the peoples living in subSaharan Africa. (pg. 131)
This is a bullshit just-so story. Africans in Africa have lower levels of testosterone than Western men (Campbell, O’Rourke, and Lipson, 2003; Lucas and Campbell, and Ellison, 2004; Campbell, Gray, and Ellison, 2006).
Note also that a difference in testosterone level frequently affects not
only the sexual behavior of a young male, but also his aggressiveness.
No it does not (Archer, Graham-Kevan, and Davies, 2005).
Thankfully, that’s all he wrote about testosterone. There is so much bullshit out there. Though, people who like and seek out the truth will learn that there are no racial differences and that testosterone does not cause crime/aggression/prostate cancer and that it’s just hereditarian bullshit.
The evidence I have amassed and the arguments I have given point to a few things: 1) the races do not differ in testosterone/there is a small negligible difference; 2) testosterone does not cause crime; 3) testosterone does not cause aggression; 4) black women do not have higher levels of testosterone than white women; 5) high levels of testosterone do not cause prostate cancer; and 6) even allowing a 19 percent black/white difference will not have hereditarian claims hold true.
So for anyone who comes across my old articles on testosterone and sex/race, do a bit more reading of my newer material here to see my new viewpoints/arguments. DO NOT cite these articles as proof for your claims of higher levels of black men/women. DO cite the old articles ALONG WITH the new ones to show how and why my views changed along with the studies I have cited that changed my view. (Actually understanding the production of testosterone in the body was a huge factor too, which I talk about in Why Testosterone Does Not Cause Crime.)
Edit: (The correlation between aggression and testosterone isn’t .14 as Book et al (2001) state; the true correlation is .08 (Archer, Graham-Kevan and Davies, 2005) So it’s even lower than I thought. This is one of the many reasons why testosterone does not cause crime. It’s just feminist bullshit and fear mongering from people who do not understand the hormone and what it does in the body. The misconceptions come from Rushton’s r/K selection bullshit which has been summarily refuted.)
Recently, I’ve written at length on racial differences in testosterone and how the correlation between testosterone and physical aggression is .14. Pitifully low to account for the cause of crime and any overall differences in racial crime (that will be touched on at length in the future). Tonight I will show, yet again, why testosterone does not cause crime by looking at what times most crimes are committed by both adults and children under the age of 18. This will definitively put the ‘testosterone causes crime’ myth to bed for good.
Before I get into the time of day that most crimes are committed, I must talk about the production of testosterone in the body. There are no ‘genes for’ testosterone (although men who had three certain alleles had a 6.5 fold higher risk of having low testosterone; Ohlsson et al, 2011, I am unaware of there being a variation by race; over 10,000 Caucasian men were studied). There is, however, an indirect control of testosterone synthesis by DNA. DNA regulates the production of testosterone by coding for enzymes that convert cholesterol to testosterone (testosterone is a cholesterol-based hormone).
There are five simple steps to the production of testosterone: 1) DNA codes for mRNA; 2) mRNA codes for the synthesis of an enzyme in the cytoplasm; 3) luteinizing hormone stimulates the production of another messenger in the cell when testosterone is needed; 4) this second messenger activates the enzyme; 5) the enzyme then converts cholesterol to testosterone (Leydig cells produce testosterone in the presence of luteinizing hormone). That’s how testosterone is produced in the body. It is indirectly controlled by DNA.
Above is a graph from the Office of Juvenile Justice and Delinquency Prevention which shows the time of day that most crimes are committed. Notice how crime goes up as the time of day goes on and since kids are at school, they’re more likely to fight. This then peaks at 3 pm when kids are getting out of school.
Now look at rates of crime for adults. At its peak of 10 pm, it’s vastly lower than that of people under the age of 18, which is important to keep in mind. You can see how at 8 am that rates of crime are low for adults and high for kids, right when they would be entering school so there would be a lot of other kids around and the chance for violence goes up. Keep the times of 8 am (kids when they enter school), 12 pm (when most kids go on lunch) and 3 pm (when most kids get out of school) along with the hours of 12 pm to 8 pm for adults (when 74 percent of crimes are committed by adults).
- In general, the number of violent crimes committed by adults increases hourly from 6 a.m. through the afternoon and evening hours, peaks at 10 p.m., and then drops to a low point at 6 a.m. In contrast, violent crimes by juveniles peak in the afternoon between 3 p.m. and 4 p.m., the hour at the end of the school day.
- Nearly one-third (29%) of all violent crime committed by juvenile offenders occurs between 3 p.m. and 7 p.m. In comparison, 26% of all violent committed by adult offenders occurs between 8 p.m. and 12 p.m.
So since testosterone varies by day and levels are highest at 8 am and lowest at 8 pm (Brambilla et al, 2009; however testing men aged 45 years of age and older is fine before 2 pm due to a blunted circadian rhythm; Long, Nguyen, and Stevermer, 2015), then how could testosterone account for why men commit most of their crimes at night and why the crime that children commit spikes when they go to school, go to lunch and get out of school? The answer is that it doesn’t because testosterone does not cause crime. What testosterone does cause, however, are feelings of confidence and dominance, which does not—surprisingly—lead to increased aggression and assault on others (Booth et al, 2006).
What testosterone does cause, however, is social dominance and success, not physical aggression and maladjustment (Shcaal et al, 1996). The effects of environment are also more notable on testosterone than are genetics at 5 months of age (Carmaschi et al, 2010). Furthermore, aggressive behavior is first noticed in infancy and reaches its peak before school age (Tremblay et al, 2004; Cote et al, 2006). Though testosterone does seem to have an effect on aggression in preschool boys, however genetic and environmental causality has not been established (Sanchez-Martin et al, 2000).
Nevertheless, the meta-analyses I cited last week show that testosterone has an extremely low correlation of .14, so other factors must be at play. However, Sanchez-Martin et al (2000:778-779) also note that “Tremblay et al (1998) suggested that associations between testosterone titer and physical aggression are likely to be observed in contexts where such attack leads to social dominance. This may be true of the preschool boys in the present study. The data generated in the present study generally support Scerbo and Kolko (1994), who studied older children (7 to 14 years of age). They found a significant relationship between testosterone levels and aggression (as assessed by clinical staff).”
It’s interesting to note that in the case of Scerbo and Kolko (1994) that after controlling for age and size, testosterone correlated with aggression when rated by staff but not parents or teachers. ‘Staff’ refers to clinic staff at a facility where the children were assessed for hyperactivity disorders. Of course, the staff would rate higher levels of aggression compared to parents of teachers—people who are around the children every day—since they would want a higher chance for diagnosis for certain drugs to ‘cure’ the hyperactivity, but I digress. Testosterone does not induce aggression in children, but it does induce social dominance and confidence which does not lead to aggression (Rowe et al, 2004; Booth et al, 2006).
There was also little difference in testosterone between socially dominant prisoners and aggressive prisoners (Ehrenkraz, Bliss, and Sheard, 1974). Furthermore, the testosterone increase leading to pubertal development in boys is not associated with increased aggression (Tremblay et al, 1998; Booth et al, 2006: 171). Indeed, increased body size is a marker for physical aggression in children, and I doubt these children have high muscle mass so, I assume, they have high levels of body fat and thusly lower levels of testosterone than they would have if they were leaner. Yet another strike against the ‘testosterone causes crime/physical aggression’ hypothesis.
Indeed, this has some implications for the honor culture hypothesis of why low-income blacks have higher levels of testosterone than similarly aged blacks with some college (Mazur, 2016). The patterns for crime as shown by the OOJDP shows that crime rises as the day progresses from the morning until its peak at 3 pm for children and then sharply declines while for adults it peaks at 10 pm.
Testosterone does increase when a challenge is issued; when one man feels his reputation is threatened, the propensity for violence is increased, but this was most notably seen in Southern men (Cohen et al, 1996). So the same would be said for this ‘culture of honor’ found in low-income black neighborhoods, the so-called ‘code of the street’ as stated by Anderson (1994: 88): “Moreover, if a person is assaulted, it is important, not only in the eyes of his opponent but in the eyes of his “running buddies,” for him to avenge himself. Otherwise, he risks being “tried” (challenged) or “moved on” by any number of others. To maintain his honor, he must show he is not someone to be “messed with” or “dissed.””
