Lewontin's legacy

 

Lewontin assumed that genetic diversity between populations is qualitatively similar to genetic diversity within populations. So comparing the two would be like comparing apples with apples. He was wrong. The second kind of diversity is less functionally significant.

 

 

The geneticist Richard Lewontin died last Sunday at the age of 92. He became prominent during the 1970s, particularly through his 1972 paper "The Apportionment of Human Diversity." Using data from blood groups, serum proteins, and red blood cell enzymes, he found far more genetic diversity within human populations than between them:

 

The results are quite remarkable. The mean proportion of the total species diversity that is contained within populations is 85.4%, with a maximum of 99.7% for the Xm gene, and a minimum of 63.6% for Duffy. Less than 15% of all human genetic diversity is accounted for by differences between human groups!

 

It is clear that our perception of relatively large differences between human races and subgroups, as compared to the variation within these groups, is indeed a biased perception and that, based on randomly chosen genetic differences, human races and populations are remarkably similar to each other, with the largest part by far of human variation being accounted for by the differences between individuals.

 

His reasoning seems sound. It ignores, however, two aspects of population genetics:

 

1. Genetic differences between populations are qualitatively different from genetic differences within populations. A population boundary is usually a boundary between different environments, either natural environments or cultural environments. It is thus a boundary between different pressures of natural selection and, hence differences in adaptation. An allele may work just fine on one side of the boundary, but not so well on the other side. Conversely, genetic diversity within a population is less meaningful because the end result tends to be the same. Everyone is adapting to the same environment. Genetic differences are less likely to produce real functional differences.

 

2. Genetic differences vary considerably in their functional significance, with the overwhelming majority having little or none. Many of these differences are found in junk DNA.

 

Lewontin discovered the obvious. Most genetic differences have little or no functional significance, and such differences account for most of the diversity within human populations. The more a genetic difference has real consequences, the less likely it will be found within a population because that is where the pressures of selection are uniform. It will more likely be found at a population boundary where the pressures of selection are different.

 

We see this, for example, in dog breeds. Although they differ considerably in anatomy and behavior, they are barely discernable in the genetic data. There is much more diversity within breeds than between them:

 

... genetic and biochemical methods ... have shown domestic dogs to be virtually identical in many respects to other members of the genus. ... Greater mtDNA differences appeared within the single breeds of Doberman pinscher or poodle than between dogs and wolves. ... there is less mtDNA difference between dogs, wolves, and coyotes than there is between the various ethnic groups of human beings, which are recognized as a single species. (Coppinger & Schneider 1995)

 

Well, dog breeds have been created through human-directed selection. What about subspecies that have arisen through natural selection? We see the same fuzziness, not only between subspecies but also between many sibling species that are anatomically distinct. In the deer family, genetic diversity is greater within some species than between some genera (Cronin 1991). Some masked shrew populations are genetically closer to prairie shrews than they are to other masked shrews (Stewart et al. 1993). Only a minority of mallards cluster together on an mtDNA tree, the rest being scattered among black ducks (Avise et al. 1990). All six species of Darwin's ground finches seem to form a genetically homogeneous genus while showing very little concordance between mtDNA, nuclear DNA, and morphology (Freeland & Boag 1999). In terms of genetic distance, redpoll finches from the same species are not significantly closer to each other than they are to sibling species (Seutin et al. 1995). Different species of haplochromine cichlids cannot be easily told apart by means of nuclear or mitochondrial genes, yet they are well differentiated morphologically and behaviorally (Klein et al., 1998). Neither mtDNA nor allozyme alleles can distinguish the various species of Lycaedis butterflies, despite clear differences in morphology (Nice & Shapiro 1999). An extreme example is a dog tumor that spreads through sexual contact: canine transmissible venereal sarcoma. It looks and acts like an infectious pathogen, yet its genes would show it to be a canid, and some beagles may be genetically more similar to it than they are to Great Danes (Yang 1996; see Frost 2011 for a full discussion).

 

When populations diverge under the impact of divergent pressures of natural selection, changes initially occur only within a fraction of the genome. Later, with the passage of time, the two populations will drift apart over the rest of the genome. But the human species is still young. The genetic split between Africans and non-Africans goes back only 60,000 years, and other splits are younger still.

 

This doesn't mean that genetic diversity between human populations is trivial. In fact, almost the opposite is true. It is the diversity within populations that is largely trivial.

 

 

References

 

Avise, J.C., C.D. Ankney, and W.S. Nelson. (1990). Mitochondrial gene trees and the evolutionary relationship of mallard and black ducks. Evolution 44: 1109-1119.

https://doi.org/10.1111/j.1558-5646.1990.tb03829.x

 

Coppinger, R. and R. Schneider (1995). Evolution of working dogs. In: J. Serpell (ed.) The Domestic Dog: Its Evolution, Behaviour and Interactions with People. Cambridge: Cambridge University Press, pp. 21-47.

https://books.google.ca/books?id=4fB7DQAAQBAJ&printsec=frontcover&hl=fr&source=gbs_ge_summary_r&cad=0#v=onepage&q&f=false

 

Cronin, M. (1991). Mitochondrial-DNA phylogeny of deer (Cervidae). Journal of Mammalogy 72: 533-566.

https://doi.org/10.2307/1382139

 

Freeland, J.R. and P.T. Boag. (1999). The mitochondrial and nuclear genetic homogeneity of the phenotypically diverse Darwin's ground finches. Evolution 53: 1553-1563.

https://doi.org/10.1111/j.1558-5646.1999.tb05418.x

 

Frost, P. (2011). Human nature or human natures? Futures 43: 740-748.

