Polygenic scores and Black Americans

 

Sunday Morning in Virginia (1877), by Winslow Homer. 

The ability to acquire language may be the mental domain where people of sub-Saharan African descent have undergone the most cognitive evolution since their separation from other humans.

 

 

 

If we look at SNP alleles associated with educational attainment, we see differences between Europeans and sub-Saharan Africans. In a previous post I asked whether the cause was genetic drift or natural selection (Frost 2021).

 

That post brought a comment on Twitter:

 

Or maybe the fact that educational attainment is based on whiteness and familial wealth in the USA but not in Africa? And familial wealth tends to be concentrated in specific closed groupings of people who only breed with each other?

 

I don’t think so. First, the alleles were identified in subjects from the Netherlands Twin Registry, the Finnish Twin Cohort, the Swedish Twin Registry, the Avon Longitudinal Study of Parents and Children, the UK Biobank and 23andme. Of those sources, only 23andme had American subjects.

 

Second, let's suppose that those alleles are incidentally related to educational attainment. Maybe they are just something that wealthy Europeans share with each other through inbreeding, a bit like the Habsburg jaw. Those alleles should therefore be useless for predicting educational attainment in other populations. Are they?

 

Let me answer that question by discussing two recent studies:

 

 

The Guo et al. study

 

Guo et al. (2019) used the same alleles to predict success on a cognitive test (verbal ability) by 8,078 Americans of different ethnic backgrounds. Two polygenic scores were calculated: one based on alleles associated with educational attainment (education PGS) and the other based on alleles associated with IQ (IQ PGS).

 

The polygenic scores significantly correlated with test results for all major ethnic backgrounds, except one:

 

The education PGS was significantly predictive of verbal ability in all estimated models and its coefficients were similar in size except for the black sample in which the coefficient was much smaller. The IQ PGS significantly predicted verbal ability in all samples except the black sample. (Guo et al. 2019)

 

[...] The incremental R2 s or the R2 s of "pure" PGS effects were 1.8%, 0.1%, 1%, 1.8%, 1.7%, and 1% for whites, blacks, Asians, Hispanic whites, the combined sample and the overall sample, respectively.

 

The literature is showing a consistent trend: polygenic scores have much less power to predict cognitive ability in people of sub-Saharan African descent than in people of European or Asian descent. In this case, the polygenic scores were ten to eighteen times worse at predicting verbal ability in Black Americans than they were at predicting verbal ability in White, Asian, and Hispanic White Americans.

 

Why? The reason may be that Eurasians and sub-Saharan Africans have different gene pools. Some alleles for higher cognitive ability are available in one gene pool but not in the other. There is undoubtedly overlap between the two, but not total overlap. Intelligent Nigerians, for instance, may owe their intelligence to alleles that exist only in sub-Saharan Africa.

 

To return to the Twitter comment, it seems clear that polygenic scores are predicting something that correlates with cognitive ability, and that "something" is not an artefact of wealthy people being related to each other and sharing the same genes. It's already a stretch to believe that close family ties are shared by high achievers throughout the United Kingdom, the Netherlands, Sweden, and Finland. Does the same family clique also include high achievers of Asian American origin? 

 

 

The Rabinowitz et al. study

 

Rabinowitz et al. (2019) used an education PGS to predict cognitive ability in Black American participants, specifically three cohorts from first grade to young adulthood (at which point their DNA was collected and analyzed).

 

The results? The PGS significantly correlated with pursuit of postsecondary education. The correlation was weak or insignificant, however, for performance on school tests. The PGS did not predict performance on a standardized reading test for any of the three cohorts, and it predicted performance on a standardized math test for only one of them. In addition, the PGS negatively correlated with having a criminal record (but only in the male subjects).

 

A problem here may be the young age of the participants. Cognitive ability seems to become less malleable and more hardwired with age. We can help children do better on IQ tests, but the improvement tends to disappear by adulthood (Frost 2008). Consequently, academic success in childhood may be too clouded by environmental factors to show a significant correlation with genetic factors.

 

On the other hand, the PGS did predict some things better than others. It predicted general academic success (pursuit of postsecondary education) and compliance with rules (absence of a criminal record). For actual school tests, it had some power to predict success on the math test but none at all on the reading test. The ability to acquire language may be the mental domain where people of sub-Saharan African descent have undergone the most cognitive evolution since their separation from other humans. The PGS cannot predict superior reading ability among Black Americans because too many of the relevant alleles are exclusive to the sub-Saharan African gene pool and remain to be identified by scientific studies.

