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A commenter by the name of bbloggz alerted me to a new paper by Lee Ellis published this year titled Race/ethnicity and criminal behavior: Neurohormonal influences in which Ellis (2017) proposed his theory of ENA (evolutionary neuroandrogenic theory) and applied it to racial/ethnic differences in crime. On the face, his theory is solid and it has great explanatory power for the differences in crime rates between men and women, however, there are numerous holes in the application of the theory in regards to racial/ethnic differences in crime.
In part I, he talks about racial differences in crime. No one denies that, so on to part II.
In part II he talks about environmental causes for the racial discrepancies, that include economic racial disparities, racism and societal discrimination and subordination, a subculture of violence (I’ve been entertaining the honor culture hypothesis for a few months; Mazur (2016) drives a hard argument showing that similarly aged blacks with some college had lower levels of testosterone than blacks with less than high school education which fits the hypothesis of honor culture. Though Ellis’ ENA theory may account for this, I will address this below). However, if the environment that increases testosterone is ameliorated (i.e., honor culture environments), then there should be a subsequent decrease in testosterone and crime, although I do believe that testosterone has an extremely weak association with crime, nowhere near high enough to account for racial differences in crime, the culture of honor could explain a good amount of the crime gap between blacks and whites.
Ellis also speaks about the general stress/strain explanation, stating that blacks have higher rates of self-esteem and Asians the lowest, with that mirroring their crime rates. This could be seen as yet another case for the culture of honor in that blacks with a high self-esteem would feel the need to protect their ‘name’ or whatever the case may be and feel the need for physical altercation based on their culture.
In part III, Ellis then describes his ENA theory, which I don’t disagree with on its face as it’s a great theory with good explanatory power but there are some pretty large holes that he rightly addresses. He states that, as I have argued in the past, females selected men for higher rates of testosterone and that high rates of testosterone masculinize the brain, changing it from its ‘default feminine state’ and that the more androgens the brain is exposed to, the more likely it is for that individual to commit crime.
Ellis cites a study by Goodpaster et al (2006) in which he measured the races on the isokinetic dynamometry, pretty much a leg extension. However, one huge confound is that participants who did not return for follow-up were more likely to be black, obese and had more chronic disease (something that I have noted before in an article on racial grip strength). I really hate these study designs, but alas, it’s the best we have to go off of and there are a lot of holes in them that must be addressed. Though I applaud the researchers’ use of the DXA scan (regular readers may recall my criticisms on using calipers to assess body fat in the bench press study, which was highly flawed itself; Boyce et al, 2014) to assess body fat as it is the gold standard in the field.
Ellis (2017: 40) writes: “as brain exposure to testosterone surges at puberty, the prenatally-programmed motivation to strive for resources, status, and mating opportunities will begin to fully activate.” This is true on the face, however as I have noted the correlation between physical aggression and testosterone although positive is low at .14 (Archer, 1991; Book et al, 2001). Testosterone, as I have extensively documented, does cause social dominance and confidence which do not lead to aggression. However, when other factors are coupled with high testosterone (as noted by Mazur, 2016), high rates of crime may occur and this may explain why blacks commit crime; a mix of low IQ, high testosterone and low educational achievement making a life of crime ‘the smart way’ to live seeing as, as Ellis points out, and that intelligent individuals find legal ways to get resources while less intelligent individuals use illegal ways.
ENA theory may explain racial differences in crime
In part IV he attempts to show how his ENA theory may explain racial differences in crime—with testosterone sitting at the top of his pyramid. However, there are numerous erroneous assumptions and he does rightly point out that more research needs to be done on most of these variables and does not draw any conclusions that are not warranted based on the data he does cite. He cites one study in which testosterone levels were measured in the amniotic fluid of the fetus. The sample was 59 percent white and due to this, the researchers lumped blacks, ‘Hispanics’ and Native Americans together which showed no significant difference in prenatal testosterone levels (Martel and Roberts, 2014).