This culture of honor is found all over the world, including Brazil where homicide can be explained by the need to maintain honor and can be understood by taking into account cultural factors; biological, psychological and socioeconomic factors do not explain murder in Northeast Brazil as well as honor and culture (de Souza et al, 2015). People in honor cultures also have a higher chance of self-harm (Osterman and Brown, 2011) as well as a higher chance of committing violence in school (Brown, Osterman, and Barnes, 2009).
Testosterone does not cause crime; it does not cause aggression. Increases in testosterone before, during and after events are a physiologic process to prime the body for competition. As cited above, dominant behavior does not necessarily lead to violence in most cases, which may be surprising for some. Indeed, honor and culture may explain a nice amount of the homicide and violence rate in the South. Since testosterone is highest at 8 am and lowest at 8 pm and the rates of crime committed by adults and children are vastly different than the diurnal variance in the day, then testosterone does not cause crime and its increase is not associated with crime, but social dominance and confidence which does not lead to crime.
Hopefully—if anyone still believes testosterone to be the boogeyman its made out to be—I’ve put those misconceptions to rest. Racial differences in testosterone cannot be the cause of racial differences in crime—because there is either no statistical difference in testosterone between the races or the difference is non-existent. Testosterone is clearly a beneficial hormone—as I have extensively documented. Misunderstandings of the hormone are abound—especially in the HBD sphere—only due to literally a few paragraphs in a book (Rushton, 1997) and one study that showed blacks have higher testosterone than whites which was the cause of their higher rates of prostate cancer (Ross et al, 1986). The study is hard to find so I had to buy access to it. I will cover this in the future, but I discovered that they assayed the subjects when it was convenient for them—between the hours of 10 am and 3 pm—which is unacceptable. You cannot gauge racial differences in testosterone from a small study (n=50) and a non-representative sample (college students). For these reasons, the study should be thrown in the trash—especially when formulating evolutionary hypotheses.
Testosterone is one of the most important hormones for vital functioning. By knowing how it is processed in the body and that there are no ‘genes for’ testosterone (‘low testosterone genes’ notwithstanding) along with how testosterone has a low relationship with physical aggression one should not be scared of having high levels, on the contrary, one should be scared of having low levels. I have once again proven my case that testosterone is not related to violence in showing the diurnal variation in testosterone levels in adults, as well as the time of day that crimes are committed by both adults and children. High testosterone means high confidence and high dominance—and those two traits have a lot to do with masculinity—which do not lead to violence.
I know why testosterone does not cause crime—because I have an understanding of the hormone, how its produced in the body and what its effects on the body are. The most important thing to note here, is that even if blacks had 15 percent higher testosterone than whites, it still wouldn’t explain higher rates of crime or disease such as prostate cancer. So those who try so hard to prove that blacks have higher levels of the hormone do so in vain, because even if they did it wouldn’t mean anything for any theories they may have. The myth of testosterone causing aggression and crime need to be put to bed for good.
by Scott Jameson
RaceRealist and I have been ruminating on a lot of stuff lately. Here’s a fun one: what economic system works best relative to what we know about human health? In my mind there are two approaches: the libertarian approach, and quasi-fascism.
In the libertarian approach, there’s no regulation of sugar placed in our food. That’s already the case. But here’s an improvement: you don’t have to pay for anyone’s gastric bypass after they overeat that sugar.
In the fascist approach, there is regulation of sugar, because a fascist state does not allow people to poison each other for profit. You still have to pay for others’ medical expenses, but those expenses will be lower.
Here’s an advantage to the libertarian approach. In that society, the people who stuff their faces and refuse to get off the couch- who are dumber and lazier on average, probably- will have a higher mortality rate on average. Eugenics need not cost a dime.
But you run into a snag, sand in the gears of your hands-off system, when Big Food kicks out a whole bunch of crappy dietary advice, at which point a minority of reasonably intelligent people will be led astray, perhaps to the grave. How could a libertarian society stop that from taking place? Would it even bother? Could the system broadly work in spite of this snag?
A libertarian society doesn’t pay for idiots to have children. That’s good, but half of your population (women) are unlikely to ever support it. Women don’t do libertarianism; observe Rand Paul’s demographic Achilles Heel on page 25. When women asked men what to do about so-and-so’s eighth unpaid for child, we’d have to look them in the eyes and give a deadpan “let’s hope private charity can handle it.” There was a time, before FDR, when women would’ve accepted that answer. They were still in the kitchen back then, and I don’t know how to put them back there.
A fascist society has more hands-on eugenics, possibly genome editing or embryo selection. Also good. Expensive, but obviously worth it.
We welcome your input on these issues.
As an aside, White men are well-known as the most conservative, small government, nationalist group out there in our current political atmosphere. I always hear people spewing the schmaltziest nonsense about the values of the Founding Fathers. They were, relative to our political compass, nationalist libertarians. Accordingly, modern nationalists and libertarians do best with the exact same demographics that used to vote on candidates back then: property-owning White men. The sole reason that Ron and Rand Paul couldn’t get elected is that they are too similar to the Founding Fathers. Any other candidate who blathers on about the Founding values is simply a liar, and their obvious lies show a disrespect of your intelligence.
If you’re a libertarian, but not an ethno-nationalistic and patriarchal thinker, then you simply haven’t gotten the memo: women and minorities do not want to create the same world that you do, nor will they ever. Evolution gave us women who want social safety nets and other races which are better off if they parasitize off of your tax dollars. All of the most libertarian societies that ever existed (early US, ancient Athens, Roman Republic) were entirely run by White men, and adding women to the electorate gave us the welfare state. Aristophanes was right.
We’re also ruminating on the difference between IQ and expertise. I know of no mentally complicated task of which one can be a master without being intelligent. Take the IQs of chess grandmasters and you will find no morons.
Contrast that with purely physical activities. I bet you there are some really stupid people out there who are great at dancing for example. A prodigiously capable cerebellum may not predict an equally capable frontal lobe.
Discounting tasks which exclusively require things like simple physical coordination, muscle memory, etc, I ought to think that IQ is the biggest component of expertise.
When critics of the mainstream approach towards modern African-American grievance questions the agency of the population to improve their standards of living, they often cite either how minorities such as poor European immigrants of the Early 20th century assimilated better despite discrimination, or how Black immigrants from Africa occupy a higher mode of living.
While multiple factors contribute to the discrepancy, one caught my attention which struck me a paradoxical but soon started to make sense as I dug deeper. That trait being the lack of effective widespread “unity” among not just Black Americans but many other populations, especially those in Africa.
– The Situation
As for my titular use of “chaos” to describe it, I owe it to an Unz commenter who contrasted it from individualism or collectivism. For an intra-regional example, you have riots or protests regarding threats seen as pertaining to the racial mass, yet you have commonly cited the lack of the same regard for those killed by perpetrators of the same race.
From an inter-regional example I refer to the words of my father that, despite the beliefs of some, there is no “Black America” in which the interests or beliefs of blacks due to having comparatively looser connections than others based on a national level. This is noted by regional variance in ideology between blacks during the Progressive Era or better yet modern African conflicts, many of which can be classified as Christians versus Muslims on the larger scale yet can even be observed on a finer, pre-colonial level of identities (Osaghae and Suberu 2005).
“There are numerous examples of pre-colonial migration, usually stimulated by wars or natural disasters, which have continued to generate bitter conflicts today owing to continuing discrimination against the immigrants by the original settlers. These include the eighteenth century mass migration of Oyo Modakeke into Ife in search of a safe haven from the internecine wars of the Oyo empire; the movement of Urhobo and Ijaw into Warri, where the Itsekiri claim to have been the original settlers; the migration of the Jukun-Chamba from Cameroon to parts of the present Taraba state, originally settled by the Kuteb; and the sixteenth century settlement of Hausa merchants in Zangon Kataf within a territory occupied by the Kataf (Isumonah 2003; Mustapha 2000). “
I attribute three reasons why this would be.
One being geography, as these behaviors are most notable with African nations that often overlap in cultural spheres despite living on a huge continent, and also how Black Americans probably covering the largest area relative to other New World African descent populations thus making diversification more enabled.