 

The take-home message? At present, we can create polygenic scores that provide a rough idea of cognitive ability in people of sub-Saharan African descent. To get more than a rough idea, we need to identify the relevant alleles specific to that population.

 

 

References

 

Frost, P. (2008). IQ: Interaction between race and age. The Unz Review, May 20

https://www.unz.com/pfrost/iq-interaction-between-race-and-age/?highlight=Minnesota

 

Frost, P. (2021). The mismeasure of genetic differentiation. Evo and Proud, April 13

http://evoandproud.blogspot.com/2021/04/the-mismeasure-of-genetic.html

 

Guo, G., Lin, M.J., and K.M. Harris. (2019). Socioeconomic and Genomic Roots of Verbal Ability. bioRxiv, 544411.

https://www.biorxiv.org/content/10.1101/544411v1

 

Rabinowitz, J.A., S.I.C. Kuo, W. Felder, R.J. Musci, A. Bettencourt, K. Benke, ... and A. Kouzis. (2019). Associations between an educational attainment polygenic score with educational attainment in an African American sample. Genes, Brain and Behavior, e12558.

https://pubmed.ncbi.nlm.nih.gov/30793481/

The mismeasure of genetic differentiation

 

Red Tree, Piet Mondrian (1908-10)

If we look at SNP alleles associated with educational attainment, we see differences between Europeans and sub-Saharan Africans. Is genetic drift the cause? Or natural selection?

 

 

IQ has long been the yardstick of cognitive ability. As such, it describes phenotype, not genotype: it measures how your inborn potential has developed in your environment. Genotype is the inborn component of IQ. It can be inferred from twin studies, family studies, and adoption studies, but those approaches are indirect and far from perfect.

 

To measure genotype directly, we need to identify the alleles that affect the development of cognitive ability. We also need to measure the size of each allele’s effect. Recently, much progress has been made. By using genome-wide association studies (GWAS), researchers have identified many alleles that are associated with educational attainment (EA). EA is not quite the same as IQ—it also includes things like sitting still in class and brownnosing the teacher—but it's a good approximation.

 

In the most recent study of this sort, Lee et al. (2018) identified 1,271 single-nucleotide polymorphisms (SNPs) that are significantly associated with high EA in a sample of over one million people of European ancestry. Together, the SNPs can explain 11-13% of the variance in EA among individuals. This new yardstick is called the "polygenic score."

 

The polygenic score is more accurate for populations than for individuals. If we compare the mean polygenic score of a population and its mean IQ, the correlation is 90% (Piffer 2019). This high correlation is due to the logic of sampling: to estimate the mean cognitive ability of a population, we don't have to identify all of the relevant SNPs, just a large enough sample.

 

Like mean IQ, the mean polygenic score differs among human populations. It seems to have increased during the northward spread of modern humans out of Africa and into the temperate zone of Europe and Asia, with East Asians having the highest scores. This geographic pattern is in line with IQ data. The mean polygenic score is also very high among Ashkenazi Jews and Finns, again in line with IQ data (Piffer 2019).

 

 

Kevin Bird’s paper

 

The above findings have been disputed by the American researcher Kevin Bird in a recent paper. Although Europeans and sub-Saharan Africans have different alleles at genes associated with educational attainment, he argues that these differences correspond to small differences in cognitive ability. In fact, they are more consistent with genetic drift than with natural selection.

 

To prove his argument, he performed two analyses of the data: an Fst and a test for polygenic selection. In my opinion, both analyses have serious problems.

 

The Fst

 

This is the most common measure of genetic differentiation. If the Fst is low, differentiation is trivial and consistent with genetic drift. If it is high, differentiation is significant and consistent with natural selection.

 

For SNPs associated with EA, Kevin Bird reports an Fst of 0.111. Is that low or high? When Sewall Wright (1978, pp. 82-85) created this measure, he defined four categories of differentiation:

 

0 to 0.05 - little genetic differentiation

0.05 to 0.15 - moderate genetic differentiation

0.15 to 0.25 - great genetic differentiation

0.25 to 1 - very great genetic differentiation

 

Those categories are widely cited in the literature. A search in Google Scholar for "moderate genetic differentiation" and "0.05 - 0.15" shows over two hundred papers.

 

So does an Fst of 0.111 mean moderate genetic differentiation? Not according to Kevin Bird, who sees nothing at all below a benchmark of 0.118. That benchmark may be valid, but it cannot be easily verified and does not appear elsewhere in the literature. Nor does Kevin explain why it is better than the ones put forward by Sewall Wright. In fact, he makes no reference to them.