https://www.researchgate.net/profile/Peter_Frost2/publication/251725125_Human_nature_or_human_natures/links/004635223eaf8196f0000000.pdf  

 

Klein, J., A. Sato, S. Nagl, and C. O'hUigin. (1998). Molecular trans-species polymorphism. Annual Review of Ecology and Systematics 29: 1-21.

https://doi.org/10.1146/annurev.ecolsys.29.1.1

 

Lewontin, R.C. (1972). The apportionment of human diversity. Evolutionary Biology 6: 381-398.

https://emilkirkegaard.dk/en/wp-content/uploads/Lewontin-1972-The-Apportionment-of-Human-Diversity.pdf

 

Nice, C.C. and A.M. Shapiro. (1999). Molecular and morphological divergence in the butterfly genus Lycaeides (Lepidoptera: Lycaenidae) in North America: evidence of recent speciation. Journal of Evolutionary Biology 12: 936-950.

https://doi.org/10.1046/j.1420-9101.1999.00111.x

 

Seutin, G., L.M. Ratcliffe, and P.T. Boag. (1995). Mitochondrial DNA homogeneity in the phenotypically diverse redpoll finch complex (Aves: Carduelinae: Carduelis flammea-hornemanni). Evolution 49: 962-973.

https://doi.org/10.1111/j.1558-5646.1995.tb02331.x

 

Stewart, D.T., A.J. Baker, and S.P. Hindocha. (1993). Genetic differentiation and population structure in Sorex Haydeni and S. Cinereus. Journal of Mammalogy 74: 21-32.

https://doi.org/10.2307/1381902

 

Yang, T.J. (1996). Parasitic protist of metazoan origin. Evolutionary Theory 11: 99-103.

Are identical twins really identical?

 

Sibling similarity in personality for monozygotic twins, dizygotic twins, and adoptees (Wikicommons)

 

 

Monozygotic and dizygotic twins who were separated early in life and reared apart (MZA and DZA twin pairs) are a fascinating experiment of nature. They also provide the simplest and most powerful method for disentangling the influence of environmental and genetic factors on human characteristics. (Bouchard et al. 1990)

 

Monozygotic twins are identical twins. They develop from a single fertilized egg and are assumed to be genetically identical. Any differences between them in mind or behavior must therefore have an environmental cause. Of course, "environmental cause" does not mean only things like diet, upbringing, education, or parental help with homework. It can also mean accidents during pregnancy or childbirth.

 

But are monozygotic twins really identical? Monozygotic twins begin to go their own ways long after the zygote has made its first division. It's actually around a week later that they begin to develop separately, when the zygote has already divided several times to form a mass of about sixteen cells. During that time, mutations may have occurred in one cell lineage or another, and not all of those mutations will be inherited by both twins. A twin may in fact develop from a single lineage or several lineages within the cell mass. The two twins may thus be genetically different.

 

Jónsson et al. (2021) have quantified these genetic differences between twins. They examined the body tissues of adult twins, specifically one sample from adipose tissue, 204 samples from buccal tissue, and 563 blood samples.  On average, one of the twins had 14 postzygotic mutations that were not present in the other. There was, however, considerable variability: 39 twin pairs differed at more than 100 loci, whereas 38 pairs did not differ at all.

 

Germ cells develop from a subset of cell lineages very early in embryonic development, and it is possible to see how twins differ genetically in their germ lines by looking at their offspring. In this case, there was a difference of 5.2 mutations between twins. Again, there was considerable variability, ranging from a minimum of no mutations at all in 207 offspring to a maximum of 8 mutations in 3 offspring.

 

If monozygotic twins are not genetically identical, we will have to revise upwards our estimates of the relative importance of nature versus nurture in different human traits:

 

Phenotypic discordance between monozygotic twins has generally been attributed to the environment. This assumes that the contribution of mutations that separate monozygotic twins is negligible; however, for some diseases such as autism and other developmental disorders, a substantial component is due to de novo mutations. Our analysis demonstrates that in 15% of monozygotic twins a substantial number of mutations are specific to one twin but not the other. This discordance suggests that in most heritability models the contribution of sequence variation to the pathogenesis of diseases with an appreciable mutational component is underestimated. (Jónsson et al. 2021)

 

In particular, we will have to revise upwards our estimates of the genetic component of intelligence, such as the 70% estimate offered by Bouchard et al. (1990):

 

Since 1979, a continuing study of monozygotic and dizygotic twins, separated in infancy and reared apart, has subjected more than 100 sets of reared-apart twins or triplets to a week of intensive psychological and physiological assessment. Like the prior, smaller studies of monozygotic twins reared apart, about 70% of the variance in IQ was found to be associated with genetic variation. On multiple measures of personality and temperament, occupational and leisure-time interests, and social attitudes, monozygotic twins reared apart are about as similar as are monozygotic twins reared together.

 

Or the 41% to 66% estimate offered by Haworth et al. (2020):

 

Although common sense suggests that environmental influences increasingly account for individual differences in behavior as experiences accumulate during the course of life, this hypothesis has not previously been tested, in part because of the large sample sizes needed for an adequately powered analysis. Here we show for general cognitive ability that, to the contrary, genetic influence increases with age. The heritability of general cognitive ability increases significantly and linearly from 41% in childhood (9 years) to 55% in adolescence (12 years) and to 66% in young adulthood (17 years) in a sample of 11 000 pairs of twins from four countries, a larger sample than all previous studies combined.

 

My criticisms

 

Why focus on germline differences?

 

I have two criticisms of the study by Jónsson et al. (2020). First, their abstract highlights the median of 5.2 mutational differences in the germline, and not the larger median of 14 mutational differences in somatic tissues.