The second being the process of slavery in New World populations giving various forms of cultural transmission amongst black slaves by region who as well came through different tribes, either producing the typical “Scot-Irish” Black culture or a “Creole” culture, like the Gullah people of the South East. The Third, the Basal reason, being the effects of Genetic interests at hand as put by RR and how African Diversity works.
Here Razib Khan explains that when Foreign Admixture is removed, African diversity is higher among individuals than for major geographical groups.In other words, while geographically diverse, the actual organization of the diversity in the context of cultural boundaries is more stratified due to the lack of breeding, be it outbreeding or replacement involved in nations.
This suggestion is strengthened by famous blogger Jayman attributing this to the lack of large states in Africa to the lack of especially large states in Africa. Granted, you did have relatively large ones in the Sahel but the didn’t last as long as those in Eurasia, falling mainly due to internal struggles.
In the presence of cultural homogeneity, reflecting of a shared lineage, you see improvements in places such as Botswana (Tswana-Sotho) or Ghana (Akan people) partially due to better cultural, and thus likely genetic, unity due to past nationhoods. Apparently, though for short duration, the Tswana formed a political body as large as France,
This is also consistent with the observations made by Sir Harry Hamilton Johnston, a famous colonialist researcher on African and US blacks, on African born blacks on the sea Islands of the South East, which he describes as of “Yoruba Stock” in semblance.
“Also they are when away from white influence inclined to sparsity of clothing-not nowadays a common trait in the United States negro. They are also pure negroes entirely without any infusion of white blood. Crime is very rare among them.” The Negro in the New World by Harry Hamilton Johnston p. 470
A good modern example would be the demographics of West Africa Immigrants, being principally Akan of Ghana and the Yoruba or Igbo of Nigeria, who each come from relatively well constructed precolonial formations. What is also of note is how their prominence seems to be correlated to the extent in which Cousin Marriage is practiced, possibly reflective of the precolonial patterns of cousin marriage
Application for the U.S population in kin networks, where it does not work.
PP, in which he discussed the ethnocentrism of different groups, said this regarding blacks and kin altruism.
“And yet eventually these extremely different tribes mixed, and so you would have parents raising kids who have genetic variants very alien to their own, and this probably contributed to the breakdown of the black family: it’s harder for kin altruism to get selected when the kids you are altruistic to, don’t resemble you that much genetically because their other parent is so unlike you that they don’t inherit your high degree of kin altruism or inherit it as a recessive unexpressed trait. And when kin altruism gets only weakly selected for, racial loyalty (which is probably just an outgrowth of kin loyalty) is probably weakly selected for too.”
Which would be incorrect. Yes, while crossing over does occur, a child would be overall close to their parent’s overall genetic background on the level of relatedness. Leaping from that neglected detail, he assumes from his evidence of “lack of racial loyalty” would that blacks have less ethnic nepotism and thus weaker kin altruism despite not taking into account of selection occurring within subgroups of various constructs like you see in Africa which would apply to families inside them.
If this theory was even supportable, one would expect the opposite that actually occurs with the percentage of Black children to return to relatives compared to White children.
“Of the 94,483 black children discharged from foster care, 12,860, or 13%, were discharged to a relative guardian. Of the 182,941 white children discharged from foster care in 2004, 20,453, or 11%, were discharged to a relative guardian.Of the 15,087 black children adopted from foster care, 4077, or 27%, were adopted by a relative. Of the 29,244 white children adopted from foster care, 5861, or 20%, were adopted by a relative. Of the 279,421 black kids living in foster care for some portion of the year, 69,888 or 25% were living with relatives. Of the 474,734 white children living in foster care for some portion of the year, 101,300, or 21%, were living with relatives.
So black children getting adopted from foster care are somewhat more likely to be adopted by relatives than white kids (27% vs. 20%), black kids exiting foster care are slightly more likely to be discharged to a relative guardian than white kids (13% to 11%), and black kids in foster care are slightly more likely to be living with relatives than white kids (25% vs. 21%). The differences support the hypothesis that blacks are more likely to utilize kinship care networks, but not by a lot, at least in regard to the foster care system.”
From Audacious Epigone, who also notes that despite the higher likelihood of such networks that doesn’t explain disproportion in foster care. Though evidence for IQ is at best moderate, interpersonal indicators were stronger (Azar, Stevenson, and Johnson 2012)).
“SIP problems were associated with direct measures of neglect (e.g., cognitive stimulation provided children, home hygiene, belief regarding causes of child injuries). Further, for the direct measures that were most closely linked to CPS Neglect Status, IQ did not add significant predictive capacity beyond SIP factors in preliminary model testing. Implications for intervention with PID discussed.”
This is possibly linked to EI scores found to differ between Whites and Blacks (Whitman, Kraus, and Rooy 2014)
“The present work examines applicant reactions to a test of emotional intelligence (EI) using an organizational sample of 334 job applicants. Results indicated that Blacks had higher face validity and opportunity to perform perceptions of EI than Whites, but that Whites performed significantly better than Blacks on the EI test. Although exploratory analyses revealed that test performance was positively related to test reactions, we also found that the magnitude of this relationship differed between Blacks and Whites for the opportunity to perform perceptions. We discuss our findings by offering practical advice for organizations considering or using a measure of EI for selection and assessment.”
Evidence for Kin networks is also supported by more data (Taylor 2013).
“Turning first to findings for family support networks, four significant differences were observed in this analysis. African Americans gave assistance to their family members more often than non-Hispanic Whites, were more likely to have daily contact with their extended family members than both non-Hispanic Whites and Black Caribbeans, and had more frequent interactions with their family than Black Caribbeans. Three general conclusions can be drawn from these findings for family assistance and interaction. First, these findings are consistent with prior work indicating that African Americans have similar or higher levels of involvement with kin than non-Hispanic Whites, but are inconsistent with reports that African Americans have lower levels of family support than Whites (e.g., Hogan et al., 1993). As noted in previous reviews of this literature (Sarkisian & Gertsel, 2004), comparisons across studies are problematic given important differences in the dependent variables used. The present study’s investigation of several dimensions of family support relationships (e.g., enacted support, emotional support, contact, negative interaction) in diverse groups of the population and using a common set of sociodemographic correlates clarifies the nature of race/ethnic differences in these relationships.”
It also found, however, weaker ties outside the family, which strengthen my suggestion of finer stratification of kin ties than just simply less selection.
“Several significant differences in friendship networks were observed in this analysis. Non-Hispanic Whites interacted with their friends and gave support to their friends more frequently than African Americans. Additionally, non-Hispanic Whites received support from friends more frequently than both African Americans and Black Caribbeans. Many of the differences between African Americans and non-Hispanic Whites could reflect basic differences in their levels of involvement in friendship networks. For instance, 16.7% of African-Americans, 16.1 % of Black Caribbeans and 9.7% of non-Hispanic Whites report that they never receive help from friends. Similarly, African Americans (11%) were twice as likely as non-Hispanic Whites (4.7%) to indicate that they hardly ever or never interact with friends. Lower levels of involvement with friends among African Americans could be due to estrangement from friends, isolation from friends or exclusive involvement with kinship networks (Ajrouch et al., 2001). Collectively, these results, and previous research (Griffin et al., 2006; Waite & Harrison, 1992), indicate that non-Hispanic Whites are more likely than African Americans to interact with friendship networks and to identify friends as an important source of support.”
This lack of support was not seen, however, with fictive kin or congregational members. So perhaps wither the perception of relationship or differences in genetic similarity may answer some of these questions.
People talk a lot about intelligence and brain size. Something that’s most always brought up is how the human brain increased in size the past 4 million years. According to PP, the trend for bigger brains in hominins is proof that evolution is “progressive”. However, people never talk about a major event in human history that caused our brains to suddenly increase: the advent of fire. When our ancestors mastered fire, it was then possible for the brain to get important nutrients that influenced growth. People say that “Intelligence is the precursor to tools”, but what if fire itself is the main cause for the increase in brain size in hominins the past 4 million or so years? If this is the case, then fire is, in effect, the ultimate cause of everything that occurred after its use.