 

One may also question the Fst of 0.111. For the data source, the reader is referred to Lee et al. (2018), but that study was done only with European subjects. Moreover, Kevin Bird used 1,259 SNPs to calculate that Fst, even though he found only 685 SNPs that had data on both Africans and Europeans.

 

The Fst of 0.111 seems to be the diversification of those SNPs in Europeans. That value is what would be expected, but it says nothing about diversification between Europeans and sub-Saharan Africans.

 

The polygenic selection analysis

 

The other analysis is more on subject. Kevin Bird compared European data with African data as follows:

 

1. First, he looked through the 1000 Genomes Project for SNP data on Europeans and sub-Saharan Africans. He found data on five European-descended populations (Utah residents, Tuscans, Finns, British, Iberians) and five African populations (Yoruba, Luhya, Gambians, Mende, Esan). The two datasets had information on 685 of the 1,271 SNPs associated with educational attainment.

 

2. For each SNP, he noted the allele frequencies in Europeans and the allele frequencies in sub-Saharan Africans.

 

3. He calculated the differences in allele frequencies between the two groups. He then weighted the differences for the allele's effect size (its estimated positive or negative effect on educational attainment). For each allele, he used two different estimates of effect size: one from between-family data and the other from within-family data.

 

4. Alongside this list of weighted alleles, he created a second list to simulate genetic drift by randomly flipping the sign of effect size for 10,000 permutations.

 

5. When effect size was calculated from between-family data, the two lists clearly differed from each other. When it was calculated from within-family data, the overall difference was much smaller and easily explained by genetic drift.

 

Bird (2021) prefers the second dataset to the first, whereas Piffer (2019) prefers the first. Who is right? All things being equal, data should come from within families. There is less statistical noise because siblings have similar upbringings. With less noise, group differences can more easily be identified.

 

Yet, here, we have the opposite. We see a significant difference between Europeans and Africans in the between-family data, but not in the within-family data. Why? The reason is that the between-family data came from over a million subjects whereas the within-family data came from 20,000 sibling pairs. Being smaller, the second dataset had a lot more noise. Sure, there should have been less noise, all things being equal. But some things weren't.

 

 

Doing the comparison again but better

 

I suspect Kevin Bird still prefers within-family data. Fine. Let's repeat the comparison with a much larger sample of sibling pairs. There would then be less noise and probably a significant difference between African and European alleles in their effect on educational attainment. Kevin seems to anticipate this eventuality:

 

While the results presented here are more consistent with neutral evolution rather than divergent natural selection, it is not possible to rule out that data sets with more power could present different results. Additionally, although within-family effect sizes are recommended over between-family effect sizes, if the within-family effect sizes are re-estimated for SNPs ascertained by a between-family GWAS, there is still likely to be some level of confounding from population structure. (Bird 2021, p. 7)

 

He elaborates on the last point:

 

[...] the [polygenic] scores might be biased by a variety of factors, including the nonrandom ways that society is geographically structured [...]. For instance, Black people in the US, for reasons unrelated to genetics, live in areas with poorer air quality and more exposure to environmental toxins (Bird 2021, p. 8)

 

Yet, as he notes further on, these SNP alleles were identified only in European subjects, and their effects on educational attainment were estimated only from European data. So how could different alleles among Europeans be spuriously associated with differences in educational attainment among Europeans because of socioeconomic deprivation among Black Americans? Where and when do the latter come into this presumably spurious association?

 

Kevin Bird is right to point out that the allele effects were calculated from European data and may be less applicable to people of other origins. In fact, there is growing evidence that the genetic architecture of cognition is different in sub-Saharan Africans (Frost 2019). By ignoring that factor, however, we introduce even more noise into the data and muddle even more any differences that may exist between Africans and Europeans. The data may indeed be of low quality, but that shortcoming would, if anything, obscure group differences. Again, Kevin is making a coherent point within an incoherent argument.

 

 

Other ways?

 

There are other ways to distinguish between genetic drift and natural selection. One way is to measure the ratio of nonsynonymous alleles to synonymous alleles. If a trait has little functional value and is thus vulnerable to genetic drift, nonsynonymous alleles will tend to proliferate and become as numerous as synonymous alleles (Tomoko 1995). Of course, if nonsynonymous alleles greatly outnumber synonymous alleles, there may be natural selection for diversity (Rana et al. 1999).

 

An SNP, by its very nature, has alleles that differ from each other by only one base substitution, and this fact limits our ability to distinguish between genetic drift and natural selection. It would thus be interesting to identify genetic polymorphisms that are associated with educational attainment but have several nucleotides.