 

Here we show that monozygotic twins differ on average by 5.2 early developmental mutations and that approximately 15% of monozygotic twins have a substantial number of these early developmental mutations specific to one of them. (Jónsson et al. 2021)

 

Yes, "heritability" refers to genes that are passed on to the next generation, but most twin studies don't include the offspring of twins. The researchers simply examine pairs of monozygotic twins and see how they differ. Any differences would therefore reflect differences in somatic tissues and not the germline, or at least not solely the germline.

 

Undoubtedly, some of the somatic mutations occurred later in development, but they would still be relevant for any study on adult monozygotic twins.

 

Do these differences really make a difference?

 

We estimate the genetic component of a mental or behavioral trait by comparing monozygotic and dizygotic twins, i.e., identical and fraternal twins. A difference between monozygotic twins is assumed to be 100% environmental, and a difference between dizygotic twins is assumed to be partly environmental and partly genetic. Therefore, we can estimate the genetic component by subtracting one from the other, right?

 

This is where the study by Jónsson et al. (2021) comes in. They argue that the genetic component is always underestimated because some of the difference between monozygotic twins is also genetic. But is that additional genetic difference large enough to make a difference? If monozygotic twins differ from each other, on average, at 14 loci, and dizygotic twins differ from each other, on average, at 1400 loci, we might as well assume that monozygotic twins are genetically identical. Any upward revision of the heritability estimate would be slight.

 

Of course, the key lies in the words "on average." Some of the twins in this study differed at more than 100 loci. More importantly, around 15% of the twins had a substantial number of "near-constitutional" mutations, i.e., absent from one twin and present in almost all the tissues of the other. In those cases, we could see big differences in development between the two.

 

It's difficult to say without a point of comparison. In other words, the same kind of study should be done on dizygotic twins. How much more variable are they genetically?

 

 

References

 

Bouchard Jr., T.J., D.T. Lykken, M. McGue, N.L. Segal, and A. Tellegen. (1990). Sources of human psychological differences: the Minnesota Study of Twins Reared Apart. Science 250(4978): 223-228. https://doi.org/10.1126/science.2218526

 

Haworth, C.M.A., M. J. Wright, M. Luciano, N.G. Martin, E.J.C. de Geus, et al. (2010). The heritability of general cognitive ability increases linearly from childhood to young adulthood. Molecular Psychiatry 15: 1112-1120. https://doi.org/10.1038/mp.2009.55

 

Jónsson, H., E. Magnusdottir, H.P. Eggertsson, O.A. Stefansson, G.A. Arnadottir, et al. (2021). Differences between germline genomes of monozygotic twins. Nature Genetics 53: 27-34 (2021). https://doi.org/10.1038/s41588-020-00755-1

A new yardstick

If we look at ancient DNA from 4,560 to 1,210 years ago, we see a steady increase over time in the number of genetic variants that are linked to high educational attainment (Woodley et al. 2017)

Four years ago I discussed genetic variants that seem to favor high educational attainment (Frost 2014). They’re found at single nucleotide polymorphisms (SNPs), and their incidence varies from one human population to another. In all but one case, they are specific to humans and not shared with ancestral primates. 

Davide Piffer has been interested in these SNP variants, seeing them as a possible way to measure how genes contribute to intelligence in different populations. By looking up population data, he can calculate their average incidence for a given group of people. This measure is called the “cognitive polygenic score.”

When he wrote up his latest paper (Piffer 2017a), only nine of these variants were known. For each geographic region, the scores were as follows:

Sub-Saharan Africans – 18%

Amerindians – 25%
North Africans – 30%
Oceanians (Papuans, Melanesians) – 34%
Southeast Asians – 35%
West Asians – 38%
Middle Easterners – 40%
Europeans – 41%
Siberians – 43%
East Asians – 45%

This regional breakdown is open to criticism. Sardinians (32%) were not included in the European category, and Mongolians (49%) were grouped with East Asians rather than with Siberians. The distinction between Middle Easterners and West Asians is not clear to me. The Amerindian category is based on a few small groups. And who is included in the Southeast Asian category? Only Cambodians?

When Piffer compared these scores with the results of IQ tests in these regions, he found a high correlation of 0.9. That is high, higher than what I would expect, given the quality of the data, especially for mean IQ, and the very disparate nature of the two datasets.

Over a two-year period Piffer submitted his paper to Intelligence, resubmitted it, had it rejected, and then resubmitted it to Frontiers in Psychology, where it was accepted by the reviewers before being rejected by the editor. It is now sitting in the limbo of a preprint repository (Piffer 2017a).

Meanwhile, the number of these SNPs has continued to grow. A research team led by Aysu Okbay identified 74 SNPs that are associated with educational attainment (Okbay et al. 2016). Another team led by David Hill reported 107 in their initial preprint and 187 in their published paper (Hill et al. 2018). 

Piffer (2017b) repeated his analysis, now using the 107 SNPs that Hill’s team had identified. The geographic pattern still held up but was weaker, the correlation being only 0.64. This lower score is actually more in line with what I would expect. It diverges the most from mean IQ in two geographic areas:

1. South Asia (Pakistan, India) - South Asians seem to do worse on IQ tests than their genetic endowment predicts. Why? Is it the culture? The diet? Inbreeding? Perhaps language. IQ tests are often administered in a language (English, Hindi, Urdu) that may be the second language of the person taking it. Or perhaps South Asian educational attainment is determined not only by IQ but also by qualities like the ability to sit still and not make a ruckus in class.

2. The Mende of Sierra Leone - For some reason, the Mende have a higher cognitive polygenic score than any other African population. This might be a real finding, or a typo.

