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Climate, Violence, r/K Selection Theory and the Vindication of JP Rushton

1850 words

Why do violent crimes increase as temperatures increase? Why do violent crimes decrease as the temperatures decrease? These phenomena are noticed every year, and criminologists set out to find the relationship between climate and violence and whether or not there is a curvilinear hypothesis, which crime increases as the temperature increases, but at extremely high temperatures the crime rate begins to dip down.

When the weather gets colder, crime decreases. All though crime does decrease in the Winter months, crimes that take more planning, such as property crime and robbery increase. This is due, obviously, to the fact that people don’t want to spend too much time outside so they plan their crimes ahead to minimize the time spent outside whereas in hotter temperatures this does not occur. It is known that when it’s colder, resulting criminal actions are less random than those committed in hotter temperatures.

The two trains of thought for the temperature/crime theory are the curvilinear hypothesis, as noted above, and the linear hypothesis, which argues for that as the temperature increases, so does crime without a drop in extremely high temperatures.

Mishra (2014) showed that the relationship is not a curvilinear one, but that crime rises steadily as the temperature increases. Looking at Allahabad city, India from a 62 year period from the years 1952 to 2013 with the variables being temperature, humidity and rainfall, the results of the analysis shows that temperature has a significant effect on the proclivity to commit crime, as well as murder. Relative to the temperature, humidity shows a strong correlation with crime with rainfall showing a negative correlation.

Mishra took annual data from the National Crime Record Bureau with monthly data taken from the various police stations of Allahabad city. The temperature and rainfall data was taken from local news stations and the Indian Meteorological Department.

Results of his analysis showed significant correlations with violent crime and temperature (r=.75) with murders increasing as temperatures increase. The relationship between relative humidity and crime was strong as well (r=.68) with rainfall having a negative correlation (r=-.14). Out of all three of these variables, the average temperature has more of an effect on crime than relative humidity. Using a regression model, Mishra discovered a correlation of .56, showing that temperature alone accounts for 56 percent of the variation in crime pattern. Including all three variables in the regression model shows a correlation of .61. This confirms that among the climate elements tested that temperature itself had the highest effect on crime.

Figure 2 of the paper shows that as temperatures rise (starting at about 25 degrees celsius), that the crime rate increases.Since very high temperatures are associated with rainfall, there is a reduction in crime when this occurs, thermal stress is reduced. However, when rainfall and humidity were both unchanged, higher temperatures would not cause a decrease in violence. This result is inconsistent with the curvilinear hypothesis and does not support the claim that extremely high temperatures cause decreased violence.

Van Lange, Rinderu, and Bushmen (2016) thought of the model CLASH (CLimate, Aggression, and Self-control in Humans) which shows differences within and between countries and their proclivities for aggression and criminal behavior. With lower temperatures, along with seasonal variation like what is seen in Northern Europe, peoples had to adopt a slower life history strategy with more focus on planning for the future as well as a need for self-control due to the differing variations in climate and how that has an effect on acquiring food. The CLASH model further shows that slow life history strategy, thinking into the future and self-control are important determinants in predicting violence.

As I have discussed here before, r/K Selection Theory (Life History Theory) shows that those who live in colder temperatures adopt slower strategies which lead to more future planning along with more self-control along with more altruistic behaviors shown. In a more harsh environment, such as Africa, Latin America and other locations situated near the equator, faster life history strategies are needed to offset the harsh environment, which leads to evolutionary causes for earlier menarche in black and Mexican-American girls. Faster life history strategies are needed in locations near the equator due to the harshness of the environment. This is why Africans and other peoples located at or near the equator have more children, to offset the harsher environment. No planning ahead was needed, as most likely populations near the equator wouldn’t have lived long enough to see the delayed payoff. Conversely, those in northerly climes live longer due to the need to plan ahead,  and along with this ability to plan ahead came higher intelligence, which leads to yet another selector for high intellect in populations that evolved further from the equator, earlier childbirth. On top of that selector, deleterious Neanderthal alleles decreased historic fitness levels 1 percent in non-African populations, which further lead to evolution of the ability to think into the future due to less children beared. Since the future becomes more predictable the further you travel away from the equator, it becomes adaptive for peoples to adopt a slower life history strategy out of necessity, as that’s the only way to survive and they will see the fruits of their self-control due to having a longer life expectancy due to superior future time orientation in comparison to those in southerly climes.

Since a faster life history strategy is correlated with threats of harshness and higher morbidity and mortality, from the life history perspective we would reason that those with lower SES would have to adopt a faster life history strategy in order to offset the fact that they are more likely to suffer premature disability or death. Lower SES is also correlated with other r-selected strategies such as earlier sexual activity (a variable correlated with lower IQ), higher rates of childhood pregnancy and childbearing, greater number of offspring and less care and attention shown to those offspring, this study. For the third time this month, proves Rushton right with his application of r/K Selection Theory on the three races of humanity.

Van Lange, Rinderu, and Bushmen state that neighborhood deterioration, assaults, muggings, drug addicts, and presence of gangs are associated with earlier and higher rates of sexual activity. Not coincidentally, this is seen in many majority black and ‘Hispanic’-majority cities in America. They also say that as resources become scarce that women gravitate towards men with more access to resources and those that will invest in their children’s reproductive values. Though this is hardly seen in low-income communities around America, you do see a lot of black women who gravitate towards the drug dealer or another black male who is involved with illegal activities who then acquire mass amounts of capital. This is an evolutionary strategy for all women, since money is correlated with intelligence and therefore a mate with more money has better means to take care of any offspring conceived.

The CLASH model extends r/K Selection Theory, particularly where r/K Selection Theory emphasizes unpredictability and harshness as a source of environmental stress, the CLASH model emphasizes predictability over environmental stress. That is, those who evolved in northerly climes can deal with stress better than those who evolved near the equator, therefore lessening the amount of crime in those populations due to them being able to constrain themselves more. The CLASH model proposes that the combination of predictability and control shape a slow life history strategy, future time orientation, with a focus on self-control. Moreover, in an analysis of 40 work-related values in 40 countries, it was found that the countries located the furthest from the equator tended to place a greater value on future rewards, such as perseverance and thrift.

In countries closer to the equator, according to the 2014 World Fact Book, the average age of first birth for a female was 20 years of age (the countries were the Gaza strip, Liberia, Bangladesh, Kenya, Mali, Tanzania, Uganda and  various other middle African countries). Conversely, for countries further away from the equator, the average age of first birth was 28 years of age (Japan, Canada, and most European countries). Those populations that evolved in warmer climates where the changes in season are minimal with unpredictable harshness tend to enact faster life history strategies than those in colder climates.

The researchers state on page 31:

One standard deviation increase in temperature was associated with a 11.3% increase in intergroup conflict and a 2.1% increase in interpersonal conflict. Examples of interpersonal conflict include spikes in domestic violence in India and Australia, greater likelihood of assaults and murders in the USA and Tanzania, ethnic violence in Europe and South Asia, and civil conflicts throughout tropical climates. Hence, we conclude that it is both differences in average temperature and differences in seasonal variation in temperature that help explain cross-national differences in aggression and violence around the world.

And on page 41:

Assuming CLASH is accurate, it is interesting to consider that people’s thoughts and behaviors may be quite different, based on the physical circumstances their ancestors faced and that they face themselves. The world is getting smaller and smaller. Electronic and social media (e.g., WhatsApp, Twitter, Facebook, email) connect us to people all over the world. Yet, people coming from differing ancestral histories and living in different locations face challenges of self-control in a variety of ways. A businessperson from London may expect a response the next day, but the alliance in Nairobi may want to take at least an extra day. If CLASH is correct, the same pattern should hold for within-country differences between a businessperson working in Chicago and the alliance working in New Orleans, or between a businessperson working in Melbourne and the alliance in Brisbane or Cairns (with London, Chicago, and Melbourne being relatively more remote from the equator, and facing greater variation in climate).

The correlation between temperature, crime and life history strategies is shockingly high. JP Rushton is now vindicated from all of the derision he experienced in the 30 plus years he was pushing his r/K Theory. This shows implications for the European ‘refugee’ crisis as well, due to the higher rates of all violent crime occurring ever since this mass exodus from MENA (Middle Eastern North African) countries.