Umbilical cord and testosterone exposure
Ellis then talks about testosterone in the umbilical cord, and if the babe is exposed to higher levels of testosterone in vitro, then this should account for racial/ethnic differences in crime. However, the study he cited (Argus-Collins et al, 2012) showed no difference in testosterone in the umbilical cord while Rohrmann et al (2009) found no difference in testosterone between blacks and whites but found higher rates of SHBG (sex hormone-binding globulin) which binds to testosterone and makes it unable to leave the blood which largely makes testosterone unable to affect organ development. Thusly, if the finding of higher levels of SHBG in black babes is true, then they would be exposed to less androgenic hormones such as testosterone which, again, goes against the ENA theory.
He also cites two more studies showing that Asian babes have higher levels of umbilical cord testosterone than whites (Chinese babes were tested) (Lagiou et al, 2011; Troisi et al, 2008). This, again, goes against his theory as he rightly noted.
Next he talks about circulating differences in testosterone between blacks and whites. He rightly notes that testosterone must be assayed in the morning within an hour after waking as that’s when levels will be highest, yet cites Ross et al (1986) where assay times were all over the place and thusly testosterone cannot be said to be higher in blacks and whites based on that study and should be discarded when talking about racial differences in testosterone due to assay time being between 10 am and 3 pm. He also cites his study on testosterone differences (Eliss and Nyborg, 1993), but, however, just as Ross et al (1986) did not have a control for WC (waist circumference) Ellis and Nyborg (1993) did not either, so just like the other study that gets cited to show that there is a racial difference in testosterone, they are pretty hugely flawed and should not be used in discussion when discussing racial differences in testosterone. Why do I not see these types of critiques for Ross et al (1986) in major papers? It troubles me…
He also seems to complain that Lopez et al (2013) controlled for physical activity (which increases testosterone) and percent body fat (which, at high levels, decreases testosterone). These variables, as I have noted, need to be controlled for. Testosterone varies and fluctuated by age; WC and BMI vary and fluctuate by age. So how does it make sense to control for one variable that has hormone levels fluctuate by age and not another? Ellis also cites studies showing that older East Asian men had higher levels of testosterone (Wu et al, 1995). Nevertheless, there is no consensus; some studies show Chinese babes have higher levels of testosterone than whites and some studies show that whites babes have higher levels of testosterone than Chinese babes. Indeed, this meta-analysis by Ethnicmuse shows that Asians have the highest levels, followed by Africans then Europeans, so this needs to be explained to save the theory that testosterone is the cause of black overrepresentation of violence (as well as what I showed that testosterone is important for vital functioning and is not the boogeyman the media makes it out to be).
Bone density and crime
Nevertheless, the next variable Ellis talks about is bone density and its relationship to crime. Some studies find that blacks are taller than whites while other show no difference. Whites are also substantially taller than Asian males. Blacks have greater bone density than the other three races, but according to Ellis, this measure has not been shown to have a relationship to crime as of yet.
Penis size, race and crime
Now on to penis size. In two articles, I have shown that there is no evidence for the assertion that blacks have larger penises than whites. However, states that penis length was associated with higher levels of testosterone in Egyptian babes. He states that self-reported penis size correlates with self-reports of violent delinquency (Ellis and Das, 2012). Ellis’ main citations for the claim that blacks have larger penises than other races comes from Nobile (1982), the Kinsey report, and Rushton and Boagert (1987) (see here for a critique of Rushton and Boagert, 1987), though he does cite a study stating that blacks had a longer penis than whites (blacks averaging 5.77 inches while whites averaged 5.53 inches). An HBDer may go “Ahah! Evidence for Rushton’s theory!”, yet they should note that the difference is not statistically significant; just because there is a small difference in one study also doesn’t mean anything for the totality of evidence on penis size and race—that there is no statistical difference!
He then cites Lynn’s (2013) paper which was based on an Internet survey and thus, self-reports are over-measured. He also cites Templer’s (2002) book Is Size Important?, which, of course, is on my list of books to read. Nevertheless, the ‘evidence’ that blacks average larger penises than whites is extremely dubious, it’s pretty conclusive that the races don’t differ in penis size. For further reading, read The Pseudoscience of Race Differences in Penis Size, and read all of Ethnicmuses’ posts on penis size here. It’s conclusive that there is no statistical difference—if that—and any studies showing a difference are horribly flawed.