Another research team, led by Michael Woodley, has compared the Okbay dataset with ancient DNA to see whether the cognitive polygenic score has increased over time, specifically between 4,560 and 1,210 years ago. The DNA was retrieved from European sites and a few sites from southwest and central Asia. The result? The cognitive polygenic score did increase over time. People on average had more and more of the alleles that favor educational attainment. The authors note that IQ alone may not be responsible:

[...] While the increase in these variants over time is certainly consistent with the expectation of rising GCA [general cognitive ability], the possibility that their increase indicates a simultaneous rise in other factors that make unique contributions to educational attainment (such as 'slow' life history or 'high-K' social cognitive characteristics) cannot be ruled out. (Woodley et al. 2017; references within quote removed)

The new mental/behavioral package developed through a process of feedback with the cultural environment. This gene-culture coevolution likely continued into recent times:

This process likely continued until the Late Modern Era, where it has been noted that among Western populations living between the 15th and early 19th centuries, those with higher social status (which shares genetic variance with, and is therefore a proxy for GCA) typically produced the most surviving offspring. These in turn tended toward downward social mobility due to intense competition, replacing the reproductively unsuccessful low-status stratum and effectively 'bootstrapping' those populations via the application of high levels of skill to solving problems associated with production and industry, eventually leading to the Industrial Revolution in Europe. (Woodley et al. 2017; references within quote removed)

Conclusion

More and more SNPs are being linked to educational attainment. The total is now in the triple digits. That’s still less than the thousands of genes that influence intelligence, but there is no need to identify most of them to spot general trends. Selection acts on phenotype, not on genotype. Selection for intelligence should therefore impact all of these SNPs in the same direction. It’s like estimating the proportions of different colors in a bowl of Smarties. You don’t have to count every last one. Just pick out a handful at random and count the colors.

Four years ago only 7 SNPs had been linked to educational attainment. Now we have 187. In another four years we’ll probably have more than a thousand. All the same, I doubt that the overall geographic pattern will change much. The problems lie elsewhere:

-          Genetic data may be lacking for some unmixed groups, particularly Amerindians.

-          The relationship between intelligence and cognitive polygenic score may not be linear.

-          We may be relying too much on educational attainment as a proxy for IQ (which itself is a proxy for intelligence).

When I was in public school, girls did better than boys in almost every subject. They had good attendance, always took notes, and did their homework. Boys got bored more easily and spent more time fidgeting, daydreaming, and drawing pictures in their notebooks. This sex difference exists in all cultures, but it seems greater in some than in others.

How useful is educational attainment as a proxy for IQ? Yes, these two measures correlate highly with each other (Rindermann 2018, pp. 51-54), but this high correlation is based on studies from WEIRD countries (Western, educated, industrialized, rich, and democratic). Does it hold up on a global scale? I’m not so sure.

References

Frost, P. (2014). Population differences in intellectual capacity: a new polygenic analysis, Evo and Proud, March 8

http://evoandproud.blogspot.ca/2014/03/population-differences-in-intellectual.html

Hill, W. D., R.E. Marioni, O. Maghzian, S.J. Ritchie, S.P. Hagenaars, A.M. McIntosh, C.R. Gale, G. Davies, I.J. Deary. (2018). A combined analysis of genetically correlated traits identifies 187 loci and a role for neurogenesis and myelination in intelligence. Molecular Psychiatry

https://doi.org/10.1038/s41380-017-0001-5

Okbay, A., J.P. Beauchamp, M.A. Fontana, J.J. Lee, T.H. Pers, C.A. Rietveld, et al. (2016). Genome-wide association study identifies 74 loci associated with educational attainment. Nature 533: 539-542.

http://www.nature.com/articles/nature17671

Piffer, D. (2017a) Evidence for Recent Polygenic Selection on Educational Attainment and Intelligence Inferred from GWAS Hits: A Replication of Previous Findings Using Recent Data. Preprints, June 8

https://www.preprints.org/manuscript/201706.0039/v1

Piffer, D. (2017b). Piffer's results replicated (again) by latest GWAS (N=147,194), toppseudoscience, July 21

https://topseudoscience.wordpress.com/2017/07/21/piffers-results-replicated-again-by-latest-gwas-n147194/comment-page-1/#comment-95

Rindermann, H. (2018). Cognitive Capitalism. Human Capital and the Wellbeing of Nations. Cambridge University Press.

Woodley, M.A., S. Younuskunju, B. Balan, and D. Piffer. (2017). Holocene selection for variants associated with general cognitive ability: comparing ancient and modern genomes. Twin Research and Human Genetics 20(4): 271-280.

https://doi.org/10.1017/thg.2017.37 

An idea abandoned by its father

Italian wall lizard (Podarcis sicula) (Credit: Charles J. Sharp). Five mating pairs were taken from one island to another, and over the next thirty generations the transplanted population became remarkably different from the parent population.

Unlike other animals, we adapt not only to natural environments but also to cultural environments of our making. We thus direct our own evolution. At the same time we are busy redesigning our cultural environment, the latter is just as busy redesigning us. Like the natural environment, it favors the survival and reproduction of those who best fit in.

This concept of gene-culture coevolution began with anthropologist Claude Lévi-Strauss in a 1971 lecture:

... Among early humans, biological evolution may have selected for pre-cultural traits like upright posture, manual dexterity, sociability, symbolic thinking, and ability to vocalize and communicate. It was culture, however, once it came into being, that consolidated these traits and propagated them. When cultures specialize, they consolidate and favor other traits, like resistance to cold or heat in societies that have willingly or unwillingly had to adapt to extreme climates, like dispositions to aggressiveness or contemplation, like technical ingenuity, and so on. In the form these traits appear to us on the cultural level, none can be clearly linked to a genetic basis, but we cannot exclude that they are sometimes linked partially and distantly via intermediate linkages. In this case, it would be true to say that each culture selects for genetic aptitudes, which then, via a feedback loop, influence the culture that had initially helped to strengthen them.