The human brain consumes 20-25 percent of our daily caloric intake. How could such a metabolically expensive organ have evolved? The first hominin to master fire was H. erectus. There is evidence of this occurring 1-1.5 mya. Not coincidentally, brain size began to tick upward after the advent of fire by H. erectus. Erectus was now able to consume more kcal, which in turn led to a bigger brain and the beginnings of a decrease in body size. The mastery and use of fire drove our evolution as a species, keeping us warm and allowing us to cook our food, which made eating and digestion easier. Erectus’s ability to use fire allowed for the biggest, in my opinion, most important event in human history: cooking.
With control of fire, Erectus could now cook its foods. Along with pulverizing plants, it was possible for erectus to get better nutrition by ‘pre-digesting’ the food outside of the body so it’s easier to digest. The advent of cooking allowed for a bigger brain and with it, more neurons to power the brain and the body. However, looking at other primates you see that they either have brains that are bigger than their bodies, or bodies that are bigger than their brains, why is this? One reason: there is a trade-off between brain size and body size and the type of diet the primate consumes. Thinking about this from an evolutionary perspective along with what differing primates eat and how they prepare (if they do) their food will show whether or not they have big brains or big bodies. How big an organism’s brain gets is directly correlated with the amount and quality of the energy consumed.
There is a metabolic limitation that results from the number of hours available to feed and the low caloric yield of raw foods which then impose a trade-off between the body size and number of neurons which explains why great apes have small brains in comparison to their bodies. Metabolically speaking, a body can only handle one or the other: a big brain or a big body. This metabolic disadvantage is why great apes did increase their brain size, because their raw-food diet is not enough, nutritionally speaking, to cause an increase in brain size (Azevedo and Herculano-Houzel, 2016). Can you imagine spending what amounts to one work day eating just to power the brain you currently have? I can’t.
Energy availability and quality dictates brain size. A brain can only reach maximum size if adequate kcal and nutrients are available for it.
Total brain metabolism scales linearly with the number of neurons (Herculano-Houzel, 2011). The absolute number of neurons, not brain size, dictates a “metabolic constraint on human evolution”, since people with more neurons need to sustain them, which calls for eating more kcal. Mammals with more neurons need to eat more kcal per day just to power those brains. For instance, the human brain needs 519 kcal to run, which comes out to 6 kcal per neuron. The brain is hugely metabolically expensive, and only the highest quality nutrients can sustain such an organ. The advent of fire and along with it cooking is one of, if not the most important reason why our brains are large (compared to our bodies) and why we have so many neurons compared to other species. It allowed us to power the neurons we have, 86 billion in all (with 16 billion in the cerebral cortex which is why we are more intelligent than other animals, number of neurons, of course being lower for our ancestors) which power human thought.
The Expensive Tissue Hypothesis (ETA) explains the metabolic trade-off between brain and gut, showing that the stomach is dependent on body size as well as the quality of the diet (Aiello, 1996). As noted above, there is good evidence that erectus began cooking, which coincides with the increase in brain size. As Man began to consume meat around 1.5 million years ago, this allowed for the gut to get smaller in response. If you think about it, it makes sense. A large stomach would be needed if you’re eating a plant-based diet, but as a species begins to eat meat, they don’t need to eat as much to get the adequate amount of kcal to fuel bodily functions. This lead to the stomach getting smaller, and along with it so did our jaws.
So brain tissue is metabolically expensive but there is no significant correlation between brain size and BMR in humans or any other encephalized mammal, the metabolic requirements of relatively large brains are offset by a corresponding gut reduction (Aiello and Wheeler, 1995). This is the cause for the low, insignificant correlation between BMR and our (relatively large brains, which correlates to the amount of neurons we have since our brains are just linearly scaled-up primate brains).
Evidence for the ETA can be seen in nature as well. Tsuboi et al (2015) tested the hypothesis in the cichlid fished of Lake Victoria. After they controlled for the effect of shared ancestry and other ecological variables, they noted that brain size was inversely correlated with gut size. Perhaps more interestingly, they also noticed that when the fish’s’ brain size increased, increased investment and paternal care occurred. Moreover, more evidence for the ETA was found by Liao et al (2015) who found a negative correlation between brain mass and the length of the digestive tract within 30 species of Anurans. They also found, just like Tsuboi et al (2015), that brain size increase accompanied an increase in female reproductive investment into egg size.
Moreover, another cause for the increase in brain size is our jaw size decreasing. This mutation occurred around 2.4 million years ago, right around the time frame that erectus discovered fire and began cooking. This is also consistent with, of course, the rapid increase in brain size which was occurring around that time. The room has to come from somewhere, and with the advent of cooking and meat eating, the jaw was, therefore, able to get smaller along with the stomach which increased brain size due to the trade-off between gut size and brain size. Morphological changes occurred exactly at the same time changes in brain size occurred which coincides with the advent of fire, cooking, and meat eating. Coincidence? I think the evidence strongly points that this is the case, the rapid increase in brain size was driven by fire, cooking, and meat eating.
The rise of bipedalism also coincided with the brain size increase and nutritional changes. Bipedalism freed the hands so tools could be made and used which eventually led to the control of fire. Lending more credence to the hypothesis of bipedalism/tools/brain size is the fact that there is evidence that the first signs of bipedalism occurred in Lucy, our Australopithecine ancestor who had pelvic architecture that showed she was clearly on the way to bipedalism. There is more evidence for bipedalism in fossilized footprints of australopithecines around 3 mya, coinciding with Lucy, tool use and eventually the advent and use of fire as a tool to cook and ward off predators. Ancient hominids could then better protect their kin, have higher quality food to eat and use the fire to scare off predators with.
The nutritional aspect of evolution and how it co-evolved with us driving our evolution in brain size which eventually led to us is extremely interesting. Without proper nutrients, it’s not metabolically viable to have such a large brain, as whatever kcal you do eat will need to go towards other bodily functions. Moreover, diet quality is highly correlated with brain size. Great apes can never get to the brain size that we humans have, and their diet is the main cause. The discovery and control of fire, the advent of cooking and then meat eating was what mainly drove the rapid increase of brain size starting 4 mya.
In a way, you can think of the passing down of the skill of fire-making to kin as one of the first acts of cultural transference to kin. It’s one of the first means of Lamarckian cultural transference in our history. Useful skills for survival will get passed down to the next generation, and fire is arguably the most useful skill we’ve ever come across since it’s had so many future implications for our evolution. The ability to create and control fire is one of the most important skills as it can ward off predators, cook meat, be used to keep warm, etc. When you think about how much time was freed up upon the advent of cooking, you can see the huge effect the control of fire first had for our species. Then think about how we could only control fire if our hands were freed. Then human evolution begins to make a lot more sense when put into this point of view.
When thinking about brain size evolution as well as the rapid expansion of brain size evolution, nutrition should be right up there with it. People may talk about things like the cold winter hypothesis and intelligence ad nauseam (which I don’t doubt plays a part, but I believe other factors are more important), but meat-eating along with a low waist-to-hip ratio, which bipedalism is needed for all are much more interesting when talking about the evolution of brain size than cold winters. All of this wouldn’t be possible without bipedalism, without it, we’d still be monkey-like eating plant-based diets. We’d have bigger bodies but smaller brains due to the metabolic cost of the plant-based diet since we wouldn’t have fire to cook and tools to use as we would have still been quadrupeds. The evolution of hominin intelligence is much more interesting from a musculoskeletal, physiological and nutritional point of view than any simplistic cold winter theory.
What caused human brain size to increase is simple: bipedalism, tools, fire, cooking, meat eating which then led to big brains. The first sign of big brains were noticed right around the time erectus had control of fire. This is no coincidence.
Bipedalism, cooking, and food drove the evolution of the human brain. Climate only has an effect on it insofar as certain foods will be available at certain latitudes. These three events in human history were the most important for the evolution of our brains. When thinking about what was happening physiologically and nutritionally around that time, the rebuttal to the statement of “Intelligence requires tools” is tools require bipedalism and further tools require bigger brains as human brains may have evolved to increase expertise capacity and not IQ (more on that in the future), which coincides with the three events outlined here. Whatever the case may be, the evolution of human intelligence is extremely interesting and is most definitely multifaceted.