 

If such a polymorphism is undergoing genetic drift, the most frequent alleles will be the ancestral allele and those that differ from it by one base substitution. The less frequent ones will be those that differ by two or more base substitutions. In short, the frequency of an allele will be inversely related to the number of base substitutions that separate it from the ancestral allele.

 

The picture is different with natural selection. The most frequent alleles will not necessarily be the ones that differ the least from the ancestral allele. If allele frequency is graphed as a function of base substitutions, the result will not be a smoothly decreasing exponential curve. The most successful allele may differ from the ancestral one by several base substitutions.

 

 

References

 

Bird, K.A. (2021). No support for the hereditarian hypothesis of the Black-White achievement gap using polygenic scores and tests for divergent selection. American Journal of Physical Anthropology. Feb. 1-12, DOI: 10.1002/ajpa.24216.

https://www.gwern.net/docs/genetics/selection/2021-bird.pdf

 

Frost, P. (2019). Differences in the genetic architecture of cognition? Evo and Proud, September 25

https://evoandproud.blogspot.com/2019/09/differences-in-genetic-architecture-of.html

 

Lee, J. J., Wedow, R., Okbay, A., Kong, E., Maghzian, O., Zacher, et al. (2018). Gene discovery and polygenic prediction from a genome-wide association study of educational attainment in 1.1 million individuals. Nature Genetics 50(8): 1112-1121.

https://academicworks.medicine.hofstra.edu/cgi/viewcontent.cgi?article=5038&context=articles  

 

Tomoko, O. (1995). Synonymous and nonsynonymous substitutions in mammalian genes and the nearly neutral theory. Journal of Molecular Evolution 40 (1): 56-63

 

Piffer, D. (2019). Evidence for Recent Polygenic Selection on Educational Attainment and Intelligence Inferred from Gwas Hits: A Replication of Previous Findings Using Recent Data. Psych 1(1): 55-75. https://doi.org/10.3390/psych1010005   

 

Rana, B.K., D. Hewett-Emmett, L. Jin, B.H.J. Chang, N. Sambuughin, M. Lin, et al. (1999). High polymorphism at the human melanocortin 1 receptor locus. Genetics 151(4): 1547-1557.

https://www.researchgate.net/profile/M-Ramsay/publication/13190390_High_Polymorphism_at_the_Human_Melanocortin_1_Receptor_Locus/links/596b13eeaca2728ca6821b9e/High-Polymorphism-at-the-Human-Melanocortin-1-Receptor-Locus.pdf

 

Wright S. (1978). Evolution and Genetics of Populations, Volume 4. University of Chicago, Chicago, IL.

No, blacks aren't all alike. Who said they were?

 

In 1915, Paul Robeson became the third African American ever enrolled at Rutgers College, being one of four students selected for its Cap and Skull honor society. His father was of Igbo descent (Wikicommons)

 

Chanda Chisala has written another piece on IQ and African immigrants to the UK:

One of the biggest problems I had with the commenters were readers who apparently were only exposed to the statistical concept of Regression to the Mean from outside the IQ debate. [...]. The problem is not that the black immigrant children were not regressing to the point of equaling their source population mean IQ (that's also not what hereditarians predict either), but that they were clearly not even moving (or being pulled) towards that extremely low IQ, as hereditarians predict.

The correct term is not "regression to the mean." It's "non-inheritance of acquired characteristics." In other words, each person has a single genotype and a range of possible phenotypes. A culture can push its members to either limit of this range, thus creating a phenotype unlike that of other people with the same genetic endowment. But this phenotype has to be recreated with each succeeding generation. For instance, there used to be a Chinese custom of binding a girl's foot to make it four inches long and of limited use for walking. When the custom was outlawed, the next generation of women had normal feet. The phenotype bounced back to its initial form, so to speak, much like an elastic band when you stop stretching it (see note 1).

Regression to the mean is something else. It happens because of genetic change. For instance, a man with above-average IQ will likely marry a woman with above-average IQ. But only part of their above-averageness is genetic. The rest is due to favorable circumstances. Or simply luck. So their children's IQ will likely be a bit closer to the mean of the overall population. That second generation will in turn marry people with similar IQs. And their children will likewise be closer still to the population mean. Eventually, several generations later, the descendants of that original couple will have a mean IQ that matches the population mean.

That's regression to the mean. It's a multigenerational genetic change. It's not what happens when genes stay constant and culture changes.

Chanda is really talking about what happens when a culture stops pushing people to excel. The phenotype reverts to its usual state and the pressure to excel comes only from within. This is a legitimate argument, and it may have great explanatory value. When people from certain cultures move to Western countries, the second and third generations do a lot worse than the first generation over many indicators—academic achievement, crime rates, family stability, etc. This is a frequent outcome when people move from an environment where behavior is tightly controlled by family and community to one where behavior is much more self-controlled.