Credit is usually given, however, to geneticist Luigi Luca Cavalli-Sforza. In 1976, he developed the first mathematical models for gene-culture coevolution with another geneticist, Marcus Feldman, and in 1978-1979 he spoke on this subject to a cultural evolution class at Stanford (Feldman & Cavalli-Sforza 1976; Stone & Lurquin 2005, p. 108). Two of his students were Robert Boyd and Peter Richerson, who later wrote a seminal book on gene-culture coevolution (Boyd & Richerson 1985). In the mid-1980s, he decided to test this concept in the field by investigating the cultural and genetic bases of artistic talent among the Inuit:

One of the most remarkable phenomena in the contemporary Canadian Arctic is the presence of highly-acclaimed art forms — carving in stone and ivory, and printing on paper. The question we ask is: how can we account for the wide-spread distribution of such talent in a small dispersed population? (Berry & Cavalli-Sforza 1986, p. 2)

To answer this question, he organized a joint project with psychologist John W. Berry at Queen's University and anthropologist Bernard Saladin d'Anglure at Université Laval. The Inuit were chosen for study because their high rate of adoption made it possible "to distinguish cultural from biological inheritance by studying correlations of adopted children with foster relatives on one hand and biological relatives on the other" (Berry & Cavalli-Sforza 1986, p. 5). Also, until recently, Inuit had lived off the land and, as such, had "abilities [that] are considered to be adaptive to a nomadic and hunting life style" (Berry & Cavalli-Sforza 1986, p. 3). Berry argued that the artistic talent of the Inuit came from certain mental skills that helped them during hunting.

Hunters, by this way of thinking, require good visual acuity, keen disembedding skills and a well-developed sense of spatial orientation. To hunt successfully, the hunter must be able to discern the object of the quest (which is often embedded in a complex visual landscape), then disembed the object, and finally return to home base. In contrast, agriculturalists need not develop these particular skills, but rather they need to invest in other areas of development, such as conservation (in both the economic and the Piagetian senses) and close social interactions. (Berry 2008, p. 3)

The project fell through. Cavalli-Sforza said he had to quit because of illness. Neither of his biographies, however, mention any illness during that time period (Frost 2014). Interestingly, his American biography ascribes his interest in culture at that time to a desire to disprove the existence of mental differences between human populations:

Yet another source of his interest in culture was the idea that the concept of human cultural learning was a valid weapon against racist arguments that differences between people (for example, different IQ scores among ethnic groups) were due to biologically determined "racial" differences. (Stone & Lurquin, 2005, p. 86)

The reality was a bit different. He believed in the importance of culture, but not as an entity separate and distinct from biology. This put him in opposition not only to the racists he denounced in the 1960s but also to the antiracists who increasingly viewed him with suspicion from the late 1980s onward.

With Cavalli-Sforza out of the picture, research on gene-culture coevolution languished over the next quarter-century. This field of research needed a high-profile champion in academia, and all of the possible candidates were either unable or unwilling.  Cavalli-Sforza never was suited for the job, being too timid and, frankly, too easy to blackmail. (Do you really think his wartime research on anthrax involved only mice?)

Lately, there seems to have been a renewal of interest, as seen in this review article on "Human biological and psychological diversity":

Humans migrated out of Africa at least 50,000 years ago and occupied many different ecological and climatological niches. Because of this, they evolved slightly different anatomical and physiological traits. For example, Tibetans evolved various traits that help them cope with the rigors of altitude; similarly, the Inuit evolved various traits that help them cope with the challenges of a very cold environment. It is likely that humans also evolved slightly different psychological traits as a response to different selection pressures in different environments and niches. One possible example is the high intelligence of the Ashkenazi Jewish people. Frank discussions of such differences among human groups have provoked strong ethical concerns in the past. We understand those ethical concerns and believe that it is important to address them. However, we also believe that the benefits of discussing possible human population differences outweigh the costs. (Winegard et al. 2017)

This article is a good read, and I was intrigued by its examples of fast evolution, particularly the Italian wall lizards. Five mating pairs were taken from one island to another, and over the next thirty generations the transplanted population became remarkably different from the parent population. The lizards were now larger, had shorter hind limbs, and could bite with much more force. Even more remarkably, they had a new morphological trait: a cecal valve—a muscle between the large and small intestines that slows down food movement and allows digestion of cellulose. This is an adaptation to the abundance of plant food on that island, but it is surprising that an entirely new trait could evolve so fast.

As far back as Darwin, biologists have described evolutionary change as slow. This is true only when organisms live in slowly changing environments. Transplant them into a very different one, and they will evolve very fast. This has been especially true for modern humans, who over the past 50,000 years have spread into a wide range of natural environments from the tropics to the arctic and into an even wider range of cultural environments:

Humans, like many animals, actively alter their environment, which changes the selection pressures they face (Laland et al. 2001; Laland and Sterelny 2006). In fact, humans may be the paradigmatic example of a niche-creating species, using brains rather than brawn to conquer the world (Baumeister 2005; Pinker 2010). Across the globe, humans devised distinctive cultural systems to cope with their environments, creating vastly different selective regimes from one culture to another. (Winegard et al. 2017)

Humans are indeed niche creators who have speeded up their own diversification. Nonetheless, they aren't alone in diversifying so fast. For example, some animal and plant species have spread into a wide range of new habitats since the last ice age, thereby giving rise to many new populations. Whether these recent populations are "sibling species," "subspecies," or "races"—the distinction is often arbitrary—their example can help us understand our own genetic diversity (Frost 2011).