2d/4d ratio and race
Then he talks about 2d/4d ratio, which supposedly signifies higher levels of androgen exposure in vitro (Manning et al, 2008) however these results have been challenged and have not been replicated (Koehler, Simmons, and Rhodes, 2004; Yan et al, 2008, Medland et al, 2010). Even then, Ellis states that in a large analysis of 250,000 respondents, Asians had the lowest 2d/4d ratio, which if the hypothesis of in vitro hormones affecting digit length is to be believed, they have higher levels of testosterone than whites (the other samples had small ns, around 100).
Prostate-specific antigens, race, and prostate cancer
He then talks about PSA (prostate-specific antigen) rates between the races. Blacks are two times more likely to get prostate cancer, which has been blamed on testosterone. However, I’ve compiled good evidence that the difference comes down to the environment, i.e., diet. Even then, there is no evidence that testosterone causes prostate cancer as seen in two large meta-analyses (Stattin et al, 2003; Michaud, Billups, and Partin, 2015). Even then, rates of PCa (prostate cancer) are on the rise in East Asia (Kimura, 2012; Chen et al, 2015; Zhu et al, 2015) which is due to the introduction of our Western diet. I will cover the increases in PCa rates in East Asia in a future article.
He then reviews the evidence of CAG repeats. There is, however, no evidence that the number of CAG repeats influences sensitivity to testosterone. However, intra-racially, lower amounts of CAG repeats are associated with higher spermatozoa counts—but blacks don’t have higher levels of spermatozoa (Mendiola et al, 2011; Redmon et al, 2013). Blacks do have shorter CAG repeats, and this is consistent with the racial crime gap of blacks > whites > Asians. However, looking at the whole of the evidence, there is no good reason to assume that this has an effect on racial crime rates.
Intelligence and education
Next he talks about racial differences in intelligence and education, which have been well-established. Blacks did have higher rates of learning disabilities than whites who had higher levels of learning disabilities then Asians in a few studies, but other studies show whites and South Asians having different rates, for instance. He then talks about brain size and criminality, stating that the head size of males convicted for violent crimes did not differ from males who committed non-violent crimes (Ikaheimo et al, 2007). I won’t bore anyone with talking about what we know already: that the races differ in average brain size. However, a link between brain size and criminality—to the best of my knowledge—has yet to been discovered. IQ is implicated in crime, so I do assume that brain size is as well (no matter if the correlation is .24 or not; Pietschnig et al, 2015).
Prenatal androgen exposure
Now to wrap things up, the races don’t differ in prenatal androgen exposure, which is critical to the ENA theory; there is a small difference in the umbilical cord favoring blacks, and apparently, that predicts a high rate of crime. However, as noted, blacks have higher levels of SHBG at birth which inhibits the production of testosterone on the organs. Differences in post-pubertal testosterone are small/nonexistent and one should not talk about them when talking about differences in crime or disease acquisition such as PCa. DHT only shows a weak positive correlation with aggression—the same as testosterone (Christiansen and Winkler, 1992; however other studies show that DHT is negatively correlated with measures of physical aggression; Christiansen and Krussmann, 1987; further, DHT is not so evil after all).
Summing it all up
Blacks are not stronger than whites, indeed evidence from the races’ differing somatype, grip strength and leverages all have to do with muscular strength. Furthermore, the study that Ellis cites as ‘proof’ that blacks are stronger than whites is on one measure; an isokinetic dynamometry machine which is pretty much a leg extension. In true tests of strength, whites blow blacks away, which is seen in all major professional competitions all around the world. Blacks do have denser bones which is due to androgen production in vitro, but as of yet, there has been no research done into bone density and criminality.