In my first article on this matter, I showed how Richard Lynn claims the average IQ in Italy is around “89-92” for Sicily and the South and around 103 for the North. I showed how he was wrong and what data he overlooked to fit his hypothesis. Lynn’s 2011 article IQs in Italy are higher in the north: A reply to Felice and Giugliano was a reply to Myth and reality: A response to Lynn on the determinants of Italy’s North–South imbalances. Felice and Giugliano brought up Lynn’s four main theses: a) the South’s “economic backwardness” in terms of economics ‘throughout history’; b) the evidence provided by Lynn wasn’t enough to ‘prove’ a cause of lower IQ for S. Italians; c) the evidence provided by Lynn wasn’t enough to show that S. Italians score lower than N. Italians; and d) the supposed ‘high rates of MENA admixture’ in S. Italians. I blew up all of these claims in the beginning of the year, more specifically I blew up up the claims about MENA admixture back in January. I’ll be going through Lynn’s 2010b article correcting any discrepancies. It’s worth noting that he still pushes the so-called ‘MENA admixture’ as being a substantial CAUSAL factor when there is NO evidence for this big of a ‘gap’ between the North and the South. The Lynn quotes will be from his 2010 paper linked above. I had also thought that ‘migrants’ from MENA countries could have contributed to the gap between the North and South, but since this isn’t the case for France then it shouldn’t be so for Italy. However, since Italy is a hub for these people when they first illegally enter Europe, they may stay and get counted as citizens and the children of these immigrants grow up and get accounted in the data. This is plausible, since a lot of ‘migrants’ may stay where they first get which is Southern Europe, mainly Sicily and Southern Italy.
We now present new data showing that IQs are higher in the north of Italy than in the south. In the previous study, data were presented for 12 Italian regions from the PISA (Program for International Student Assessment) 2006 study of the reading comprehension, mathematics and science performance of 15 year olds, regarded as measures of intelligence. We are now able to give similar data on the reading comprehension, mathematics and science performance of 15 year olds in 20 Italian regions obtained in the 2009 PISA study (OECD, 2010). These are given in Table 1. This shows, reading from left to right, the latitude of the Italian regions, the mean PISA scores for 12 regions for 2006 given in Lynn (2010a), the mean scores of 15 year olds on reading comprehension, mathematics and science understanding for the 20 Italian regions obtained in the 2009 PISA study, and the averages of the three 2009 PISA scores given because it provides a convenient summary of the scores on the three tests.
I already went through this in my previous article, but for clarity, I’ll go through this again.
Cornoldi, Giofrè, and Martini (2013) showed how there are problems inferring Italian IQ from the very PISA data that Lynn cites. There was a relevant decrease between the North and South. If the PISA test showed genetic proclivities between the North and South, why was there a relevant decrease in the three-year period? Because it is not an intelligence test, but a test of educational achievement. D’Amico et al (2011) conclude:
Our examination of intelligence test score differences between the north and south of Italy led to results that are very different from those reached by Lynn (2010a). Our results demonstrate that by using intelligence tests to assess differences in ability rather than using achievement scores as a proxy for intelligence, children from the south of Italy did not earn lower scores than those from the north of Italy. Rather, they were even higher in Raven’s CPM. However, we see no advantage in claiming that children in the south are “more intelligent” than children in the north, because these groups are different on a number of variables (e.g., environmental factors, educational influences, composition of the samples) that influence differences in test scores.
Either no difference or Southern Italians scored higher. When using purer measures of intelligence (Raven’s Progressive Matrices) so-called “differences” in “intelligence” disappear.
It will be noted that the regional differences in both language and math ability increase with age. For example, in language ability the regional differences in the youngest children (P2) range between 1.6 and −3.8, a difference of 5.4, while the differences in the oldest children (2S) range between 3.6 and −4.4, a difference of 8.0. Similarly, in math ability the regional differences in the youngest children (P2) range between 0.8 and −1.0, a difference of 1.8, while the differences in the oldest children (2S) range between 4.3 and −5.4, a difference of 9.7. These age differences would be predicted from the thesis that the regional differences have a genetic basis, because the heritability of intelligence increases during childhood (Plomin, DeFries, & McClearn, 1980, p. 334).
On other measures of achievement, such as the INVALSI examinations, Southern Italians do not score lower, and in some cases may even score higher (Robinson, Saggino, and Tommasi (2011). Moreover, the N/S differences in ‘cognitive ability’ don’t exist at age 7, the IQ/income relationship didn’t exist in the past, and the MENA admixture in Southern Italians is minute (Daniel and Malanima, 2011). The so-called MENA admixture that Nordicists and Lynn like to say is the subject of my next point.
Further data for the proportion of North African ancestry in the Italian regions are available in the frequency of the haplogroup E1b1b allele. This is a marker for North African ancestry, where it reaches frequencies above 50% and peaks at around 82% in Tunisia (Zalloua et al., 2008). The frequencies of the haplogroup xR1 and the E1b1b alleles are taken from Capelli et al. (2006), Capelli et al. (2007), Di Giacomo et al. (2003), Balaresque et al. (2010), Scozzari et al. (2001), and Semino et al. (2000). These data are given in columns 11 and 12 of Table 1 and the correlations between these and the other variables are given in Table 2.
As said and cited above, the so-called admixture from MENA populations in Southern Italians accounts for an extremely small fraction of the overall Southern Italian genome. The cause for lower achievement (“IQ” according to Lynn) in Southern Italians rests on this very pertinent point. And it’s wrong. Furthermore, and this is for Sicilians, the contribution of their genome by the Greeks is 37 percent, with the North African contribution being 6 percent. Daniel and Malanima (2011) ask ” Can the Greek heritage to the Western culture really be associated to a lower IQ?” The answer is, clearly, no. Moreover, a Central Italian province has the highest amount of MENA admixture, yet they have higher scores than Southern Italy. What does that tell you?
Richard Lynn’s Italian IQ data is garbage. Purer measures of intelligence such as Raven’s Colored Progressive Matrices show a decrease in the “intelligence gap” and in some cases, Southern Italians score higher than Northern Italians. When using measures of “IQ” from PISA data, these so-called differences disappear. Lynn’s data he cites in his 2010a paper don’t control for socio-cultural differences and school quality. There is numerous data that suggests the school quality in Southern Italy is worse than that of the North; this difference in school quality then affects educational achievement. Since PISA is a test of educational achievement and not intelligence (D’Amico et al, 2011), what accounts for these differences in achievement in the various studies may (and in my opinion, does) account for the differences in educational achievement between Northern and Southern Italians. The measurements in various studies may be influenced by the larger between-schools variability that is present in the South (Cornoldi et al, 2010; Daniel and Malanima 2011).
Finally, some people may point to the GDP differences between North and South Italy as proof of genetic/intelligence differences between them. However, the Mafia accounts for around a 20 percent drop in GDP in Southern Italy. To say that any differences in GDP can be accounted for without first controlling for things like this is dishonest. The presence of Mafia in areas shows lower growth and a sharper increase in murders. Each time homicides rise, GDP falls between 16-20 percent (Pinolli 2012). The presence of the Mafia had a devastating effect on the economies in that area between the 70s and 00s.
In sum, PISA is garbage to infer intelligence from as they are tests of achievement and not intelligence. Other tests of achievement show a decrease in the gap and/or Southern Italians scoring higher. Moreover, no substantial genetic differences exist between the North and the South, falsifying Lynn’s thesis for the causality of the differences between the North and the South. The oft-cited GDP difference between Northern and Southern Italy can be accounted for by the presence of the Mafia. Whenever the murder rate rises (due to Mafia activity), the GDP decreases. None of these factors have been taken into account and they explain the difference between the North and the South. It is environmental in nature–not genetic. Lynn’s Italian IQ data is garbage and should not be cited. It’s just a Nordicist fantasy that Southern Italians score lower than Nothern Italians.
Ethnic differences in the prevalence of obesity occur, majorly in part due to differences in the rates of metabolic syndrome (which is actually a few variables including high blood pressure, high blood sugar which leads to insulin resistance, excess visceral fat around the waist which is the ‘skinny fat‘ phenomenon, and abnormal blood pressure levels) and obesity. Ethnic differences in these variables do, in part, show how the three ethnies differ in rates of obesity. I will discuss the differences between each ethny in regards to metabolic syndrome and sleep and how it leads to the differences in ethnic obesity rates.