These populations, like our own, seem to have evolved much more anatomically than they have genetically. Their anatomies are often distinct from each other, with no overlap, yet their genomes overlap considerably—there is far more genetic variation within each population than between them. So they are easier to tell apart by their appearance than by their genes. 

Why this discordance between genes and anatomy? Genes don't lie, do they? To make sense of this puzzle, we need to understand three points:

• When a gene has different "alleles" or versions of itself, these alleles vary in their degree of similarity, some performing very differently and others identically or almost so—often because the gene itself is little more than "junk DNA.
• Population boundaries separate not only different populations but also different natural or cultural environments. This is especially true for humans. The cultural environment usually differs, even when the natural environment is the same.
• If the alleles of a gene perform differently, some of them will be more useful to one population than to another because they do better in one environment than in another. The more differently they perform, the more their frequencies will differ across population boundaries, with some alleles being more common in some populations than in others. Conversely, if the alleles perform identically, they will do equally well in all environments and tend to be equally common in all populations. To the extent that different alleles are present within a single population, the reasons will be more stochastic and less related to the usefulness of any one allele. Genetic variation within a population is therefore disproportionately due to alleles that perform similarly.

So genetic variation between populations differs qualitatively from genetic variation within each population. The first kind matters a lot more than the second kind. There are exceptions to this rule, e.g., balanced polymorphisms, founder effects, genetic drift, but that's the general picture. So when you read that genes vary far more within human populations than between them, you should keep in mind that we see the same pattern with many sibling species that are nonetheless anatomically and behaviorally distinct. This pattern tells us only that the populations in question are very young. It doesn't tell us how different they really are from each other, since real evolutionary change can happen very fast—as we saw with the Italian wall lizards. 

References

Berry, J.W. (2008). Models of Ecocultural Adaptation and Cultural Transmission: The Example of Inuit Art, paper presented at the conference Adaptation et socialisation des minoritiés culturelles en région, June 3-4, Quebec City.

Berry, J.W., and L.L. Cavalli-Sforza. (1986). Cultural and genetic influences on Inuit art. Report to Social Sciences and Humanities Research Council of Canada, Ottawa.

Boyd, R. and P.J. Richerson. (1985). Culture and the Evolutionary Process, Chicago: Chicago University Press.

Feldman, M.; Cavalli-Sforza, L. (1976). Cultural and biological evolutionary processes, selection for a trait under complex transmission, Theoretical Population Biology, 9: 238-59.

Frost, P. (2014). L.L. Cavalli-Sforza. A bird in a gilded cage, Open Behavioral Genetics, March 28,

http://openpsych.net/OBG/2014/03/l-l-cavalli-sforza-a-bird-in-a-gilded-cage/

Frost, P. (2011). Human nature or human natures? Futures, 43: 740-748.

https://www.researchgate.net/profile/Peter_Frost2/publication/251725125_Human_nature_or_human_natures/links/004635223eaf8196f0000000.pdf  
Lévi-Strauss, C. 1971). Race et culture, conférence de Lévi-Strauss à l'UNESCO le 22 mars 1971 (Audio). Polit'productions
http://politproductions.com/content/%C2%ABrace-et-culture%C2%BB-conf%C3%A9rence-de-l%C3%A9vi-strauss-%C3%A0-lunesco-le-22-mars-1971-audio  

Stone, L. and P.F. Lurquin. (2005). A Genetic and Cultural Odyssey. The Life and Work of L. Luca Cavalli-Sforza, New York: Columbia University Press.

Winegard, B., B. Winegard, and B. Boutwell. (2017). Human biological and psychological diversity, Evolutionary Psychological Science, 3(2): 159-180.

http://atavisionary.com/wp-content/uploads/2017/05/Human-Biological-and-Psychological-diversity.pdf  

A modern myth

 

Your blood group cannot reliably identify your ethnicity, your race ... or even your species (Wikicommons, Etan Tal).

 

What sort of ideas will guide our elites twenty years from now? You can find out by observing university students, especially those in the humanities and social sciences. One popular idea is that race doesn't exist, except as a social construct. Its proponents include Eula Biss, a contributor to the New York Times Magazine:

Whiteness is not a kinship or a culture. White people are no more closely related to one another, genetically, than we are to black people. [...] Which is why it is entirely possible to despise whiteness without disliking yourself. (Biss, 2015, h/t to Steve Sailer)

The last sentence needs little explanation. It's possible to like yourself a lot while despising your own people. Such individuals have existed since time immemorial. But what about the second sentence? One often hears it among the educated, even those who dislike genetics and biology. Where does it come from?

From a study by geneticist Richard Lewontin, in 1972. He looked at human genes with more than one variant, mostly blood groups but also serum proteins and red blood cell enzymes. His conclusion:

The results are quite remarkable. The mean proportion of the total species diversity that is contained within populations is 85.4%, with a maximum of 99.7% for the Xm gene, and a minimum of 63.6% for Duffy. Less than 15% of all human genetic diversity is accounted for by differences between human groups! Moreover, the difference between populations within a race accounts for an additional 8.3%, so that only 6.3% is accounted for by racial classification.

[...] It is clear that our perception of relatively large differences between human races and subgroups, as compared to the variation within these groups, is indeed a biased perception and that, based on randomly chosen genetic differences, human races and populations are remarkably similar to each other, with the largest part by far of human variation being accounted for by the differences between individuals. (Lewontin, 1972)

The problem here is the assumption that genetic variation within a human group is comparable to genetic variation between human groups. In fact, the two are qualitatively different. When a gene varies between two groups the cause is more likely a difference in natural selection, since the group boundary also tends to separate different natural environments (vegetation, climate, topography) or, more often, different cultural environments (diet, means of subsistence, sedentism vs. nomadism, gender roles, state monopoly of violence, etc.). Conversely, when a gene varies within a population, the cause is more likely a random factor without adaptive significance. That kind of variation is less easily flattened out by the steamroller of similar selection pressures.