The races don’t differ on penis size—and if they do it’s by tenths of an inch which is not statisitcally significant and I won’t waste my time addressing it. It seems that most HBDers will see a racial difference of .01 and say “SEE! Rushton’s Rule!” even when it’s just that, a small non-significant difference in said variable. That’s something I’ve encountered a lot in the past and it’s, frankly, a waste of time to converse about things that are not statistically significant. I’ve also rebutted the theory on 2d/4d ration as well. Finally, Asians had a similar level of androgen levels compared to blacks, with whites having the least amount. Along with a hole in the theory for racial differences in androgen causing crime, it’s yet another hole in the theory for racial differences in androgens causing racial differences in penis size and prostate cancer.
On intelligence scores, no one denies that blacks have scored about 1 SD lower than whites for 100 years, no one denies that blacks have a lower educational attainment. In regards to learning disabilities, blacks seem to have the highest rates, followed by Native Americans, than non-Hispanic whites, East Asians and the lowest rates found in South Asians. He states only one study links brain size to criminal behavior and it showed a significant inverse relationship with crime but not other types of offenses.
This is a really good article and I like the theory, but it’s full of huge holes. Most of the variables described by Ellis have been shown to not vary at all or much between the races (re: penis size, testosterone, strength [whites are stronger] prostate cancer caused mainly by diet, 2d/4d ratio [no evidence of it showing a digit ratio difference], and bone density not being studied). Nevertheless, a few of his statements do await testing so I await future studies on the matter. He says that androgen exposure ‘differs by race and ethnicity’, yet the totality of evidence shows ‘not really’ so that cannot be the cause of higher amounts of crime. Ellis talks about a lot of correlates with testosterone, but they do not pass the smell test. Most of it has been rebutted. In fact, one of the central tenets of the ENA theory is that the races should differ in 2d/4d ratio due to exposure of differing levels of the hormone in vitro. Alas, the evidence to date has not shown this—it has in fact shown the opposite.
ENA theory is good in thought, but it really leaves a lot to be desired in regards to explaining racial differences in crime. More research needs to be looked into in regards to intelligence and education and its effect on crime. We can say that low IQ people are more likely to drop out of school and that is why education is related to crime. However, in Mazur (2016) shows that blacks matched for age had lower levels of testosterone if they had some college under their belt. This seems to point in the direction of the ENA theory, however then all of the above problems with the theory still need to be explained away—and they can’t! Furthermore, one of the nails in the coffin should be this: East Asian males are found to have higher levels of testosterone than white males, often enough, and East Asian males actually have the lowest rate of crime in the worle!
This seems to point in the direction of the ENA theory, however then all of the above problems with the theory still need to be explained away—and they can’t! Furthermore, one of the nails in the coffin should be this: East Asian males are found to have higher levels of testosterone than white males, often enough, and East Asian males actually have some of the lowest rate of crime in the world (Rushton, 1995)! So this is something that needs to be explained if it is to be shown that testosterone facilitates aggression and therefore, crime.
I’ve shown—extensively—that there is a low positive correlation between testosterone and physical aggression, why testosterone does not cause crime, and have definitively shown that, by showing how flawed the other studies are that purport to show blacks have higher testosterone levels than whites, along with citing large-scale meta-analyses, that whites and blacks either do not differ or the differences is small to explain any so-called differences in disease acquisition or crime. One final statement on the CAG repeats, they are effect by obesity, men who had shorter CAG repeats were more likely to be overweight, which would skew readings (Gustafsen, Wen, and Koppanati, 2003). So depending on the study—and in most of the studies I cite whites have a higher BMI than blacks—BMI and WC should be controlled for due to the depression of testosterone.
It’s pretty conclusive that testosterone itself does not cause crime. Most of the examples cited by Ellis have been definitively refuted, and his other claims lack evidence at the moment. Even then, his theory rests on the 2d/4d ratio and how blacks may have a lower 2d/4d ratio than whites. However, I’ve shown that there is no significant relationship between 2d/4d ratio and traits mediated by testosterone (Kohler, Simmons, and Rhodes, 2004) so that should be enough to put the theory to bed for good.