Such social atomization is less toxic for people of Northwest European descent because they have adapted to it over a longer time. For at least the past millennium, they have had weaker kinship ties and stronger tendencies toward individualism than any other human population. This cultural environment has favored individuals who rely less on external means of behavior control and more on internal means, specifically guilt proneness and affective empathy (Frost, 2014).

But that isn't Chanda's argument. That's the argument he attributes to something called "the HBD position." In reality, there are at least three HBD positions:

1. African immigrants to the UK perform better than whites academically because they are a select group, either because they have elite backgrounds or because they tend to be more motivated than the people who stay behind.

2. African immigrants perform better than whites academically, but this academic performance is weakly linked to the heritable component of IQ, especially in modern Britain. Teachers tend to "over-reward" black students who satisfy basic requirements (regular attendance, assignments turned in on time, non-disruptive behavior, etc.). African parents also invest in private tutoring to improve exam results.

3. Most African immigrants perform worse than whites academically. Only certain African groups excel, notably the Igbo of Nigeria. Igbo excellence is due to their specific evolutionary history and cannot be generalized to all sub-Saharan Africans.

Are African immigrants better than the Africans left behind?

Chanda attacks the first argument, saying that the average African immigrant is very average:

I actually know that the average African immigrants to the UK from any nation or tribe are not from the African elite class, economically or intellectually (even if there is a small segment from the super-professional class)

He also points to the example of African American families. The children of middle-class and even upper-class African Americans do worse on IQ tests than the children of lower-class Euro-American families. So even if you select from the black elite, the next generation will still underperform whites.

One could counter that the African American middle class largely works for the government. In Africa, the middle class is more likely to be self-made men and women. Also, a selection effect may exist despite the averageness of most African immigrants to the UK. Even if most are average, it may be that fewer are below-average. Below a certain level of ability, many Africans may not bother to emigrate.

Fuerst (2014) has studied this question and found that black immigrants to the U.S. have a mean IQ that is one third of a standard deviation above the mean IQ of their home countries. So there is a selection effect. But it seems too weak to explain the difference in IQ—more than one standard deviation and possibly two—between African immigrants to the UK and Africans back home, unless one assumes that migration to the UK is a lot more selective than migration to the US.

What does the GCSE actually measure?

We now come to the second explanation. It is assumed in this debate that the GCSE (General Certificate of Secondary Education) is a good proxy for IQ, which in turn is a proxy for the heritable component of intelligence. Is this true? Or does the GCSE largely measure something that is culturally acquired rather than heritable? Perhaps something as simple as showing up for class, doing one's assignments, or having a private tutor. This point is raised by one commenter:

[...] black Africans in London, even if poor and living in social housing, hire private tutors for their children. White British do not, especially the working class. This much better explains the GCSE results, a very tuition friendly test [...]

Furthermore, many African immigrants may be targeting those exams they can do best on and avoiding those they are less sure about:

[...] one needs to know how many children from each racial group take the exams. For example, the pass rate for Higher Mathematics is very high, not because the exams are easy, but because they are hard, and frighten off most applicants.

Interestingly, Chanda replies to this GCSE skepticism by pointing out that the same "Nigerians" (Igbos) who do well on the GCSE also do well in Nigeria:

For example, the subgroups within the Nigerian group that are the best in Nigeria or even in the US etc are also the best on the GCSEs. Also, the Traveller white (or whatever precise race) groups are placed by the GCSEs exactly where you would expect to find them.

The Igbo factor

This brings us to the third explanation. It's the one I favor, although the other two probably play a role. African excellence in the UK seems largely driven by a single high-performing people: the Igbo of southeastern Nigeria. Let's begin with the example of Harold Ekeh, whom Chanda describes in glowing terms:

Harold Ekeh showing off his acceptance letters to all 8 Ivy League Schools. He was born in Nigeria and migrated with his parents at age 8.