The CLASH model is a great compliment to r/K Selection Theory and goes deeper into why behaviors differ in human populations based where ancestral evolution occurred. As temperatures increase, so does crime starting at 76 degrees Fahrenheit, with there being a negative correlation for crime committed during rainfall. The CLASH model vindicates Rushton’s supposedly ‘wacky theories’ on race, evolution and behavior. Further, the CLASH model also shows another cause for the current situation occurring in Europe. The people flooding into the continent have ancestral ties to hotter climes. They then bring their genetic proclivity to commit crimes with them to the new area, which then increases crime. This is one of many  reasons for the cucking of Europe. As we look more into evolutionary causes for behavior and those behaviors that lead to more crime committed, Rushton and others will be further vindicated and when this occurs, with ample data, of course, sensible immigration policy can be had to quell the amount of crime committed by ‘migrants’ and other immigrants into our countries.


Black American Men with More African Ancestry Less Likely to Be Obese

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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.

Blacks Are Less Violent Than Whites?

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I’ve read a lot of crazy things in my life, though this must be the craziest. Someone really believes that “blacks are less violent than whites“. To believe such a claim, you would have to close your eyes to all of the relevant data. From naming outright falsities to obscuring data to fit his narritive, this article will show and refute a distorted reality, one that the Left wishes to show, to one simply looking for the truth to interracial crime.

Don’t be modest, Caucasians. The Holocaust

The Holocaust is really beyond the scope of this blog, but check out the CODOH Library for the truth on this matter.

ethnic cleansing

This is not unique to Europeans. The Rwandan Genocide (which was due to ethnocentrism) and the ethnic cleansing currently occurring in Central Africa aren’t real? Fact of the matter is, is that every ethnicity has participated in ‘ethnic cleansing’, which is really just protecting genetic interests. This is a non-factor as this has gone on before European colonialism.

colonization of Africa and the Caribbean

Colonialism was good for the native inhabitants of Africa. Speaking of the Caribbean, how well did it end for the Haitians after they defeated Napolean?

American slavery

Oh? You mean how a majority of the slaveholders were Sephardic Jews? Or how there are reports from New Orleans from their 1860 census that showed 3000 freed blacks owned slaves, accounting for 28 percent of the city’s population? In 1860 Louisiana, at least 6 blacks owned more than 65 slaves, with the biggest number of slaves being 165 slaves who worked on a sugar plantation. How about the Jews’ role in American slavery? Moreover, at the height of slavery, a paltry 6 percent of Southern whites owned slaves, when combined with the North it was 1.4 percent. An estimated 3000 blacks had about 20000 slaves in 1860. But tall is only about the whites who did slavery, and not about the Arabs and how they started enslaving Africans FIRST, in 650 AD.

Native American Genocide

The Alternative Hypothesis just had a post the other day about the non-genocide of American Indians. Basically, their population was anywhere between 1.5 and 2 million people. Population reduction for the Native Americans was only 0.22 percent!! Doesn’t seem like such a ‘genocide’ to me. If so, that’s the slowest genocide I’ve ever heard of.

Jim Crow

People segregate naturally. We’re more segregated now than we were 50 years ago! Must be those residual effects from Jim Crow huh?

But somehow in the media it’s the black man who is portrayed as the savage.

I wonder why??

It’s just not fair. We white folks are so much better at race-based aggression than our darker complected brothers.

More intelligent than them, that’s why.

Just this Wednesday a white guy walked into a historic African American Church in South Carolina, was accepted as part of the service, stayed for about an hour before shouting a spiteful message and gunning down several parishioners!

Now that’s some hate right there!

One person does something and that means….what exactly?  It shows one person is hateful! Look at averages, not singular events.

Whenever anyone brings up race and violence, the first thing people mention is crime.

Because they are linked to each other. Why wouldn’t the two things be mentioned in the same breath?

There is more black-on-black crime than white-on-black crime, they say. And they’re correct!

According to a 2013 FBI Uniform Crime Report, when it comes to murder, 90 percent of black victims were killed by black offenders.

However, what people fail to mention is that according to the very same report, 83 percent of white victims were killed by white offenders, too.

These numbers don’t show black people are more violent than white people. They show that BOTH white and black people would rather kill within their own race.

Yea they show that both would rather kill within race, however you miss something very important here:  Interracial crime!

First, we find that during the 2012/2013 period, blacks committed an average of 560,600 violent crimes against whites, whereas whites committed only 99,403 such crimes against blacks. This means blacks were the attackers in 84.9 percent of the violent crimes involving blacks and whites. This figure is consistent with reports from 2008, the last year DOJ released similar statistics. Perhaps not coincidentally, that was the year Mr. Obama was elected president.

In terms of raw numbers, black people and white people actually commit about the same number of murders. But you wouldn’t know that from the media.

Not really. Per capita rates are more important than raw numbers, luckily we have data on that!

As of 2008, young black men kill at a rate of 7 times higher than white men.

Homicide Trends in the United States, 1980-2008 Annual Rates for 2009 and 2010 pg 11

Is that the same number of murders?? I’m looking at the same stat in a completely different way than you are.

The FBI is charged under the Hate Crime Statistics Act with compiling statistics on spite-based legal transgressions. In its most recent report, for 2013, hate crimes based on race are far more numerous than any other kind.

  1. The FBI is biased towards blacks and ‘hate crimes’. How about all of the countless times we here about blacks attacking whites using racial epithets during the attack? Too many to count. They are, however, not counted as hate crimes by the FBI because it doesn’t fit their narritive.
  2. I wonder how those numbers would look if actual hate crimes were included in this data (black on white included).

According to the FBI statistics, 54.5 percent of the reported single-bias hate crimes that were racially motivated in 2013 targeted blacks. Only 16.3% target whites.

Want to talk bias? The amount of black on white hate crimes that are NOT categorized as such. This skews the statistics considerably.

Would our economy really have been so robust without the free labor of all those slaves?

Yes. Whites could have done it, but getting blacks to do it was cheaper and more efficient. Using brains to get ahead is what life is all about. Whites build great societies anywhere. Our economy would have been as robust as it is now without America never having a history of slavery.

Heck! Would we even have a country at all if we hadn’t murdered all those indigenous peoples in the first place?

Is a population decline of 0.22 percent per year ‘murdering all those indigenous peoples’?

So let’s put it to rest. When it comes to hate crimes, white folks kill! But don’t feel too bad, black folks. There are things you’re good at, too. Like nonviolent resistance.

This guy is delusional. Just because MLK preached non-violence doesn’t mean that blacks as a whole are non-violent. Look at crime stats from anywhere in the world.

After all this time, black people have very rarely used violence as a means to achieve their ends, to try to secure the rights and freedoms white America guards so jealously.

Is this guy living in the same America as I am?

In just the past year or so, unarmed black folks have been assaulted or killed for holding toy guns

Go ahead and pick out the real one, then do it from a distance when you get a phone call that there is a kid walking around while waving a gun.

being suspected of selling loose cigarettes

He died due to asthma, obesity, and heart disease, that’s why he couldn’t breathe; he was 350 pounds. He also did not comply with the officers’ orders, which is why he needed to be taken down in such a fashion.

listening to music at a gas station

Dunn did say that Davis said he was going to kill him with a shotgun and that’s when he grabbed his gun out of his glove box.

asking for help after a car accident

Freak accidents happen that get blown up? Damn, that proves whites are more violent huh!?!?

wearing hoodies

Yea, people still believe that Trayvon got killed for ‘wearing a hoody’. We have jurys for a reason. We have trials for a reason. We have laws like Stand Your Ground for a reason. Trayvon was killed because if Zimmerman hadn’t of protected his life, he would be dead. All of these people complaining about the verdict, if you were put into that same situation, would you allow yourself to be killed for fear of being called ‘racist’?

wearing bikinis

Listen to police when they tell you to do something. Especially during an investigation. This shouldn’t even need to be said.


1) The Baltimore Six are going to get off for it. They caused no harm. 2) He threw himself around in the back of the van causing his own death.

and now just going to church!

Right. They were killed just for going to Church. eyeroll

And the response from the black community has been pretty darn nonviolent. Yeah there’s been some shouting and looting, but very little beating or killing.

‘Pretty darn non-violent. Which is why immediately after, blacks began false flagging Church burnings in an attempt to pin them on whites. So ‘peaceful’, right?

White folks, can you imagine having to undergo such indignity on a daily basis and NOT responding in kind!?

Can’t tell if serious. Just recently, a beta Trump supporter was thrown down on the ground by a ‘young black male’ and did not retaliate.

No wonder a blonde white girl from a Christian fundamentalist home darkened her skin, curled her hair and tried to pass as black! Sometimes – often really – it’s darn embarrassing to be white! Black folks have the moral high ground.