This point isn't merely theoretical. In other animals, as Lewontin himself noted, we often see the same genetic overlap between races of one species. But we also see it between many species that are nonetheless anatomically and behaviorally distinct. Some two decades after Lewontin’s study, this apparent paradox became known when geneticists looked at how genes vary within and between dog breeds:

[...] genetic and biochemical methods ... have shown domestic dogs to be virtually identical in many respects to other members of the genus. [...] Greater mtDNA differences appeared within the single breeds of Doberman pinscher or poodle than between dogs and wolves. Eighteen breeds, which included dachshunds, dingoes, and Great Danes, shared a common haplotype and were no closer to wolves than poodles and bulldogs.

[...] there is less mtDNA difference between dogs, wolves, and coyotes than there is between the various ethnic groups of human beings, which are recognized as a single species. (Coppinger and Schneider, 1995)

Initially, this paradox was put down to the effects of artificial selection. Kennel clubs insist that each breed should conform to a limited set of criteria. All other criteria, particularly those not readily visible, end up being ignored. So artificial selection targets a relatively small number of genes and leaves the rest of the genome alone.

But is natural selection any different? When a group buds off from a population and moves into a new environment, its members too have to conform to a new set of selection pressures that act on a relatively small number of genes. So the new group will diverge anatomically and behaviorally from its parent population, and yet remain similar to it over most of the genome. This is either because most of the genes respond similarly to the new environment—as with those that do the same housekeeping tasks in a wide range of species—or because they respond weakly to natural selection in general. Many genes are little more than "junk DNA"—they change slowly over time, not through the effects of natural selection but through gradual accumulation of random mutations.

With the extension of population studies to nonhuman species, geneticists have often encountered this paradox: a gene will vary much less between two species than within each of them. This is notably the case with sibling species that have emerged since the last ice age, when many new and different environments came into being.

Thus, the genetic overlap between dog breeds also appears between many natural species. In the deer family, genetic variability is greater within some species than between some genera (Cronin, 1991). Some masked shrew populations are genetically closer to prairie shrews than they are to other masked shrews (Stewart et al., 1993). Only a minority of mallards cluster together on an mtDNA tree, the rest being scattered among black ducks (Avise et al., 1990). All six species of Darwin's ground finches form a genetically homogeneous genus with very little concordance between mtDNA, nuclear DNA, and morphology (Freeland and Boag, 1999). In terms of genetic distance, redpoll finches from the same species are not significantly closer to each other than they are to redpolls from different species (Seutin et al., 1995). The haplochromine cichlids of Lake Victoria are extremely difficult to identify as species when one looks at their nuclear or mitochondrial genes, despite being well differentiated anatomically and behaviorally (Klein et al., 1998). Neither mtDNA nor allozyme alleles can distinguish the various species of Lycaedis butterflies, despite clear differences in morphology (Nice and Shapiro, 1999). An extreme example is a dog tumor that has developed the ability to spread to other dogs through sexual contact. It looks and acts like an infectious microbe, yet its genes would show it to be a canid and, conceivably, some beagles may be genetically more similar to it than they are to Great Danes (Cochran, 2001; Yang, 1996).

We see this genetic overlap not only between sibling species, but even between some species that have long been separated, like humans and other primates. This is the case with ABO blood groups:

Remarkably, the A, B, and H antigens exist not only in humans but in many other primates [...], and the same two amino acids are responsible for A and B enzymatic specificity in all sequenced species. Thus, primates not only share their ABO blood group, but also the same genetic basis for the A/B polymorphism. O alleles, in contrast, result from loss-of-function alleles such as frame-shift mutations and appear to be species specific. (Segurel et al., 2012)

Just think. Lewontin used the same blood group polymorphisms for his study. While the O alleles are specific to each primate species, the A and B alleles show considerable overlap between primates that have been separated for millions of years. So it's not surprising that this polymorphism should vary much more within human races than between them, as Lewontin found. Little did he know that the same pattern can continue above the species level.

Some have argued that this genetic overlap between humans and apes is only apparent. In other words, the same antigens have evolved independently in each species. Well, no. It seems that this polymorphism has survived one speciation event after another for millions of years:

That different species share the same two A/B alleles could be the result of convergent evolution in many lineages or of an ancestral polymorphism stably maintained for millions of years and inherited across (at least a subset of) species. The two possibilities have been debated for decades, with a consensus emerging that A is ancestral and the B allele has evolved independently at least six times in primates (in human, gorilla, orangutan, gibbon/siamang, macaque, and baboon), in particular, that the human A/B polymorphism arose more recently than the split with chimpanzee. We show instead that the remarkable distribution of ABO alleles across species reflects the persistence of an old ancestral polymorphism that originated at least 20 million years (My) ago and is shared identical by descent by humans and gibbons as well as among distantly related Old World monkeys. (Segurel et al., 2012)

Are blood groups a special case? Perhaps. But there seem to be quite a few trans-species polymorphisms, at least between humans and chimpanzees:

Instances in which natural selection maintains genetic variation in a population over millions of years are thought to be extremely rare. We conducted a genome-wide scan for long-lived balancing selection by looking for combinations of SNPs shared between humans and chimpanzees. In addition to the major histocompatibility complex, we identified 125 regions in which the same haplotypes are segregating in the two species, all but two of which are noncoding. In six cases, there is evidence for an ancestral polymorphism that persisted to the present in humans and chimpanzees. (Leffler et al., 2013)

Many of these appear to be "disease polymorphisms." If an epidemic sweeps through a community, it pays to have surface antigens that differ somewhat from your neighbor’s. The result is selection that inflates within-group variability, especially for the sort of structural proteins that are easy to collect and examine for studies on population genetics.