There is a ‘missing hour of sleep‘ when comparing blacks and whites. On average, blacks get 6.05 hours of sleep while whites get 6.85 hours of sleep. Of course, the same old racism argument comes up, which, if one ‘percieves’ discrimination, I wouldn’t doubt that it would have an effect on sleep due to a rise in cortisol, which affects sleep due to the raised levels making you restless and not able to fall asleep. Insulin levels then rise due to the rise in cortisol, which is the cause of obesity.
Some studies may try to say that racism and other forms of discrimination are a factor, without even thinking of genetic factors. Another study that Frost cites says that duration of deep sleep and duration of stage 2 (light sleep) is correlated correlated in African Americans with perceived discrimination. The authors defined ‘perceived discrimination’ as the extent to which one believes that their ethnic group have been discriminated against by society. Still even when controlling for discrimination, there were still marked differences between blacks and whites and how long they slept.
Frost then talks about how sleep patterns are heritable and cites studies done on Africans in Africa. One study found that there was an hour sleep difference between Ghanaians and Norwegians on the week days and between a quarter to half hour less on weekends. He shows another study showing that Nigerian college students sleep 6.2 hours a day while getting 70-minute naps in the afternoon.
Frost concludes that the African sleep patterns is normal on Africa. Africans are more active during the cooler times of the day and sleep during the bitter periods. Frost says those who evolved in more northerly climes are particularly adapted to a certain sleep pattern with the same holding true for Africans.
However, these sleep patterns in first world countries have negative effects on metabolism and rates of obesity.
Here are some more studies showing that blacks sleep less than whites:
The sleep of African Americans: a comparative review: The researchers found that blacks take longer to fall asleep than whites, report poorer sleep quality, have more light and less deep sleep, and nap more often and longer. This is a huge recipe for risk factors for obesity, and it shows in their demographics.
Unfair Treatment is associated with Poor Sleep in African American and Caucasian Adults: Pittsburgh SleepSCORE Project: This is one of the studies spoken about above that show that discrimination leads to less sleep. Though, it holds for both black and white adults. The researchers conclude:
Taken together, the confluence of perceived unfair treatment as a chronic stressor and poor sleep and the interplay between the two may have critical roles in long-term health problems.
African Genetic Ancestry is Associated with Sleep Depth in Older African Americans: The researchers hypothesized that “racial differences in sleep phenotypes would show an association with objectively measured individual genetic ancestry in AAs.” They conclude that the slow wave sleep may have genetic underpinnings.
Mexican Americans sleep less than do Mexican immigrants. US-born Mexicans are 40 percent more likely to be short sleepers. This is attenuated by environmental factors such as smoking and stress, which shorten the duration of sleep (smoking decreases the Body Set Weight, whereas cortisol along with insulin in tandem increase it).
Also, in this study by Roane et al (2014) looked at the link between sleep disturbances and stress in Mexican Americans (average age 55) and non-‘Hispanic’ whites (average age 66). Mexicans reported higher levels of sleep disturbance (25 percent) compared to whites (17 percent). They conclude that disturbed sleep was positively correlated with depression.
So both blacks and Mexicans sleep less than whites. These differences in sleep between these three ethnies also affect the prevalence of obesity in these populations.
Obesity and Sleep
It’s long been known that poor sleep habits make people fat. This is due to the effects of insulin and cortisol. Increased insulin comes before increased cortisol–increased insulin is the cause for obesity. Sleeping less is linked to obesity. Since, as described above, the three ethnies differ in sleep patterns, the same also holds true for obesity rates (Ogden at al, 2014). The trends are as follows: 67.3% for whites, 75.6% for blacks, and 77.9% for Hispanics. Though, sleep is only one factor involved with obesity.
Getting adequate sleep is extremely important. Not doing so can lead to a myriad of negative health implications:
Sleep is an important modulator of neuroendocrine function and glucose metabolism and sleep loss has been shown to result in metabolic and endocrine alterations, including decreased glucose tolerance, decreased insulin sensitivity, increased evening concentrations of cortisol, increased levels of ghrelin, decreased levels of leptin, and increased hunger and appetite. Recent epidemiological and laboratory evidence confirm previous findings of an association between sleep loss and increased risk of obesity.
So a lack of sleep leads to an increase in ghrelin levels, decreased levels of leptin (the same effects as caloric restriction over time), increased appetite and hunger, increased evening cortisol (which insulin spikes then follow), decreased insulin sensitivity (the cortisol brings it back up and most people are insulin resistant independent of diet), decreased glucose tolerance, etc. We can see that these ethnic differences in sleep, which are partly genetic in nature, can and would have great effects on metabolism, contributing to the ethnic differences in obesity rates.
And from Harvard:
For example, in the Nurses’ Health Study, researchers followed roughly 60,000 women for 16 years, asking them about their weight, sleep habits, diet, and other aspects of their lifestyle. (2) At the start of the study, all of the women were healthy, and none were obese; 16 years later,women who slept 5 hours or less per night had a 15 percent higher risk of becoming obese, compared to women who slept 7 hours per night. Short sleepers also had 30 percent higher risk of gaining 30 pounds over the course of the study, compared to women who got 7 hours of sleep per night.
Damn!! This, pretty much, mirrors the black-white difference. I’d love to see a racial breakdown of this cohort and will keep an eye out for one, but in the meantime, those who were short sleepers had a 30 percent higher risk of gaining 30 pounds over the course of the study in comparison to women who got 7 hours of sleep per night. Blacks are the most likely group to be overweight and obese in the US, and this data from the Nurses Health Study (which tons of data can be drawn from this study) shows one reason why, however the driver is cortisol > insulin > processed carbs > increased insulin > insulin resistance > increased insulin > vicious cycle > obesity. These differences in sleep almost perfectly mirror the ethnic differences in obesity.
There are several possible ways that sleep deprivation could increase the chances of becoming obese. (1) Sleep-deprived people may be too tired to exercise, decreasing the “calories burned” side of the weight-change equation. Or people who don’t get enough sleep may take in more calories than those who do, simply because they are awake longer and have more opportunities to eat; lack of sleep also disrupts the balance of key hormones that control appetite, so sleep-deprived people may be hungrier than those who get enough rest each night.
Ah the old ‘exercise to increase the Calories Out part of the equation’. however, Calories Out does not stay constant. This also rebuts the ‘Eat Less and Move More’ CICO (Calories In/Calories Out) model of obesity, showing that because it doesn’t take insulin into account, it’s doomed to fail.
Speaking of insulin, it’s about time I focused on metabolic syndrome.
As I discussed in a previous post, Race, Obesity, Poverty, and IQ, metabolic differences exist between race/ethnicity. ‘Hispanics’ metabolize carbohydrates differently, blacks have a lower fiber intake (increased fiber protects against obesity, another correlate) while whites have a more high fat diet. Contrary to popular belief, dietary fat doesn’t make you fat as it’s the macro that spikes your insulin the least.
Diaz et al (2005) showed that minority populations are more likely to be affected by diabetes mellitus which may be due to less healthy diets and/or genetic factors. Using the National Health and Nutrition Survey for 1999-2000, they analyzed overweight, healthy adults, calculating dietary intake variables and insulin sensitivity by ethnicity. They characterized insulin resistance with fasted insulin, as those who are more likely to become insulin resistant have higher fasted insulin levels (levels taken after waking, with the subject being told not to eat the night before as to get a better reading of fasted insulin levels). Non-‘Hispanic’ whites had higher energy and fat intake while ‘Hispanics’ had higher carb intake with blacks having lower fiber intake. Blacks and ‘Hispanics’ were more likely to have lower insulin sensitivity. However, ‘Hispanics’ were more likely to have lower insulin sensitivity even after controlling for diet, showing that metabolic differences exist between ethnicities that affect carbohydrate metabolism which leads to higher rates of diabetes in those populations.
In ‘Hispanics’, several loci were discovered that play a role in hepatic (relating to the liver) fat content. Along with showing that ‘Hispanics’ have lower insulin (which due to low insulin, blood glucose builds up in the blood stream leading to diabetes) and showing that they metabolize glucose in the liver differently due to differing loci leading to more cases of fatty liver, this shows how and why ‘Hispanics’ have higher rates of Type II Diabetes Mellitus (TIIDM).