Because Dolezal is a moron.  Blacks have the moral high ground? Please show me where this occurs.

Somehow they live in an American society that heaps hatred on their every move and they respond with dignity and perseverance.

There’s no reason at all for this right? Just good old fashioned ‘racism’?

So why are black people so nonviolent?

They aren’t. See the whole of sub-Saharan Africa to see how ‘non-violent’ they are.

Damned if I know! But I wish us white folks would take a lesson from them.

Yes!! The white man has tons to learn from the criminal black man! Much to learn about taking welfare and not working!!

Blacks have 2.5 to 4.9 percent higher testosterone than whites, which is causes more violence and crime. Beaver (2014) states that blacks who have the MAOA-L 2 repeat allele have significantly highier chances of being shot, stabbed or reporting shootings and stabbings than other genotypes. Blacks also have the highest rate of the 3 repeat allele (53 percent compared to 37 percent for whites) and 2 repeat allele (5 percent compared to .1 percent for whites). Moreover, he didn’t speak about how black violent crime is genetic in nature. This is mirrored in the crime rate and how violent blacks really are.

This is the age of the Internet where we have amassed tons of human knowledge which is readily available with a few hits of a few buttons. If people still want to be ignorant spewing falsities, it’s on them. But the truth is out there for those who seek it.

Blacks are not ‘non-violent’. Go to the nearest ghetto and see how ‘non-violent’ blacks are.

Individual and Racial Differences in IQ and Allele Frequencies

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In the past 100 years since the inception of the IQ test there have been racial differences in test scores. What causes these score differences? Genetics? Environment? Both? Recently it has come out that populations do differ in allele frequencies that affect intelligence. David Piffer’s “forbidden paper on population genetics and IQ” was rejected by the new editor of the journal Intelligence. In the paper, he shows how IQ alleles vary in frequency by population. One reviewer even said it should not be put up for review, which Piffer believes there was a hidden agenda or a closed minded attitude. He even puts reviewers comments and responds to them. He says science should be transparent, which is why he’s showing the researchers’ comments on his paper.

His December, 2015 paper titled: A review of intelligence GWAS hits: Their relationship to country IQ and the issue of spatial autocorrelation shows that there are differing allele frequencies in which IQ between populations that affect IQ which are then correlated highly with average IQ by country (r=.92, factor analysis showed a correlation of .86). There was also a “positive and significant correlation between the 9 SNPs metagene and IQ”(pg. 45). However, Piffer does conclude that since the 9 alleles are present within all populations (Africans, Latin Americans, Europeans, South Asians, and East Asians) that the intelligence polymorphisms don’t appear to be race-specific, but were already present in Homo Sapiens before the migration out of Africa. He then goes on to say that it’s extremely likely that the vast majority of alleles were subject do differential selection pressure which lead increases in cognitive abilities at different rates rates in different geographical areas (pg. 49). It’s of course known that differing populations faced differing selection pressures which then lead to genotypic changes which then affected the phenotype. It’s not surprising that genes that correlate strongly with intelligence have differing frequencies in different geographical populations; it’s to be expected with what we know about evolution and natural selection. Below is the scatter plot showing the relationship between polygenic score GWAS (Genome Wide Association Studies) hits and IQ:

Scatter plot IQ-polygenic score

The fact that these differences exist should not come as a shock to those who want to seek the truth, but as seen with how David Piffer didn’t even get consideration for a revision, this shows the bias in science to studies such as this that show racial differences in intelligence exist.

Piffer’s data also corroborates Lynn and Meisenberg’s (2010) finding of a correlation of .907 with measured and estimated IQ. This shows that the differing allele frequencies affect IQ, which then affect a countries GDP, GNP, and over all quality of life.

With a sample with a huge n (over 100,000 subjects) cognitive abilities tests were performed on verbal-numerical reasoning, memory and reaction time (a huge correlate for IQ itself, see Rushton and Jensen, 2005). Davies et al (2016) discovered that there were significant genome-wide SNP based associations in 20 genomic regions, with significant gene-based regions on 46 loci!! Once we find definitive proof that intelligence differences vary between individuals, as well as the loci and genomic regions responsible, we can then move on to difference in allele frequency in depth (which Piffer 2015 was one of the starts to this project).

Moreover, genes that influence intelligence determine how well axons are encased in myelin, which is the fatty insulation that coats our axons, allowing for fast signaling to the brain. Thicker myelin also means faster nerve impulses. The researchers used HARDI to measure water diffusion in the brain. If the water diffuses rapidly in one direction, that shows the brain has very fast connections. Whereas a more broad diffusion would indicate slower signaling, thus lower intelligence. It basically gives us a picture of an individuals mental speed. Thinking of reaction time tests where Asians beat whites who beat blacks, this could possibly show how differing process times between populations manifest itself in reaction time. Since myelin is correlated with fast connections, we can make the inference that Asians have more than whites who have more than blacks, on average. The researchers also say that it’s a long time from now, but we may be able to increase intelligence by manipulating the genes responsible for myelin. This leads me to believe that there must be racial differences in myelin as well, following Rushton’s Rule of Three.

Since the mother’s IQ is the best predictor of the child’s IQ, this should really end the debate on its own. Sure on average, intelligent black mothers would birth intelligent children, but due to regression to the mean, the children would be less intelligent than the mother. JP Rushton also says that regression works in the opposite way. Both blacks and whites who fall below their racial means will have children who regress to the means of 85 and 100 respectively, showing the reality of the genetic mean in IQ between the races.

Why would differing allele frequencies lead to the same cognitive processes in the brain in genetically isolated populations? I’ve shown that brain circuits vary by IQ genes, and populations do differ in this aspect, like all other differing genotypic/phenotypic traits.

East Asians have bigger brains, as shown by MRI studies. Rushton and Rushton (2001) showed that the three races differ in IQ, brain size, and 37 different musculoskeletal traits. We know that West Africans and West African-descended people have genes for fast twitch muscle fibers (Type II) (Nielson and Christenson, 2001). Europeans and East Asians have slow twitch muscle fibers (Type I) for strength and endurance. (East Africans have this as well, which allows for ability to run for distance, which fast twitch fibers do not allow for. The same is true for slow twitch fibers and sprinting events.) Bengt Saltin showed that European distance runners have up to 90 percent slow twitch fibers (see Entine, 2000)! So are genetic IQ differentials really that hard to believe? With all of these differing variables in regards to intelligence that all point to a strong genetic cause for individual differences in other genes that lead to stark phenotypic differences between the races, is it really not plausible that populations differ in intelligence, which is largely inherited?

Is it really plausible that differing populations would be the same cognitvely? That they would have the same capacity for intelligence? Even when evolution occurred  in differing climates?  The races/ethnicities differ on so many different variables with differing genes being responsible for it. Would IQ genes really be out of the question? Evolution didn’t stop from the neck up. Different populations faced different selection pressures, so different human traits then evolved for better adaption in that environment. Different traits clearly developed in genetically isolated populations that had no gene flow with each other for tens of thousands of years. These differing evolutionary environments for the races put different pressures on them, selecting some for high IQ alleles and others for low IQ alleles.

We are coming to a time where intelligence differences between populations will become an irrefutable fact. With better technology to see how differing genes or sets of genes affect our mind as well as physiology, we will see that most all human differences will come down to differing allele frequencies along with differing gene expression. Following Rushton’s simple rule based on over 60 variables, East Asians will have the most high IQ alleles followed by Europeans and then blacks. The whole battery of different cognitive abilities tests that have been conducted over the past 100 years show us that there are differences, yet we haven’t been able to fully explain it by GWAS and other similar techniques. Charles Murray says within the next 5 to 10 years we will have definitive proof that IQ genes exist. After that, it’s only a matter of time before it comes out that racial differences in IQ are due to differing allele frequency as well as gene expression.

White Men Can’t Jump? That’s OK; Black Men Can’t Swim

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Everyone sees how athletic blacks are, for instance in football, but why don’t blacks like swimming? Black children drown at a rate almost three times higher than white children. 70 percent of black children can’t swim, compared to 60 percent of ‘Hispanic’ children and 40 percent of white children. A combination of genetic and environmental factors are involved in this.

JP Rushton writes in Race, Evolution and Behavior (pg. 163):

Body structure differences likely account for the differential success of blacks at sporting events. Blacks are disproportionately successful in sports involving running and jumping but not at all successful at sports such as swimming. For example in the 1992 Olympic Games in Barcelona, blacks won every men’s running race. On the other hand, no black swimmer has ever qualified for the U.S. Olympic swim team. The bone density differences mentioned above may be a handicap for swimming.