Ekeh is an Igbo name, and the Igbo (formerly known as Ibo) have a long history of academic success within Nigeria (Frost, 2015). Chanda himself referred to this success in his first article:

The superior Igbo achievement on GCSEs is not new and has been noted in studies that came before the recent media discovery of African performance. A 2007 report on "case study" model schools in Lambeth also included a rare disclosure of specified Igbo performance (recorded as Ibo in the table below) and it confirms that Igbos have been performing exceptionally well for a long time (5 + A*-C GCSEs); in fact, it is difficult to find a time when they ever performed below British whites. (Chisala, 2015a)

This superior achievement was widely known in Nigeria by the time of independence:

All over Nigeria, Ibos filled urban jobs at every level far out of proportion to their numbers, as laborers and domestic servants, as bureaucrats, corporate managers, and technicians. Two-thirds of the senior jobs in the Nigerian Railway Corporation were held by Ibos. Three-quarters of Nigeria's diplomats came from the Eastern Region. So did almost half of the 4,500 students graduating from Nigerian universities in 1966. The Ibos became known as the "Jews of Africa," despised—and envied—for their achievements and acquisitiveness. (Baker, 1980)

The term "Jews of Africa" recurs often in the literature. Henry Kissinger used it back in the 1960s:

The Ibos are the wandering Jews of West Africa — gifted, aggressive, Westernized; at best envied and resented, but mostly despised by the mass of their neighbors in the Federation. (Kissinger, 1969) 

To what degree is African success Igbo success? If we go back to Chanda's first article, we see that high African achievers are overwhelmingly "Nigerians" (Chisala, 2015a). This is evident in a chart that lists mean % difference from the mean English GCSE score in 2010-2011 by ethnicity:

Nigerian: +21.8

Ghanaian: +5.5
Sierra Leone: +1.4
Somali: -23.7
Congolese: -35.3

Clearly, high academic achievement is due to something that is very much present in Nigeria, a little bit in Ghana, and not at all in Somalia and Congo. Could this something be the Igbo? The Igbo make up 18% of Nigeria's population and form a large diaspora elsewhere in West Africa and farther afield. In fact, they seem to be disproportionately represented in overseas Nigerian communities, making up most of the Nigerian community in Japan and a large portion of China's Nigerian community (Wikipedia, 2015). Statistics are unfortunately lacking for the UK.

Conclusion

What happens when we remove Igbo students from the GCSE results? How well do the other Africans do? To some degree, Chanda answered that question in his first article. African excellence seems to be overwhelmingly Igbo excellence.

So why doesn't he speak of Igbo excellence? Probably because he assumes that all sub-Saharan Africans are fundamentally the same. Or maybe he assumes that all humans are fundamentally the same. Both assumptions are wrong, and neither can be construed as an "HBD position." 

We are all genetically different, even within our own families. So why the surprise that different African peoples are ... different? The Igbo have for a long time specialized in a trading lifestyle that favors a certain mental toolkit: future time orientation; numeracy, and abstract reasoning. This is gene-culture coevolution. When circumstances push people to excel in a certain way, there will be selection for people who can naturally excel in that way, without the prodding of circumstances. And it doesn't take eons of time for such evolution to work.

 

Will we hear more about the Igbo in this debate? Probably not. There is a strong desire, especially in the United Kingdom, to show that blacks are converging toward white norms of behavior, including academic performance. There is indeed some convergence, but almost all of it can be traced to the growing numbers of high-performing "Nigerians" (Igbos) and the growing numbers of biracial children (the census now has a mixed-race category, but most biracial people still self-identify as "black"). In the UK, 55% of Black Caribbean men and 40% of Black Caribbean women have a partner from another ethnic background. It's very likely that half of all "black" children in the UK are at least half-white by ancestry (Platt, 2009, p. 7).

Nor is it likely that we'll hear more about the Igbo from Chanda. As he sees it, the debate should be over. The academic excellence of Igbo students proves that the black/white IQ gap in the U.S. cannot have a genetic basis:

[It is not] a function of global racial evolution (Sub-Saharan African genes versus European genes), as most hereditarians believe, especially those who identify with the Human Biodiversity or HBD intellectual movement (generally known as "scientific racism" in academic circles, but we are avoiding such unkind terms).

Thank you, Chanda, for avoiding unkind terms. Well, I know a bit about HBD. The term was coined by Steve Sailer in the late 1990s for an email discussion group that included myself and various academics who may or may not want their names disclosed. It's hard to generalize but we were all influenced by findings that genetic evolution didn’t slow down as cultural evolution speeded up in our species. In fact, the two seemed to feed into each other. This is why genetic evolution accelerated over 100-fold about 10,000 years ago when humans began to abandon hunting and gathering for farming, which in turn led to ever more diverse societies. Our ancestors thus adapted much more to their cultural environments than to their natural environments. These findings were already circulating within our discussion group before being written up in a paper by Hawks et al. (2007) and later in a book by Greg Cochran and Henry Harpending (2009).

Yes, previously it was thought that genetic evolution slowed to a crawl with the advent of culture. Therefore, groups like the Igbo couldn't possibly differ genetically from other sub-Saharan Africans, at least not for anything culture-related. But that kind of thinking wasn't HBD or even racialist. It was simply the old anthropological narrative, and it's still accepted by many anthropologists, most of whom aren't "scientific racists."