Since TIIDM affects Mexican Americans more, better measures to address their differences in carbohydrate metabolism need to be taken. Racial and ethnic differences in TIIDM are as follows:
7.6% of non-Hispanic whites
9.0% of Asian Americans
12.8% of Hispanics
13.2% of non-Hispanic blacks
15.9% of American Indians/Alaskan Natives
Whites eat a higher fat diet, which means a decrease in carbs. Asians eat white rice which spikes blood glucose eliciting a high insulin response leading to TIIDM, ‘Hispanics’, non-‘Hispanic’ blacks, and Indians and Alaskan Natives (I wish they separated Indians and Alaskan Natives as I’m almost positive that Alaskan natives have a lower rate) all eat high carb, low fat, low protein diets. Carbohydrates are a main staple, and since they spike insulin the most, they are the cause for obesity and TIIDM rates in these populations.
Turning my attention over to metabolic syndrome and blacks and whites, we can see that black women with PCOS have an increased risk for cardiovascular disease and metabolic syndrome in comparison to white women with PCOS. The researchers say that after controlling for age and body mass index (BMI) “black women with PCOS had a significantly increased prevalence of low high-density lipoprotein and high glucose. The general CVD risk was significantly increased in black adults with PCOS.” Though, a longitudinal study needs to be carried out to assess the independent impact of race and PCOS with CVD (Cardiovascular Disease).
Blacks have a higher chance to be diagnosed with metabolic syndrome since they are also at increased risk to have elevated blood pressure (hypertension), become obese, and be diabetic. This is due to their diet, which is due to their low IQ (obesity is correlated with intelligence), and different metabolism in comparison to whites.
There are also metabolic differences between race and sex. Fat oxidation is lower in black than white men and in African American men/women and white men/women, they have a lower metabolic rate!!! 24-hour energy expenditure is lower in black women in comparison to white women, whereas physical activity energy expenditure (PAEE) is the same as whites. Contrasted with women, black men had higher PAEE than white men. The authors conclude:
In conclusion, this comparative study of 24-h energy metabolism in African Americans and whites with use of a respiratory chamber not only confirms the previous findings from ventilated-hood studies of a lower resting metabolic rate, but also suggests a lower 24EE in African American women than in white women. Although only marginal ethnic differences in metabolic rate were found in men, African American men seem to have a lower rate of fat oxidation than do white men. The underlying mechanisms for these sex differences and the significance of these findings with respect to the development and maintenance of obesity remains to be investigated in longitudinal studies.
Metabolic Syndrome and Obesity
Black American men are the least likely male ethnic group to be overweight or obese in America (69.2 percent) compared to ‘Hispanic’ men (78.6 percent) and white men (71.4 percent) (Ogden et al, 2014). As a result of being less likely to be obese, black men as a whole suffer from diabetes and other diseases that are correlated with higher body fat. Conversely, for women the rate for white women is 63.2 percent, 77.2 percent for ‘Hispanic’ women and 82.4 percent for black women. Why do black men have lower rates of obesity and chronic health diseases?
Klimentidis et al (2016) set out to find why black men have lower rates of obesity than black women despite having the same socioeconomic and environmental factors. Using 2814 self-identified African Americans from the Atherosclerosis Risk in Communities study, they estimated each individual’s degree of African ancestry using 3,314 genetic markers. They then tested whether sex modifies the association of West African genetic ancestry and body mass index, waist circumference, and waist to hip ratio. Also, they adjusted for income and education as well as examined associations of ancestry with the phenotypes of males and females separately. They recreated their results with the Multi-Ethnic Study of Atherosclerosis (n= 1611 AA).
They discovered that West African ancestry is negatively correlated with obesity as well as central obesity, which is obesity around the midsection, among black men but not black women. Also noted, was that black men with more African ancestry had a lower waist to hip ratio and less central adiposity than black men with less African ancestry. They conclude that their results suggest that a combination of male gender and West African ancestry is correlated with protection against central obesity and suggests that a portion of the difference in obesity (13.2 percent difference) may be due, in part to genetic factors. The study also suggests that there are specific genetic and physiologic differences in African and European Americans.
This study confirms two things. 1) Black women are more likely to be obese than black men as well as the general population. 2) Black men have less of a chance of becoming obese or overweight as well as less of a chance of incurring the risks that come along with being obese or overweight. The degree of African ancestry is the cause in both black men and black women for these differences in the rate of overweight and obese individuals in both populations. One of my theories also got confirmed. Since obesity is partly genetic in African Americans, and black girls have an earlier menarche (period) than white girls due to higher body fat which activates the hormone leptin, which precedes an increase in body fat to prepare for eventual menstruation, I theorize that black girls have earlier menarche than white girls due to r/K Selection Theory. It’s an evolutionary advantage to be able to have children earlier, as the population dies younger.
Evolutionarily speaking, black men needed to be more fit in order to protect the clan from predators. This is also why blacks evolved narrower hips (Rushton, 1995). Higher body fat allows for more protection for a baby in vitro, which is why an increase in leptin precedes an increase in body fat, which then causes black girls to have an earlier puberty.
One of the questions I would like answered is whether it’s the actual degree of African ancestry that is the cause of black men being less likely to be obese or it’s the cause of higher degree of European ancestry. European American men do have a slightly higher risk of being overweight or obese than African American men, so there is some credence to this hypothesis. Three SNPs were found to be correlated with obesity in African American populations as well as European American populations; this could be one cause.
Wagner and Heyward (2000) discovered biological differences exist between blacks and whites. They reviewed the literature on the differences between blacks and whites in fat-free body mass (water, mineral, and protein) fat patterning and body dimensions and proportions. Blacks, in general, have greater bone mineral density and body protein content than do whites, resulting in lower fat-free bone density. They also note racial differences in the differences of subcutaneous body fat, which is the body fat that’s just below the skin, as opposed to visceral body fat which is found in the peritoneal cavity, which can be measured with calipers to give a rough estimate of total body fat adiposity. The conclusion reached in the study was that differences in FFB (fat-free body) was statistically significant between blacks and whites. They also have a greater BMC (bone mineral content) and BMD (bone mineral density) than do whites. They also argue that for a given BMI (body mass index), blacks might have less adiposity because they tend to be more mesomorphic. Researchers push for the development of racial-specific equations to better see differences in FFB.
With the above study noting that there is a substantial difference between blacks and whites in FFB, there may be some truth to a negative effect of European ancestry on blacks in terms of obesity acquisition. However, lower FFB in black men is one reason why black men can’t swim as well as whites.
One of the causes for both racial and gender discrepancies in obesity is genetic in origin. The difference between black men and black women is 13.2 percent whereas for white men and white women the difference is 8.2 percent. There is a clear genetic difference between races that is the cause for this discrepancy. Black men and black women have the same socioeconomics status and live in the same environment, so some of the differences in obesity noticed in this population must be genetic in origin.
Freedman et al (2004) observed that, as expected, black men were more likely to choose heavier figures as an ideal body for women than white men. Also expected was that both groups would choose figures with a low waist to hip ratio, but black men would choose a lower waist to hip ratio as ideal. They also show weight to be a more important cue than waist to hip ratio in mate selection as well as supporting the theory that black men’s preferences may serve as a protective factor against eating and body image pathology in black women.
To give an example of the above study in action, we can look at Mauritania. They force feed their women up to 16,000 kcal a day in an effort to make them obese, as that’s what is seen as attractive in their society. Mauritanian love songs also describe the ideal woman as fat. Obesity is so celebrated in their society that parents beam at the fact that their daughters look obese, as they have a better chance of getting partners.
The higher the degree of West African ancestry in black men, the lower the chance they have for obesity. I do wonder, though, if it’s because they have less European ancestry or because they have more African ancestry. Black men with more African ancestry are less likely to be obese than black men with less African ancestry, so there is a correlation there that I would like to see explored in the future. Differences in fat-free body mass have been noticed between blacks and whites, but this is one of the first studies to my knowledge that shows that genetic differences between black men and black women may be part of the cause for obesity differences in that population. Cultural differences in perception of beauty, of course, come into play in regards to differences between black and white men, however, the cause of black women having higher rates of obesity is due in part to genetic factors, which then leads to black men liking that as their beauty standard.