Rushton noted above this paragraph that there are bone density differences between blacks and whites which have been noted at all ages and skeletal sites, remaining even after controlling for body mass. These differences even appear before birth, prenatally. Divergence in length and width of the bones in black and white fetus is followed by greater weight of black infants in comparison to white infants. These skeletal differences in weight obviously persist into adulthood, which then have implications for blacks with swimming, but give them advantages in other sports.

At the time of the writing of Race, Evolution, and Behavior in 1997, no black had ever qualified for the U.S. Olympic Swimming Team. However, Anthony Ervin became the first black swimmer to qualify for the Olympic swim team in the year 2000. The fact that it took so long for a black swimmer to make the Olympic swim team shows a genetic component.

Also contributing to this phenomenon is the fact that blacks have narrower chest cavities along with heavier skeletons (as mentioned above), this makes it harder for blacks to stay afloat and swim in the water. A smaller chest cavity brings with it less mobility while doing strokes in the water in comparison to one with a wider chest cavity.

Hochberg (2007) notes that fracture risk, particularly hip fractures, in whites is higher than for blacks in both sexes at 10.1 and 4.1 percent for white and black women respectively while the percentage is 4.3 and 3.1 percent for white and black men respectively. Other analyses of people aged 65 to 90 show 16.3 and 5.3 percent in white and black women while the percentage is 5.5 and 2.6 percent for white and black men respectively. Why do white women suffer more fractures? When women hit menopause, the drop in estrogen coincides with bone loss and osteoperosis. Moreover, in 2010, the Food Surveys Research Group published Fluid Milk Consumption in the United States, which shows women drink less milk then men, with seniors drinking less milk than all age groups (pg. 4). We can then infer from this that senior white women drink less milk, which is then another cause for more hip fractures and weaker bones. Though, there is of course a genetic component with blacks having stronger bones. However, stronger bones means heavier bones, which is a disadvantage when it comes to swimming.

Another funnier reason for blacks non-ability for swimming is that since blacks have a higher single mother rate (72 percent) they didn’t take them to the pool and teach their kids how to swim because they “didn’t want to get their hair wet”, as they put so much time in their hair. This may contribute to this slightly, but the physiological and biological differences mentioned above contribute a far greater amount of variance.

Blacks also wouldn’t be good swimmers due to them having more type II muscle fibers than type I, meaning their muscles fire off quicker and therefore tire quicker. This is why blacks are good sprinters, but would suffer in swimming events. Blacks also have a higher fat free bone density than whites, which leads to blacks not being able to float since fat floats.

For the same reasons why blacks wouldn’t be good swimmers, whites can’t jump, on average. Type II muscle fiber doesn’t allow for the explosive power needed to be able to jump as well as blacks. Even though blacks have a heavier skeletons than whites on average, they can still jump due to their muscle fiber typing. This is also why whites are underrepresented in the NBA (which is 74.4 percent black). Testosterone and musculoskeletal differences are the causes for racial differences in sports.

Whites drown more than blacks before 5 years of age, but after 5 years, more blacks drown in comparison to whites. Drowning in natural water settings was significantly higher for blacks than for whites, with blacks drowning more than whites at ages 7-8 through 17-18 years of age. Swimming pool drowning rates was also shown to be elevated for black children This data shows that after 5 years of age, blacks drown at a significantly greater amount than whites or ‘Hispanics’, which is attributed to the data above.

In our ‘post-racial society’, it’s become taboo to study, and even speak of differences so prevalent in our society, seeing as sports is a huge part of many peoples’ lives around the world. Most of the stars everyone speaks of are black. They must, subconsciously atleast, notice that these differences are there seeing the racial differences on the screen (except for baseball). Of course practice has a part in becoming elite in whatever sport is chosen, however, the best also have a higher inclination to want to do better as well as already being genetically gifted. Those who are more genetically different are, obviously, on the right side of the bell curve, thus, are extremely rare. Though, we can see these genetic disparities in racial differences in sports, with swimming being a huge tell.

It’s not just “a racist joke” that blacks can’t swim, there is biological and physical evidence that blacks, on average, have a more difficult time in the water due to difference in fat-free body mass as well as more narrow chest cavities and heavier skeletons than whites. The same reasons why blacks dominate other sports (football, soccer, boxing, basketball) is the same reason why blacks are underrepresented as swimmers: their biology. However, the trope that white men can’t jump is true as well, and also has it’s origin in genetic differences between the races.

The cause for racial disparities in drowning, as well as in swimming competitions is due considerably to genetic factors such as bone density and chest cavity narrowness. Other environmental factors include children not being taught how to swim due to them being more likely to be raised by single mothers. Bone density and heaviness also shows why blacks suffer less fractures than whites, with white women suffering from it the most. That same bone heaviness is also a reason why blacks are not good swimmers. Muscle fiber typing play a difference in racial differences in sports ability, which the races also vary in significantly. For these reasons, “White men can’t jump.” That’s OK, because “Black men can’t swim.”

Science Daily: Mom’s Exposure to BPA During Pregnancy Can Put Her Baby on Course to Obesity

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Science Daily came out with an article today that exposure to BPA invitro for babies is correlated with obesity at age 7. 94 percent of the women tested had detectable levels of BPA. BPA is also linked with early onset puberty, which I will also speak on later in this article as it has implications for one of my theories.

I briefly touched on BPA in my article What’s the Cause of the Cucking of Europe? where I said:

I advise all of you (women included, there are many deleterious effects of BPA on the mother as well as the baby prenatally), to discontinue use of plastics with BPA in them.

The above-linked study shows that preeclampsia is correlated with elevated levels of BPA in the blood levels in the pregnant mothers, fetal blood, and the placenta. BPA was found to be elevated in mother’s fetal tissue with preeclampsia in comparison to the mothers with lower levels of BPA in their fetal tissue. I will come back to the BPA link with preeclampsia later in the article as it has implications for ethnic groups in America.

The paper, which was just released on the 17th, called Bisphenol A and Adiposity in an Inner-City Birth Cohortcarried out tested BPA in three differing subjects: 375 babies invitro, (3rd trimester) children aged 3 (n=408) and aged 5 (n=518) (Hoepner, et al, 2016). They measured the children’s bodies as well as measuring body fat levels with bioelectrical impedance scales.** Prenatal urinary BPA was positively associated with waist circumference as well as fat mass index, which was sex-specific. When analyzed separately, it was found that there were no associated outcomes in body fat for boys (however it does have an effect on testosterone), but there was for girls (this has to do with early onset puberty as well). They found that after controlling for SES and other environmental factors, they discovered that there was a positive correlation with fat mass index – a measure of body fat mass adjusted for height, body fat percentage and waist circumference. The researchers say that since there was no correlation between BPA and increased obesity, that prenatal exposure to BPA indicates greater vulnerability in that period.

The researchers then conclude that BPA exposure invitro “may be an important underlying factor in the obesity epidemic” and that “Endocrine disrupting chemicals like BPA may alter the baby’s metabolism and how fat cells are formed early in life.”

If true, this has huge implications for the way we look at the obesity epidemic in this country. Who are the most likely to be obese? “Hispanics” and blacks (Ogden et al, 2014).

Returning to what I brought up earlier about early onset puberty: in my article on the hormone leptin being a cause for earlier menarche in black girls, I noted that since black girls were more likely to be heavier as well as mature faster than white girls, that differences in leptin were the cause of differences in menarche between the two groups.  Elevated levels of serum leptin were correlated with body fat and differences in maturation between the two groups. Differences remained, but lessened, after controlling for differences in fat mass, maturation, age, and physical fitness.

Since BPA is correlated with adiposity in children and black girls have earlier menarche DUE to there being a higher chance of black girls being overweight in comparison to white girls, BPA is yet another piece to the puzzle of this phenomena, along with, of course, evolution. Ingestion of BPA is an environmental factor, however, with these changes in body chemistry in the children invitro due to increased BPA consumption by the pregnant mothers, it leads to one cause that can be prevented from further occurring due to our new knowledge.