Oh sorry, I forgot we promised to avoid that term.

Note

(1) Of course, if the cultural pressure is maintained long enough, there may be selection for individuals who naturally produce the new phenotype—with no prodding and pushing. Let’s suppose that foot binding had never been outlawed in China. Through chance mutations, some Chinese women might be born with tiny feet, and their descendants would become more and more numerous because of their better life prospects. So what began as a new phenotype could end up becoming a new genotype. Culture pushes the limits of phenotypic plasticity, and then favors genotypes that don't have to be pushed. That's gene-culture coevolution.

References 

Baker, P.H. (1980). Lurching toward unity, The Wilson Quarterly, 4, 70-80

http://archive.wilsonquarterly.com/sites/default/files/articles/WQ_VOL4_W_1980_Article_01_2.pdf 

Chisala, C. (2015b). Closing the Black-White IQ gap debate. Part I, The Unz Review, October 5

http://www.unz.com/article/closing-the-black-white-iq-gap-debate-part-i/ 

Chisala, C. (2015a). The IQ gap is no longer a black and white issue, The Unz Review, June 25

http://www.unz.com/article/the-iq-gap-is-no-longer-a-black-and-white-issue/

Cochran, G. and H. Harpending. (2009). The 10,000 Year Explosion: How Civilizations Accelerated Human Evolution, Basic Books, New York. 

Frost, P. (2015). The Jews of West Africa? Evo and Proud, July 4

http://evoandproud.blogspot.ca/2015/07/the-jews-of-west-africa.html 

Frost, P. (2014). How universal is empathy? Evo and Proud, June 28

http://evoandproud.blogspot.ca/2014/06/how-universal-is-empathy.html 

Fuerst, J. (2014). Ethnic/race differences in aptitude by generation in the United States: An exploratory meta-analysis, June 29, Open Differential Psychology

http://openpsych.net/ODP/wp-content/uploads/2014/07/U.S.-Ethnic-Race-Differences-in-Aptitude-by-Generation-An-Exploratory-Meta-analysis-John-Fuerst-2014-07262014FINAL.pdf 

Hawks, J., E.T. Wang, G.M. Cochran, H.C. Harpending, and R.K. Moyzis. (2007). Recent acceleration of human adaptive evolution, Proceedings of the National Academy of Sciences (USA), 104, 20753-20758.

http://harpending.humanevo.utah.edu/Documents/accel_pnas_submit.pdf 

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A genetic marker for empathy?

 

The Starry Night, Vincent van Gogh (1853-1890). The more you empathize with the world, the more you feel its joy and pain, but too much can lead to overload.

 

One of my interests is affective empathy, the involuntary desire not only to understand another person's emotional state but also to make it one's own—in short, to feel the pain and joy of other people. This mental trait has a heritability of 68% and is normally distributed along a bell curve within any one population (Chakrabarti and Baron-Cohen, 2013). Does it also vary statistically among human populations? This is possible. Different cultures give varying importance to affective empathy, and humans have adapted much more to their cultural environments than to their natural environments. This is why human genetic evolution accelerated over 100-fold about 10,000 years ago when humans began to abandon hunting and gathering for farming, which in turn led to increasingly diverse forms of social organization (Hawks et al., 2007).

I have argued previously that Europeans to the north and west of the Hajnal Line (an imaginary line running from Trieste to Saint-Petersburg) have adapted to a cultural environment of weaker kinship and, conversely, greater individualism. In such an environment, the reciprocal obligations of kinship are insufficient to ensure compliance with social rules. This isn’t a new situation. Weak kinship is inherent to the Western European Marriage Pattern, which goes back to at least the 12th century, if not earlier.

This cultural environment has selected for a package of mental adaptations:

- capacity to internalize punishment for disobedience of social rules (guilt proneness)

- capacity to simulate and then transfer to oneself the emotional states of people who may be affected by rule-breaking (affective empathy)

- desire to seek out and expel rule-breakers from the moral community (ideological intolerance).

The above mental package has enabled Northwest Europeans to free themselves from the limitations of kinship and organize their societies along other lines, notably the market economy, the modern State, and political ideology. They have thus managed to meet the threefold challenge of creating larger societies, ensuring greater compliance with social rules, and making possible a higher level of personal autonomy.