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
I’ve been in a few discussion with PumpkinPerson on phenotype and if the similar phenotype found in Australoids and Pacific Islanders meant they were Negroid. However, just because two *dissimilar groups* look *phenotypically similar*, that doesn’t mean that they are *genotypically similar*. Afrocentrists have also latched on to this ridiculous theory, saying that blacks are ‘all over the world, displaced by whites yada yada yada’. Today, I’ll show that just because those two groups look similar to Africans doesn’t mean that they are similar on the genotype.
PP wrote an article last week, The importance of leaving Africa, which I will be quoting from for the remainder of this article.
The root of this debate is not so much genuine scientific disagreement, but ethnic genetic interests. The black Afrocentrists believe it’s good for black people to be seen as part of this larger, global black community, thus dispelling the claim that blacks only left Africa in chains. For leaving Africa was one of the milestones that separates humans from our closest living relatives (chimpanzees), so the claim that blacks never left Africa is seen as racist indeed.
I agree here that Ethnic Genetic Interests is the main driver of the dispute.
But if the mere leaving of Africa did indeed screen for IQ, why do the Australoids score even lower on IQ tests than sub-Saharan Africans do, and have somewhat smaller brains
Because the environment is similar it would select for similar phenotypes, but just because the environment is extremely similar doesn’t mean that no genetic change occurred in the 70 ky that Australoids left Africa in.
By contrast, the non-black HBDers think it elevates their racial status to promote the idea that their ancestors did something that blacks couldn’t accomplish: leaving Africa.
Well, as I’ve covered here last year (time flys), those who left Africa had specific alleles, the DRD7 and DRD4 alleles, which are absent from SSA populations. This ‘wanderlust’, due to the DRD7 allele, is the *cause* of the migration OoA. It has nothing to do with being more intelligent than those who stayed, it has to do with the genetic mutation that arose from a common ancestor around the time of the OoA migration. The cause of the migration does come down to genetic differences in the founder population (s), but not intelligence differences.
Two notes on the DRD4 allele: populations with a history of migration have a higher chance of having the allele in comparison to sedentary populations. And: a correlation of .85 was found between km traveled and the rate of DRDR4 allele frequency distributions. These alleles are more prevalent in South America, which is not surprising since they had to travel the furthest.
PP then starts talking about why Australoids have lower IQs, saying:
With agriculture/civilization, the dark caucasoids traveled the World, spreading their high IQ mutation to every corner of the globe except those that are most isolated. So the mean genetic IQ of the entire World increased by 13 points, with the exception of places that were too hard to get to, such as Australia and Papua New Guineas, the Congo rain forest, the Southern tip of Africa, and the Americas. Since most of sub-Saharan Africa got the genes, they suddenly leaped from having lower IQs than the Austaloids, to being smarter (only the bushmen and pygmies, who like the Australoids, were too isolated to get the genes, remained behind the Australoids).
This is a great hypothesis. It makes a lot of sense. The ‘Dark Caucasoids’ as PP calls them, better known as Anatolian/Neolithic Farmers could have had a higher chance for more high IQ mutations due to the fact that they could farm and thus have a higher population giving more of a chance for higher IQs.
The downfall for the dark caucasoids was spreading these genes to whites and East Asians. Because of cold winters, East Asians and whites were smarter than pre-mutation dark caucasoids, and now with these mutations, they were smarter once again.
I’m confused here. What we call whites today did not exist that far back in the past. Europeans are an amalgamation of four different ancient populations, basically are an amalgamation of ‘Dark Caucasoids’. Is he also saying that the Neolithic Farmers were more intelligent than East Asians?
Eurasians didn’t become a distinct breeding group until the end of the last Glacial Maximum. This is why there is ‘genetic similarity’ to modern-day Europeans with some old, 10k year plus peoples in the Americas. Because the two groups didn’t split into distinct populations, they show a similar genotype. This is what proponents of the Solutrean Hypothesis need to get through their heads. (I recently got into a nice discussion over at The Alternative Hypothesis, scroll down for comments. I’m going to make a more comprehensive post on the SH in the near future as I have come across even better data on it.)