The study was carried out on a cohort from NYC. In 2010 in NYC, the city was: 44 percent white, 25.5 percent black, 12.7 percent Asian with the rest being filled out by ‘Hispanics’ (not a racial category) and mixed-race people. Even after they matched for SES and other environmental factors, these differences persisted. However, this study was only carried out on those women who self-identified as either Dominican (basically African) and black. To quote the researchers:

Women were included if they self-identified as either African American or Dominican and had resided in Northern Manhattan or the South Bronx for at least 1 year before pregnancy. Exclusion criteria included mother’s report of: cigarette smoking or use of other tobacco products during pregnancy, illicit drug use, diabetes, hypertension, known HIV, or a first prenatal visit after the 20th week of gestation.

So, we have a full sample of Caribbean Africans and African Americans in this study. What else can we learn about those two populations and their consumption of things with BPA in them?

race differences tap and bottled water

The above Figure (7) is taken from the U.S. Department of Agriculture and the Food Surveys Research Group study on differences in drinking tap and bottled different populations in the country. As you can see in this figure (what is notable is the ages 12-19 and 20 to 60 in the table), whites at all age groups drink more tap water. Blacks and ‘Hispanics’ were pretty much even in consumption of bottled water. However, Mexican American girls, like black girls, are also entering puberty earlier. Since both populations have a substantial percentage of them overweight and obese (factor for serum leptin production which then causes early onset puberty), this again shows a strong correlation between body fat gain and early onset puberty. Moreover, this also shows that both Dominican and black populations consume more bottled water than do white populations, both populations are more likely to be obese or overweight (even after controlling for SES) which causes leptin production earlier causing periods to happen much sooner than in populations who drink less bottled water and use other products with BPA in them. .

Going back to preeclampsia, it is a condition that pregnant women develop that’s characterized by hypertension (high blood pressure) and protein in the urine. It’s known that black women suffer from it the most. More interestingly, over the past ten years, rates of preeclampsia have been increasing in the black female population. As the researchers note in the article, BPA is correlated with preeclampsia. Blacks have a higher rate and chance of being diagnosed with hypertension as well. All of these differing variables coalesce into our current obesity epidemic. With blacks and “Hispanics” being more likely to be overweight/obese drink more bottled water, have a higher risk for hypertension, higher risk for preeclampsia and having earlier menarche, these help explain, in part, racial/ethnic differences in obesity.

These differences can be attributed to consumption of bottled water, i.e., consuming things with made with and packaged in plastic as well as canned foods. From my experience with Dominican and black New Yorkers, they tend to have horrible lifestyles, tend to drink tons of bottled water and also tend to be overweight or obese at a higher rate in comparison to the general population. This leads to biologic factors changing (i.e., earlier menarche in younger girls) in these young girls, leading to devastating effects on their body chemistry.

This study, yet again, proves another underlying factor for obesity in certain populations in the country. And what do you know? It’s the populations that already have the highest rate of obesity in the country. When it becomes definitive that BPA consumption by pregnant mothers does lead to underlying factors in obesity. To quote the researchers: “Endocrine disrupting chemicals like BPA may alter the baby’s metabolism and how fat cells are formed early in life.” This will be HUGE for our understanding of underlying causes to obesity! Moreover, if (when) this is fully corroborated, it can then be said that by mothers exposing their children in the womb to excess levels of BPA, there is a chance that they are “giving their own choice to make their children have a higher chance of being obese, as they know the dangers of BPA consumption during pregnancy and all of the negative variables associated with it.”

This is an extremely interesting and important study for our understanding of obesity. Since BPA consumption invitro is correlated with higher fat mass index in girls at age 7, and since those girls who tend to be more overweight and obese than other populations, we can then say that BPA has a hand in obesity in children, which then causes serum leptin to be released, causing way menarche in these populations. An increase in sexual maturation has been linked to the obesity epidemic, which began around 60 years ago. The cause of this is due to the demonization of the fat macro and carbohydrates, all the while it was reversed. This destroyed insulin sensitivity for many Americans, leading to a huge majority of our health problems today.

In conclusion, underlying factors for obesity keep appearing. Due to racial/ethnic differences in bottled water consumption (one of the most common BPA products in households), which the effects of BPA may alter how fat cells are formed in early life, this accounts for, in part, excess adiposity in differing populations. These underlying factors could help show where some of these racial/ethnic differences in obesity come from. Since the two populations in the study (black American and Dominican) both have high levels of adiposity, both drink a lot of bottled water and both have earlier menarche than do whites (who drink LESS bottled water), this shows that some (a lot?) of the variation in obesity between ethnic/racial groupings can be explained by these underlying factors.

** I have one problem with this study. They assessed fat mass index with bioelectrical impedance.The machine sends a light electrical current through the body and measures the degree of resistance to the flow of the current, which body fat can then be estimated. Problems with measuring body fat this way are as follows: it depends on how hydrated you are, whether you exercised that day, when you last ate, even whether your feet are calloused. Most importantly, they vary depending on the machine as well. Two differing machines will give two differing estimates. This is my only problem with the study. I would like if, in a follow-up study, they would use the DXA scan or hydrostatic weighing. These two techniques would be much better than using bioelectrical impedance, as the variables that prevent bioelectrical impedance from being a good way to measure body fat don’t exist with the DXA scan or hydrostatic weighing.

Racial differences in Blood Donation

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Racial differences in blood donations pose a big problem for minorities. This has to do with altruism, which as I have covered extensively here, has a genetic basis. This pathological altruism has whites give and donate more than other races. This is due to evolving in colder climates with harsher environments, which high intellect evolved so our ancestors could survive. Why do minorities, blacks specifically, donate blood less?

Shaz and Hillyer (2010) observed that minorities were underrepresented as donors in the U.S., and that the cause was a higher deferral rate. Deferral reasons include: “low hemoglobin, travel, abnormal blood pressure, pulse or temperature, inability to find vein, tattoo/piercing, infection or taking antibiotics, and not being in good health.”  They state that blood donation rate for blacks was 25 to 50 percent of that of white individuals.

Blacks have lower levels of hemoglobin than whitesThe Red Cross defers people with low levels of hemoglobin. I don’t really know about blacks traveling too much. Abnormal blood pressure could be low or high blood pressure. Your blood pressure is determined by the amount of blood your heart pumps and the amount of resistance in your arteries.The more blood your heart pumps while arteries are clogged, the higher your blood pressure will be. The more fat and cholesterol that build up on the inner walls of the arteries, which I covered the other day, is called atherosclerosis. Called “hypertension” by the medical community, blacks also have a higher rate of this disease as wellBlacks have more genes expressed for coronary artery calcium, which is a strong indicator of atherosclerosis burden. Cardiovascular disease, more specifically coronary heart disease (CHD) is the leading cause of death for all Americans of all ages and ethnic groups (smoking is a leading cause of this). Blacks suffer the highest percentage of deaths due to CHD. And finally, inability to find a vein is due in large part to 75.6 percent of the black community being obese in America (69.2 percent for men and 82 percent for women).

Another reason for deferral is that all though Sickle Cell Disease isn’t strictly a racial disease, blacks do have the highest rate of it. Those with Sickle Cell Trait (SCT) can donate blood, though those with Sickle Cell Disease cannot.

Infections and antibiotics as well as not being in good health is yet another reason why blacks get deferred. This is due in part to “down-low bruthas” who are more likely to have diseases, and therefore cannot donate blood or plasma. Since homosexuals have some of the highest rates of disease in the country, it’s no surprise that blacks would be leading the pack in that subgroup of the country as well. This is a huge reason why blacks get deferred so much. However, in December of last year, the FDA lifted its lifetime ban of gays donating blood. I shutter to think what the deferral rates of blacks will look like in a few years due to this. That is also why “not being in good health” along with “infection or antibiotics” are such big reasons for deferrals. Blacks have all of the things they defer for, yet of course, allegations of prejudice and racism come about and the government has to step in to change things again, endangering the citizens of the country.


To quote from this AmRen article:

It has long been known that blood transfusions and organ transplants work best between people of the same race. Until the Second World War, stocks of blood were routinely segregated by race for this reason. Classification by race was ended when it was discovered to be “racist,” but blood banks are reinstituting segregation.

The distribution of the common blood types is different from race to race, and some rare types are unique to certain races. Only blacks have U negative blood; only whites have Vel negative or Lan negative blood. Dr. W. Laurence Marsh of the New York Blood Center justifies racial classification: “It makes no sense to screen 100,000 whites for U negative when no U negative white person has ever been found.”

So there is a problem with interracial blood transfusion, and they work better with co-ethnics than non-co-ethnics.

The Central Blood Bank states this about ethnicity and blood donation:

Though compatibility is not based on race, genetically similar blood is best for patients who need repeated or large volumes of blood transfusions, or those who have produced red blood cell antibodies for various diseases and conditions like sickle cell, heart disease and kidney disease.