So much for the theory. What direct evidence do we have that affective empathy is stronger on average in Northwest Europeans? We know that a higher capacity for affective empathy is associated with a larger amygdala, which seems to control our response to facial expressions of fear and other signs of emotional distress (Marsh et al., 2014). Two studies, one American and one English, have found that "conservatives" tend to have a larger right amygdala (Kanai et al., 2011; Schreiber et al., 2013). In both cases, my hunch is that "conservatives" are disproportionately drawn from populations that have, on average, a higher capacity for affective empathy.

But testing this kind of hunch would require a large-scale comparative study, which in turn would require cutting up a lot of cadavers or doing a lot of MRIs. It would be nicer to have a genetic marker that shows up on a simple test. It would also be cheaper.

We may now have that marker: a deletion variant of the ADRA2b gene. Carriers remember emotionally arousing images more vividly and for a longer time, and they also show more activation of the amygdala when viewing such images (Todd and Anderson, 2009; Todd et al., 2015). This is not to say that the ADRA2b deletion variant is the sole reason or even the major reason why some people have increased capacity for affective empathy. As with intelligence, an increase in capacity seems to have come about through changes of small effect at many genes.

Nor can we say that "emotional memory" is equivalent to affective empathy. Instead, it seems to be one component, albeit a critical one: the capacity to imagine an emotional state based on visual information (a picture of a person's face, a puppy dog, etc.) and then keep it as part of one's current emotional experience. Emotional memory may be upstream to affective empathy, being perhaps closer to cognitive empathy—the ability to imagine how another person feels without involuntarily making that feeling one's own.

Does its incidence differ among human populations?

This variant was first studied in the United States. Small et al. (2001) found a higher incidence in Caucasians (31%) than in African Americans (12%). Belfer et al. (2005) likewise found a higher incidence in Caucasians (37%) than in African Americans (21%).

In a press release, the authors of the latest study noted that this variant is not equally common in all humans:

The ADRA2b deletion variant appears in varying degrees across different ethnicities. Although roughly 50 per cent of the Caucasian population studied by these researchers in Canada carry the genetic variation, it has been found to be prevalent in other ethnicities. For example, one study found that just 10 per cent of Rwandans carried the ADRA2b gene variant. (UBC News, 2015)

Curiously, its incidence seems higher among “Canadian Caucasians” (50%) than among "American Caucasians” (31-37%). This may reflect differences in participant recruitment or in ethnic mix between the two countries. Indeed, the "Caucasian" category may prove to be problematic because it includes people from both sides of the Hajnal Line. If the average incidence is 31% to 50%, there may be populations that score much higher.

I have found only three studies on specific European ethnicities. The first study found an incidence of 50% in Swiss participants (de Quervain, 2007). The second one found an incidence of 56% in Dutch participants (Cousijn et al., 2010). The third one had two groups of participants: Israeli Holocaust survivors and a control group of European-born Israelis who had emigrated with their parents to the British Mandate of Palestine. The incidence was 48% in the Holocaust survivors and 63% in the controls (Fridman et al., 2012).

From East Asia, a study on Chinese participants reported an incidence of 68% (Zhang et al., 2005). This is surprising because Chinese seem less likely to distinguish between cognitive empathy and affective empathy (Siu and Shek,2005). Japanese participants had an incidence of 56% in one study (Suzuki et al., 2003) and 71% in another (Ishii et al., 2015). Among the Shors, a Turkic people of Siberia, the incidence was 73%. Curiously, the incidence was higher in men (79%) than in women (69%). It may be that male non-carriers had a higher death rate, since the incidence increased with age (Mulerova et al., 2015).

Conclusion

The picture is still incomplete but the incidence of the ADRA2b deletion variant seems to range from a low of 10% in some sub-Saharan African groups to a high of 50-65% in some European groups and 55-75% in some East Asian groups. Given the high values for East Asians, I suspect this variant is not a marker for affective empathy per se but rather for empathy in general (cognitive and affective).

It may be significant that a high incidence was found among the Shors, who were largely hunter-gatherers until recent times. This suggests that empathy reached high levels in Eurasia long before the advent of complex societies, or even farming. The example of the Shors also suggests that non-carriers of the deletion variant suffer from higher mortality—a somewhat surprising finding, given the evidence that carriers have a higher risk of heart disease.

More research is needed on how this variant interacts with variants at other genes. For instance, it has been found that people with at least one copy of the short allele of 5-HTTLPR tend to be too sensitive to negative emotional information. This effect seems to be attenuated by the deletion variant of ADRA2b, which either keeps one from dwelling too much on a bad emotional experience or helps one anticipate and prevent repeat experiences (Naudts et al., 2012). Nonetheless, too much affective empathy may lead to an overload where one ends up helping others to the detriment of oneself and one’s family and kin.

References 

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