A lot of people seem to confuse causes between ‘Islam’ and behavior that’s just ‘low IQ’. Whenever these attacks like shootings, sexual assaults and rapes happen, that’s due to their low IQ; not religion. I wrote about this in IQ, Inbreeding and Clannishness. All of the behavior you see is due to low IQ. 1) being in an area with a hot climate and 2) cousin marriage has been going on there ever since Jews from the Levant introduced it to them around 200 BC. To quote myself:
Those innate behaviors which result in the favoring in all areas of life, themselves and their family, is a result of genetic similarity because of the closely related genes they share (the father’s brother’s daughter type is the most common in the Muslim world). Also, first and second cousin marriages are more common, which also result in increased altruism for their own family because of the close genetic similarity, but also those in their own group, which is mediated by the brain hormone oxytocin.
In a paper on the mean IQ of Muslims and non-Muslim countries, Donald Templer states that the Muslim world, which used to be have great intellectual achievements from the 7th to 12th centuries, has seen an underrepresentation in highly creative contributions in science journals. This is because of the inbreeding effect (2.5 to 10 point drop in IQ) of close cousin marriage. He ends up saying that genetic factors are more important than social/cultural/religious values (back to the inbreeding, causing defects and lowering IQ) in regards to IQ.
I also put a map of individualism and collectivism in Europe here. You can see that the collectivist countries are fighting back more. The countries/regions where it’s more red roughly matches up to the situation. You can see how in Central, Northern and Northwestern Europe they’re more individualistic, as well as more atheist, than those collectivist countries. So that leads to what we see with this ‘welcome refugees’ signs, as well as, I would assume, more oxytocin in the brain for Europeans, which leads to more altruism towards other peoples. Of course, 1000 years ago, the high altruism was fine due to being a mostly homogeneous society. But when others move in who are not from the area, and who do not have the same biology as you due to certain selection pressures, that’s when the ‘clash of cultures’ commences. Which it’s not really a clash of culture, more like a clash of biology, because 2 groups who shouldn’t live together are being forced to live together.
This also brings me to people who confuse the causality between Islam and blacks. As I said, it’s a low IQ religion (which I have provided enough evidence for my case). So blacks who become Muslim do so because of low IQ. Anything after that doesn’t mean that being a Muslim had them do it. Lets say that Islam never popped up and the same peoples were still there, continuing such close inbreeding, would that be Islam doing it? No. It’s their biology. **
Using environmental factors (Islam, culture) is what leftists do. In my post on behavior not equaling genes plus environment, I showed how people create their own environments based on their own genetics. The environment we put ourselves in is based on our genetics. We can clearly see that Islam is bringing their culture (genetics) to Europe and are incompatible with Europe as well as all Western societies around the world. Due to this, we can see that wherever any population goes, it will be the same from the original place they emigrated from if migration in large enough numbers occurs. A country is only as good as its majority population.
In Non-Western People are Abnormal to Our Societies, I showed how due to differing cultures (genetics), these third-world immigrants coming into our countries cannot readily assimilate due to differing average IQs and other hormones that lead to crime differentials with the native population. Though Arabs are Caucasian, evolving closer to the equator lead to higher levels of testosterone as more exposure to the sun increases vitamin D levels, which is not a vitamin but actually a steroid hormone. These differences in testosterone then lead to more sex attacks with high testosterone combined with low IQ. Lower IQ people are less likely to be virgins than higher IQ people. This shows that higher IQ people have less testosterone and can also hold back urges more than lower IQ people. This then translates over to an increase of sexual assaults by ‘migrants’ to European women. These ‘abnormalities’, though, would be abnormal anywhere. Putting differing cultures (genetics) in a place with a completely different culture will lead to strife due to genetic distance between the two populations.
I wrote in Evolutionary Reasons for Suicide Bombings that Muslims who suicide bomb do so to increase inclusive fitness. The increase in inclusive fitness comes about due to the suicide bomber having no prospects as well as no kids, so he/she is just taking up resources. By committing suicide, they are freeing resources for others who have a better chance to spread their genes. Many suicide bombers come from middle-class backgrounds, which further proves the case for genetic interests being the cause for this. The majority of Al-Qaeda members come from educated, middle-class backgrounds. Even for Palestinian suicide bombers, none of them were poor, uneducated, simple minded nor depressed.
The average IQ for a criminal is 85 adult offenders, 92 for juvenile offenders. What’s the average IQ in the Middle East? 81, around 1.3 SD lower than average, and 4 points lower for chronic adult offenders in America. The lower IQ comes from being more inbred, which then manifests itself in the crime rate. The strife in the middle east can also be traced back to IQ and consanguinity rates in those populations. How inbred a population is predicts IQ as well as how much strife occurs in those populations.
Germany has said they will begin IQ testing their ‘migrants’. If it works well (I highly doubt it will, and if it is, it won’t be implemented well) this could curb some attacks that happen. Since IQ differences between populations are one of the biggest causes for crime differentials (lower IQ is also correlated with higher testosterone) between them, screening for and only allowing high IQ ‘migrants’ in would curb some violent crime and sex attacks if implemented on a wide enough scale. IQ differences between populations are one of the biggest reasons for differences between any population you can think of.
For a comparison, we can use Christian Arabs. Christian Arabs are less inbred than Muslim Arabs, which shows in the amount of terror attacks committed by Christian Arabs, which I can’t find any data for. If anyone has found any, leave a comment. hbdchick then says this about consanguinity between Christian Arabs and Muslim Arabs:
so, the rate of cousin-marriage amongst lebanese christians was 16.5% while the rate for muslims approached double that at 29.6%.
christians married cousins more distant than first cousins at a slightly higher rate than they did first cousins: 8.6% (>1C) versus 7.9% (1C). muslims, on the other hand, favored first cousin marriage: 17.3% (1C) versus 12.3% (>1C). this is a similar pattern found elsewhere in the middle east/arab world. in egypt, for instance, copts tend to marry second cousins while muslims tend to marry first cousins (no, i can’t find the reference!).
there was also more fbd marriage amongst muslims (6.4%) versus christians (3%).
This is directly mirrored in how often we hear about Christian Arab attacks and crime (I haven’t heard of this), showing that consanguinity rates can predict crime rates. Due to this extreme inbreeding, they are more genetically similar, which leads to higher amounts of altruism for their own group, in turn leading to derogation of the out-group. Europeans are, on average, less inbred than Muslims. This is why it’s said that Muslims are incompatible with our societies. They are more clannish and altruistic for their own. Like JP Rushton said, groups will proliferate ideas that are good for their genetic interests.
Even more evidence can be shown with Chechen inbreeding. I can’t find any data on Chechen IQ, so lets use the closest country to Chechnya, which is Georgia with an average of 94. Since inbreeding can depress IQ 2.5 to 10 points, Chechnya’s average IQ should be somewhere around the mid-80s. This shows similarity with the consanguinity rate. hbdchick then concludes:
it’s no wonder, then, that they still engage in blood feuds (just like the albanians). you’d half expect them to build tower houses for protection during clan disputes like the albanians or the maniots.
Muslim (Arab) populations are incompatible to Western societies due to how inbred they are. Their own societies are built on their genetics, which they then bring to the West and attempt to bring what they’re running from to their new host country.
In conclusion, whenever people say “it’s Islam doing it”, it’s low IQ behavior. Those with lower IQ are more likely to be drawn to Islam. Islam developed after 1300 years after the start of Arab inbreeding. We can draw, from IQ from American criminals, that 85 is the sweet spot for criminality, and since criminality is correlated with low IQ more so than any other variable you can think of. A good example of this is a low IQ person coaxed into committing a crime. It’s an obvious biological difference, the sociopolitical garbage is just that, garbage. The biology drives the politics. Consanguinity rates are one of the biggest factors. You should be concerned with the biology aspect.
Note: When I say “Muslim” I mean Arab. I am also not attempting to “apologize” for terror attacks. I’m simply looking at it through the lens of evolutionary psychology. Most people who read this blog know why Africans act the way they act, and African “migrants” are no different.