It says that “compatibility isn’t based on race” then says immediately after “genetically similar blood is best for patients who need repeated or large volumes of blood transfusions. . .” The fact that there are differences in blood-type rate by ethnicity, and that there is a shortage of those blood types for blacks and “Hispanics” in America.

There are varying frequencies in white blood types are found in ethnicities throughout the country, and these varying frequencies in blood type are another reason why interethnic blood transfusion cannot happen; because the differing ethnic groups vary in the different blood types, there will be a low chance of having a certain blood type if it’s rare.

Another reason why blacks donate blood less is due to fear of needles and low iron. Low iron is due to vitamin and mineral deficinecies in diet. Combined with all of the aformentioned variables, this is why blacks get deferred so much. They just don’t donate as much either.

The disparity in differences in blood donation also come down to differences in giving between the races. Whites were seen to be more altruistic than were minorities in the study. This same altruistic behavior leads to more blood donations, but it also leads to the cucking of Europe due to the increase in pathological altruism.

Racial differences in blood donation are due to a whole host of factors, mainly being SCD and other diseases as a barrier for donation, as well as differing blood type frequencies between ethnic/racial groups. Since blacks have higher frequencies of SCD, SCT, and SCA this is another cause for their deferral rate. Being highly sexually active leads to higher disease acquisition, which is another reason less blacks donate blood.  Moreover, blacks’ want to donate will not increase either; racial differences in blood donation and problems will persist to the forseeable future.

Gene Expression By Race

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Since all humans are less than 1 percent different, many people take this to mean that “Race is a social construct“. The stranglehold that race-denying individuals have had on our society for the past fifty years has had huge implications for our society. This egalitarian notion that “we are all the same” together with affirmative action has already begun its devastating effects on our society with this “Blank Slate“, “ghost in the machine” way of thinking.

However, when they engage in this fallacious reasoning, they fail to realize that we are 96 percent genetically similar to chimpanzees. They also don’t know that cats have 90 percent homologous genes with humans; 82% with dogs; 80% with cows; 79% with chimpanzees; 69% with rats and 67% with mice90% of the mouse genome could be lined up with a region on the human genome99% of mouse genes turn out to have analogues in humans. We  share 97.5 percent of our DNA with mice (which is why lab tests get carried out on them). All of this data makes it clear: what causes phenotypic differences between species that are so genetically similar is not how much genetic distance (Fst) is between them, but how those genes that differ are expressed between these populations. Knowing this, it doesn’t seem so crazy now that with less than a 1 percent difference in the genome on average between the races that there are ways to see that race exists genetically. Moreover, the fact that geneticists estimate that there is a difference of 3 million base pairs between two humans on average, shows that there are enough genetic differences between human populations to produce phenotypic differences to be able to differentiate human populations and that since genotype is the cause for the phenotype, due to the physical diversity between human populations that it doesn’t matter how “small” these differences are, but, as mentioned previously, how those differing genes are expressed is the proof that race exists.

Cheung and Speilman collected the gene sequence of a particular white blood cell in 82 Asians and 60 Europeans. They found that the amount of genetic differences was minute, though the two races had differing amounts of gene expression. 25 percent of the overall genes tested showed differing expression between the Asians and Europeans in the sample. It was noticed on one gene that Europeans expressed it at 22 times the strength that Asians did! Since Asians and Europeans split off around 40 kya, I wonder what a study done on Europeans and Africans would show in regards to gene expression strength along with overall differing genetic expression between those two races.

Hicks et al (2013) compared gene expression levels in 4 populations (whites, blacks, Asians and ‘Hispanics’). The gene expression data consisted of 126 whites, 51 ‘Hispanics’, 13 blacks and 8 Asians. They discovered that there were 300 significantly identified genes that showed differing expression in the four populations tested. Some of the genes were: PHF6 (“Mutations affecting the coding region of this gene or the splicing of the transcript have been associated with Borjeson-Forssman-Lehmann syndrome (BFLS), a disorder characterized by mental retardation, epilepsy, hypogonadism, hypometabolism, obesity, swelling of subcutaneous tissue of the face, narrow palpebral fissures, and large ears.”, BRD3 (observed to be implicit in some forms of leukemia, as well as performing cell overlapping functions), CRLF2 (“. . . which control processes such as cell proliferation and development of the hematopoietic system. Rearrangement of this gene with immunoglobulin heavy chain gene (IGH) on chromosome 14, or with P2Y purinoceptor 8 gene (P2RY8) on the same X or Y chromosomes is associated with B-progenitor acute lymphoblastic leukemia (ALL) and Down syndrome ALL.”) and finally RNF135 (known to be involved in protein-protein and protein-DNA interactions). All though this study had an extremely small sample size for Asians and blacks, with further study in the future, we will see bigger sample sizes to better test these predictions.

Analysis of 639 tumor samples (270 black, 369 white), showed that 95 genes were overexpressed involving prostate cancer from blacks relative to whites and 132 were overexpressed in whites relative to Asians. This seems like testosterone is correlated with this as well. Since blacks are twice as likely to get prostate cancer than white men, this shows another reason why there is a disparity in disease acquisition between races: genetic differences, not any allegations of racism people attempt to use.

Still, there are differences in gene expression that account for more disease rate differences between blacks and whites. Huang et al (2011) observed gene expression differences between blacks and whites that lead to atherosclerosis. They discovered 409 differently expressed genes. Genes expressed lower in black Americans also tended to express lower in blacks with lower CAC. Ontological analysis also verified that of the 409 race-associated genes, a significant amount of them “revealed significant enrichment in mobilization of calcium and immune/inflammatory response”.

With differences in testosterone, estradiol and other hormones between the races, as well as looking at disease rates between human populations and studying what genes correlate with what disease, we can better understand human evolution as well as develop new and specific drugs for individuals based on their genotype.

The gene ACTN3 has been linked to athletic performance, specifically sprinting. Those descended from West African populations have it, i.e., Jamaicans and other Caribbean Islanders along with West Africa. 70 percent of those individuals have this gene variant, so, due to this, the all-time record holders in sprinting are all descended from West African populations. This holds true for Europeans as well. This is seen in World’s Strongest Man (WSM) competition wins by country, seeing as the countries with the most wins have majority white populations. A white man has also won the WSM every year since its inception, which is yet another example of gene expression in action.  Whites and Asians have more slow twitch fibers (along with Kenyans) and West African descended blacks have more fast twitch fibers, accounting for these genetic differences which then manifest themselves in our athletic competitions.

Race does exist, and average phenotypic variation is the proof that there is a biological reality to race. The races differ in disease acquisition, as well as muscle fiber typing, which then accounts for disparities in professional championships won along with racial differences in the racial mix of certain sports. As we begin to fully understand the human genome, we will then begin to understand how and why the races differ genetically. The fact that the races differ, on average, on genetic expression shows that there is a reality to what we call “race”. Yes, race is a “social construct”, but it is a social construct of a biological reality. To put it simply, everything is a social construct, and if race doesn’t exist because it’s a social construct then nothing exists, since everything is socially constructed in our minds. But, we know this is not the case. There is a reality, and we use science to test that reality and confirm it with the scientific method.

Strong Evidence, Strong Argument: Race IQ and Adoption

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Commenter Salger brought this article to my attention, Weak Evidence, Weak Argument: Race, IQ, Adoption in which an environmentalist in the B-W IQ debate regurgitates the same old and boring long-refuted studies and the same long-refuted researchers, to attempt to prove that the gap in IQ is purely environmental in nature. I have written on this before, so his reasoning that there is “weak evidence” and “a weak argument on race and IQ” is clearly wrong, as we know the studies and researchers he cites have been disproven. Steele then references another discussion he had on the black-white IQ gap, speaking about people being “uninformed” about a position while arguing it.

My problem with this kind of data is as follows. It isn’t overly useful data in proving much of anything: small sample sizes, lack of effective controls and control groups, abundance of confounding factors, difficulty of replicability, etc.

Since he’s saying that there is a “difficulty of replicability” with IQ tests in transracial adoption studies, he hasn’t read the ones for the hereditarian argument and seeing how they show the biological origin of IQ or he’s just being willfully ignorant. I’ll go with the first one.

We know through other research that racial biases are immense in our society, and this other research tends to be of a higher quality than the adoption (and twin) research. Studies have found various forms of racial biases in a wide variety of areas, from education to policing. It’s well supported that this is systemic and institutional.