We can see from this PCA graph (from Zainel Abidin et al) that Australoids don’t even cluster in the vicinity of Africans. They are on the complete other side of the graph, showing how great of a genetic distance there is between these two populations. You can see the other Oceanic peoples (the orange dots, who Afrocentrists and others say are Negroid, Abos, Papuans, Melanesians, etc) are also clustered away from Africans. PCA graphs show that the three populations are not genetically similar and that phenotype, sometimes, isn’t enough to show who belongs to what racial grouping. PCA analysis refutes peoples ‘feelz’ on what they believe with their eyes. Even with this data, their ‘feelz’ still overrides the truth and they still believe lies.
While on this subject of similar phenotype not meaning one population is racially the same as another, people use this same fallacious reasoning for ‘white-looking’ peoples in the ME.
Quoting Razib Khan:
The final issue is that a lot of the phenotypes that we racially code are recent. This probably explains why groups like the Kalash and Nuristanis can look more like Europeans than South Asians, but they’re genetically more like South Asians.
What does any of this have to do with non-scientific things? I don’t really know. My interest in population structure is intellectual, not personal. But a certain type of person should probably stop talking about how white people have been in Europe for 40,000 years. First, the ancestors of modern Europeans 40,000 years ago were almost all residing outside of Europe. An assertion that holds until 15,000 years ago. And most would still be resident outside of Europe 8,000 years ago as depending on how you count/calculate. *** And, perhaps more importantly, the typical phenotype of Northern Europeans probably really coalesced only around ~5,000 years ago. ***
How can there be such phenotypic similarity in two populations separated by thousands of miles?
Easy. The Kalash and other ME ‘white-looking’ populations have ancient Siberian ancestry. As shown in my linked article, modern-day Europeans have a great deal of Siberian ancestry, mostly from the true Aryans, the Yamnaya peoples.
And in the comments Razib was asked:
“Could I bother you to list the top three theories/positions that you see falling into this unsupportable category?”
To which he responded:
“that phylogeny and phenotype track closely. just because you can’t tell the physical difference between two pops (e.g., solomon islanders and sub-saharan africans) they must be phylogenetically close. this is not the case.”
Pretty much seals the deal.
Just because populations look similar on the outside doesn’t mean they are genetically similar. As shown from Razib’s post, the phenotypes that we code are relatively recent, which is why there are some populations separated by thousands of miles yet look extremely similar.
This was said in the comments:
I can’t really tell about the genetics since I don’t have the scientific background, but my impression is a lot of those white identity guys have an extremely mythologised view of the past. This seems to be true even of the smarter ones; e.g. I recently read a bit of Richard Spencer’s twitter account (out of interest in the alt right phenomenon) and he throws out such totally retarded comments as “Europe has always been unified, even before Christianity” (totally ignoring what is known about the ancient Greeks’ intimate links to the Near East, the Greeks’ and Romans’ unflattering view of the northern barbarians, the emergence of Latin Christendom in the middle ages and the fairly late rise of the concept of Europe etc.) or “Europe is a nation”. There seems to be little awareness of the complexities of historical change because everything is reduced to some supposedly unchanging racial essence reaching back into the mists of prehistoric times. Now I’m pretty far right and “racist” myself, but a lot of this really seems pretty stupid…like myth-making for identity politics.
i knew the pre-WN richard spencer (we lost touch after his ideological changes ~2010). he’s smart. i have a hard time believing he doesn’t know the latest research, which was evening starting to be evident back then. so i think it’s myth-making.
p.s. a friend of mine sent me a link to a richard spencer interview with kevin macdonald last year i think, pointing to a specific segment of the podcast talking about ancient genetics. kevin was telling richard how europeans 40,000 years ago were white, and those are the ancestors of europeans. that’s wrong.
Europeans 40kya were not white those in the area at that time are *not* the ancestors of today’s Europeans.
Both Afrocentrists and Nordicists need to keep up with the new information that’s constantly coming out. Because what they say in regards to genetics and/or anything else is mostly wrong.