There are no racial biases in education nor policing. Police arrest less black offenders than are reported by the NCVS and affirmative action getting blacks ahead shows that the racial bias is for them, not whites. Saying that it’s “systemic and institutional” is a cop out since you know he doesn’t want to even entertain the idea of the hereditarian hypothesis.

It is also well supported that it is often internalized, and typically unconscious. Studies have shown that even minorities show prejudice against other minorities and that this is worse toward those with darker skin. Plus, studies show an internalized racial bias by way of stereotype threat, where the framing of a situation apparently causes the person to in a sense unintentionally sabotage themselves (because of added stress and cognitive load).

Stereotype threat, my favorite. ST can only be replicated in the lab. “Prejudice” doesn’t matter.

For any of these adoption (and twin) studies to be useful, it would require taking into account all the known confounding factors. I don’t know of a single study that does this or even attempts to come close to doing this. It would be ludicrously counterintuitive to presume that these endemic and internalized racial biases weren’t effecting the results.

All this leaves us is to speculate based on weak and probably misleading data. This means interpretation inevitably will follow ideology, as long as we limit ourselves to this data and ignore the larger context of data.

What other confounders could be controlled for that you think had a negative impact on the mean IQ of blacks at adolescence throughout adulthood? “Internalized racial biases” don’t matter since blacks have a higher self-esteeem about their physical attractiveness (Kanazawa, 2011), so “internalized racial biases” (which includes things such as one’s thoughts of one’s self physically) do not matter as they are more confident than are whites. This is due to testosterone, which makes blacks more extroverted than whites who are more extroverted than Asians (Rushton’s Differential-K Theory). If these racial biases were really to manifest themselves to actually sap 15 to 18 (1 to 1.2 SDs) IQ points from blacks, this would show in their self-confidence about themselves. Yet they are more confident, on average, than the other two major races.

All this leaves us is to speculate based on weak and probably misleading data. This means interpretation inevitably will follow ideology, as long as we limit ourselves to this data and ignore the larger context of data.

It’s been discussed ad nasueam. The data attempting to say that blacks are just as intelligent are whites are wrong, as I will show below. The data for the hereditarian hypothesis is not weak, as I have detailed on this blog extensively.

This is highly problematic, for the issues involved are complex. That is just the way reality is. If you want to deal with complex reality, you better find sophisticated ways of dealing with it. On that account, these studies fail in various ways. Still, they give us some possible insights in new directions to take with better research.

IQ has been tested for 100 years, and every time, whites outscore blacks 1 to 1.2 SDs.THAT is reality, not some made up, contorted view of reality for some egalitarian dogma.

In conclusion, my basic point is that all of this demonstrates how weak is the argument being made by hereditarians. As for those who prefer environmental explanations, they don’t need this data at all, since there is already plenty of other data that supports their position. Given what we know, all of the racial disparities, IQ or otherwise, can be explained without recourse to genetic determinism.

My basic point is that all of this demonstrates how weak the argument being made by environmentalists really is. What other data supports the environmentalist position that “they don’t need any data at all”? I’d love to see it. The gap is 80/20 genetics and environment respectively. From averaged correlations on subtests that correlate highest with g, we can say that the gap is around 80 percent genetic and 20 percent environment. Genetic determinism in terms of IQ, save extreme environmental factors, will always beat any environmental model.

This is an obvious statment, for the simple reason that race itself is a social construct, not a scientific fact. Social constructs and their social consequences need social explanations of social causes. The debate of the racial IQ gap is about as meaningful as attempting to compare the average magical intelligence of those sorted into each Hogwarts Houses by the magical sorting hat, if one were to base a society on such strange notions.

Race is not a social construct, but a biological reality. If this debate is “about as meaningful as attempting to compare the average magical intelligence of those sorted into each Hogwarts Houses by the magical sorting hat”, why waste youre time writing this post with tons of misinformation?

Steele cites Block (2005), a “philosopher of science”. Rushton and Jensen (2005, p. 279) say that those (Block) who say that gene-environment interactions are so hard to entangle, why then, do identical twins raised apart show identical signs of intelligence (among many other heritable items)?

Eyferth comes out, of course, which the study has been discredited. To be breif, 20 to 25 percent of the fathers to German women’s children weren’t sub-Saharan African, but French North Africans. 30 percent of blacks got refused in military service in comparison to 3 percent of whites due to rigorous testing for IQ in 70 years ago. One-third of the children were between the ages of 5 and 10 and two-thirds were between the ages of 10 and 13. Heritability estiamtes really begin to increase around puberty as well, so if the Eyferth study would have retested in the following 5 to 8 years to see IQ scores then, the scores would have dropped as that’s when genetic effects start to dominate and environments effects are close to 0.

He then cites Richard Nisbett, who I have discussed here, on the Moore study.

The study conducted by Elise Moore (1986) compared IQ scores of 23 7 to 10-year-old black children raised by middle-class white families and the same number of black children but raised in black families (normal adoption).The findings indicated that traditionally adopted black children raised by black parents had normal IQ scores (85), whereas those black children who were adopted by white families had IQs 1 standard deviation (100) above the black mean. Moore states that multivariate analysis indicates that the behaviors of black and white mothers were different in regards to how the black children were treated. She states that white adoptive mothers reduced stress by joking, laughing, and grinning. Whereas black adoptive mothers reduced stress in less positive ways including coughing, scowling and frowning. She also says that white adoptive mothers gave more positive reinforcement to their adoptive child’s problem solving whereas black adoptive mothers gave less (as I am arguing here, these traits are mostly genetic in origin, driven by IQ). She concludes that the ethnicity of the rearing environment exerts a significant influence on intellectual ability as well as standardized test scores. The sample sizes, however, are extremely small and to infer that the black-white IQ gap is environmental in origin because of a study with a small sample size is intellectually dishonest.

He cites a study of black children in the UK, but this is a case of super-selection, as only the most intelligent Africans emigrate.

Steele then cites this article:

These results make some common sense. We know that intelligent people tend to have intelligent children— but not always. Some studies have also suggested that intensive programs may make a large difference in disadvantaged children’s intelligence quotient (IQ) scores.

Headstart gains are temporary, and there is a fadeout over time.. Arthur Jensen was writing about this 50 years ago. IQ and scholastic achievement gains only last for a few years after Headstart, then genetics starts to take effect as the child grows older.

The article then mentions how European ancestry can be measured in American black populations. However, the studies fail to choose genetic markers with large allele frequencies between Europeans and African Americans (Jensen, 1998, p. 480).

He cites Lee Willerman and his colleagues who found that children with white mothers and black fathers scored higher on IQ tests than children with black mothers and white fathers. This is due to the mother being the best predictor of intelligence of the child. White mothers have a better prenatal environment than do black mothers.

He cites the Wikipedia article on Race and Intelligence, which brings up all the usual, Moore, Tizard (will address below) and Eyferth. The article cites Nisbett (2009) as claiming that Rushton and Jensen’s (2005) claim that the three aforementioned studies did not retest at adulthood, and that “heritability between ages 7 and 17 are quite small, and that consequently this is no reason to disregard Moore’s findings.”

That’s a lie. IQ heritability jumps from 40 percent at age 7 to 82 percent at age 18, with some studies showing heritabilities up to 90 percent.

From the same Wikipedia article:

Another study cited by Rushton & Jensen (2005), and by Nisbett et al. (2012), was Moore (1986) study which found that adopted mixed-race children’s has test scores identical to children with two black parents – receiving no apparent “benefit” from their white ancestry

As shown above, since the mother’s IQ is the best predictor of intelligence and the black-white IQ gap being 80 percent heritable, this means that the amount of white ancestry an American black has, the higher his IQ score will be.

Tizard (1972) observed 2 to 5-year-old black and white children in a nursery setting. The white and black children both had IQs at 102.6 and 106.3 respectively. She found no significant gap in the three groups tested (white, black and West Indian). However, she did note that the single significant difference was in that of non-white children. But that doesn’t mean anything as genetics doesn’t take full effect until around 18, where the IQ gap will be the largest.

Levin and Lynn (1994) disputed Weinberg et al’s conclusion with a hereditarian alternative. That the average IQ and school achievement scores of the black children directly reflected their amount of African ancestry. At both age 7 and 17, the adopted children with 2 black parents had lower average IQs and worse school achievement tests than those with one black parent and one white parent. So right here, in the MTAS, it shows that mixed-race people DO score better than just blacks, which is attributed to their white ancestry.

He then cites a bunch of quotes from Nisbett’s book Intelligence and How to Get It, yet Ruhston and Jensen have refuted this too.

Even with equalized environments these gaps still persist. Your allegations of supposed racism or any other factor you want to bring up for the racial gap in intelligence are unfounded. Environmental differences do not account for the 1.2 SD gap between blacks and whites; environment accounts for, at best, 3 IQ points, so you’ll need to explain what environmental effects cause that kind of IQ drop. In America, blacks don’t have the same environmental factors, i.e., parasitic load, bad nutrition and the high disease rate, so they can hit their phenotypic IQ, plus a bit more due to 22 percent white ancestry on average.  Why you cite discredited studies and researchers to help prove your point is beyond me.

Stereotype Threat is false. Non-replicable studies outside of a lab setting, as well as a meta-analysis that looked at 55 published and unpublished studies that showed that Stereotype Threat is discredited. As shown above, blacks have higher self-confidence than do whites, so this imaginary “stereotype threat” doesn’t affect blacks taking real tests; it only affects them in a lab setting. Steve Sailer has covered stereotype threat as well.

This debate is meaningful, and environmentalist who thinks that they can attempt to explain everything away by environmental factors are being extremely disingenuous. Even giving blacks everything they want in a school system with having one of the highest budgets at 430 million dollars did nothing to close the IQ gap or do anything for integration. Why do we have to deny reality, all for egalitarian dogma based off of philosophical musings then taken by Franz Boas to deny the biological validity of race?

To quote the concluding paragraph in Rushton and Jensen’s refutation to Nisbett:

There is no value in denying reality. While improving opportunities and removing arbitrary barriers is a worthy ethical goal, we must realize that equal opportunity will result in equitable, though unequal outcomes. Expanding on the application of his “default hypothesis” that group differences are based on aggregated individual differences, themselves based on both genetic and environmental contributions, Jensen proposed “two laws of individual differences”—(1) individual differences in learning and performance increase as task complexity increases, and (2) individual differences in performance increase with practice and experience (unless there is a low ceiling on proficiency). We must recognize that the more environmental barriers are ameliorated and everybody’s intellectual performance is improved, the greater will be the relative influence of genetic factors (because the environmental variance is being removed). This means that equal opportunity will result in unequal outcomes, within-families, between-families, and between population groups. The fact that we have learned to live with the first, and to a lesser degree the second, offers some hope we can learn to do so for the third.

Arthur Jensen’s Method of Correlated Vectors

1200 words

Arthur Jensen developed the Method of Correlated Vectors in the 1980s and presents a great explanation and analysis in his 1998 book THE g FACTOR: The Science of Mental AbilitySince IQ is correlated with g, it’s not presumable that the correlation between IQ and physical variable X does not involve g. More sufficient evidence would come from the correlation between X and thefactor’s scores. So Jensen proposed the method of correlated vectors that can determine whether there is a correlation between X (or any other factor other than X) and g. Still, it doesn’t tell us about the numerical correlations between and X, but it can prove that there is a correlation between factor X and and show if there are any other factors independent of that are not correlated with X (pg 143).

When a significant correlation is observed between g factors and factor X using the method of correlated vectors, which Rushton (1999) calls the “Jensen Effect”, it demonstrates that the test’s loading is the best predictor of that correlation with a given variable. Basically, a Jensen Effect arises when there is a correlation between a large number of biological and psychological variables and the factor. Jensen did say in his interviews with Frank Miele for the Book Intelligence, Race, and Genetics: Conversations with Arthur Jensen:

. . . it involves what I have called “Spearman’s hypothesis.” In his book The Abilities of Man, Spearman made a casual observation that the size of the average W hite-Black difference on ten diverse tests was directly related to his subjective im pression of how much each test reflected the g factor— the more g, the greater the Black-White difference. I turned Spearmans offhand conjecture into an empirically testable hypothesis by calculating the average Black-W hite difference for a number of diverse mental tests, obtaining the g loading for each test (that is, how much each test measures g), and ranking the average W-B differences and the g loadings. If the rank order of the Black White differences and the g loadings are pretty much in the same order, Spearman’s hypothesis is confirmed.

I’ve now tested Spearmans hypothesis on 25 large independent samples and it has been confirmed on every one. It has held up for many different test batteries, and at every age level from three-year olds to middle-aged adults. Nor did matching Blacks and Whites for SES diminish the effect. It even shows up in reaction-time tests that have different g loadings but require no cultural knowledge and can be performed in less than one or two seconds by elementary school children. Based on all these studies, the overall probability that Spearmans hypothesis is false is less than one in a billion! (emphasis mine)

There is less than one in a billion chance that Spearman’s hypothesis is wrong. Which brings me to the Black-White IQ gap.

Using the MCV, Dragt (2010) had his prediction confirmed when the psychometric meta-analysis of IQ batteries showed a correlation of .91, based on a large N. Their study on language bias showed a small underestimate of 2.71 points. They conclude that Spearman’s hypothesis is an empirical fact:

Spearman’s hypothesis can now be considered to be an empirical fact. Mean differences in intelligence between ethnic groups can be largely explained by the complexity of the subtests in an IQ battery. So, the present study shows clearly that there is simply no support for cultural bias as an explanation of these ethnic group differences. Apart from subtests with a strong language component, IQ batteries appear to be excellent measures of intelligence for all groups studied in our meta-analysis.

Conclusion: Mean group differences in scores on cognitive-loaded instruments are well documented over time and around the world. A meta-analytic test of Spearman’s hypothesis was carried out. Mean differences in intelligence between groups can be largely explained by cognitive complexity and the present study shows clearly that there is simply no support for cultural bias as an explanation of these group differences. Comparing groups, whether in the US or in Europe, produced highly similar outcomes. 

This proves the hereditarian hypothesis 100 percent. Since the black-white differences on subtests are greater the more the factor is involved (complex tasks, etc), that shows that a magnitude of the black-white difference in IQ is genetic in origin. IQ tests are also not “flawed” or “biased“, as all of the variables that continually get brought up have been controlled for, and genetic confounding wins out every time. Since testing blacks and whites both in America and Europe produces the same outcome, there is a clear genetic component in IQ between blacks and whites.

However, as with most statements and theories by Rushton and Jensen, Jensen’s MCV doesn’t come without any detractors.

Ashton and Lee (2005) state that the MCV produces spurious results as well as non-sources of variance, producing a vector correlation of 0, even when the item is strongly correlated with the factor. However, Nijenhuis et al (2007) state that by performing a psychometric meta-analysis on the MCV would alleviate some of the limitations with MCV. Rushton and Jensen (2010) state:

For example, Dolan et al [59] and Ashton and Lee [60] argue that the method of correlated vectors (MCV) lacks specificity so that Jensen Effects might occur even when differences are not on g, and so more powerful statistics are needed, such as multi-group confirmatory factor analysis (MGCFA). However, this criticism misses the point because there is no absolute claim that the g effects have been proven, only that what is observed is what would have been expected if an underlying g did in fact exist (see Bartholomew [61] for the logic of g inferences). Thus, the onus is on the critics of g to identify whether some other factor is operating

Which the critics cannot do. That is because the factor encompasses all mental abilities and the lower one’s g, the lower one’s overall intelligence. The MVC shows that the black-white IQ difference is largely biological in nature, seeing as the black-white IQ gap is 80 percent genetic and 20 percent environmental (Rushton and Jensen, 2005, p. 279):

. . . is that genetic and cultural factors carry the exact same weight in causing the mean Black–White difference in IQ as they do in causing individual differences in IQ, about 80% genetic–20% environmental by adulthood.

Blacks are ahead of whites at young childhood (around 4 years of age), but at around the age of 5, whites catch up and that’s when the significant racial differences in intelligence are noticed between the races. The fact that we have this debunked “blank slate” notion on the nature of not only race and intelligence but intelligence as a whole in this era of scientific knowledge is mind boggling. Changing all variables to where environments are as close as possible still produces the same occurrence: a clear 1 to 1.2 SD difference between blacks and whites.

Methods like factor analysis and the method of correlated vectors help us to understand the magnitude and heritability of the black-white difference in IQ. Since the differences are the highest on those subtests that are correlated with g, along with correlations from the MCV, with an 80/20 (Pareto Principle in action) genetic/environmental difference in black-white IQ, we can most definitively say that the 1 to 1.2 SD (the equivalent of 15 and 18 IQ points respectively) gap in IQ between whites and blacks is genetic in origin.