If such polymorphisms can remain intact despite millions of years of separation, how many more persist among human populations that have been separated for only tens of thousands of years?

In sum, if we are to believe blood groups and other genetic markers, it seems that Eula Biss may have more in common with certain apes than with the white folks she despises. Let’s hope she feels gratified.

When I discuss Richard Lewontin's study with antiracists, preferably those with some background in biology, they often agree that he misunderstood his findings. They nonetheless go on to say that their position has many other justifications, particularly moral ones. Fine. But it is above all Lewontin who gave antiracism a veneer of scientific objectivity. He still impresses people who are less impressed by academics who attack racism by attacking objectivity, like Stephen Jay Gould. "I criticize the myth that science itself is an objective enterprise, done properly only when scientists can shuck the constraints of their culture and view the world as it really is" (Gould, 1996, p. 53). It was in this spirit that he impugned the integrity of long-dead scholars who could not defend themselves—or point out that Gould himself was manipulating the data to suit his preconceived views (Frost, 2013).

When one takes Lewontin and Gould out of the picture, who is left? A lot of people, to be sure. Followers for the most part—those like Eula Biss who believe because everyone else in their milieu seems to believe, at least anyone with moral authority.

References 

Avise, J.C., C.D. Ankney, and W.S. Nelson. (1990). Mitochondrial gene trees and the evolutionary relationship of mallard and black ducks, Evolution, 44, 1109-1119.

http://www.jstor.org/stable/2409570?seq=1#page_scan_tab_contents 

Biss, E. (2015). White Debt, The New York Times Magazine, December 2

http://www.nytimes.com/2015/12/06/magazine/white-debt.html?_r=1

Cochran, G. (2001). Personal communication. 

Coppinger, R. and R. Schneider (1995). Evolution of working dogs. In J. Serpell (ed.), The Domestic Dog: Its Evolution, Behaviour and Interactions with People. Cambridge: Cambridge University Press, pp. 21-47.

https://books.google.ca/books?hl=fr&lr=&id=I8HU_3ycrrEC&oi=fnd&pg=PA21&dq=evolution+of+working+dogs&ots=BccrPzh5v3&sig=Cy-uz8gKk_epZRPTP58-k-1D9wg#v=onepage&q=evolution%20of%20working%20dogs&f=false 

Cronin, M. (1991). Mitochondrial-DNA phylogeny of deer (Cervidae), Journal of Mammalogy, 72, 533-566.

http://jmammal.oxfordjournals.org/content/72/3/553.abstract 

Freeland, J.R. and P.T. Boag. (1999).The mitochondrial and nuclear genetic homogeneity of the phenotypically diverse Darwin's ground finches, Evolution, 53, 1553-1563.

https://www.researchgate.net/profile/Peter_Boag/publication/233529125_The_mitochondrial_and_nuclear_genetic_homogeneity_of_the_phenotypically_diverse_Darwins_Ground_finches/links/0deec514a004f3a887000000.pdf 

Frost, P. (2013). Not getting the point, Evo and Proud, June 22

http://evoandproud.blogspot.ca/2013/06/not-getting-point.html  

Gould, S.J. (1996). The Mismeasure of Man, New York: W.W. Norton & Co.

http://www.amazon.com/The-Mismeasure-Man-Revised-Expanded/dp/0393314251 

Klein, J., A. Sato, S. Nagl, and C. O’hUigin. (1998). Molecular trans-species polymorphism, Annual Review of Ecology and Systematics, 29, 1-21.

http://www.jstor.org/stable/221700?seq=1#page_scan_tab_contents

Leffler, E.M., Z. Gao, S. Pfeifer, L. Ségurel, A. Auton, O. Venn, R. Bowden, R. Bontrop, J.D. Wall, G. Sella, P. Donnelly, G. McVean, and M. Przeworski. (2013). Multiple instances of ancient balancing selection shared between humans and chimpanzees, Science, 339 (6127), 1578-1582.

http://www.sciencemag.org/content/339/6127/1578.short  

Lewontin, R. (1972). The apportionment of human diversity, Evolutionary Biology, 6, 381-398.

http://www.philbio.org/wp-content/uploads/2010/11/Lewontin-The-Apportionment-of-Human-Diversity.pdf  

Nice, C.C. and A.M. Shapiro. (1999). Molecular and morphological divergence in the butterfly genus Lycaeides (Lepidoptera: Lycaenidae) in North America: evidence of recent speciation, Journal of Evolutionary Biology, 12, 936-950.

http://onlinelibrary.wiley.com/doi/10.1046/j.1420-9101.1999.00111.x/full 

Sailer, S. (2015). White Debt, The Unz Review, December 5

http://www.unz.com/isteve/white-debt/  

Ségurel, L.,  E.E. Thompson, T. Flutre, J. Lovstad, A. Venkat, S.W. Margulis, J. Moyse, S. Ross, K. Gamble, G. Sella, C. Ober, and M. Przeworski. (2012). The ABO blood group is a trans-species polymorphism in primates, Proceedings of the National Academy of Sciences U.S.A., 109, 18493-18498

http://www.pnas.org/content/109/45/18493.abstract  

Seutin, G., L.M. Ratcliffe, and P.T. Boag. (1995). Mitochondrial DNA homogeneity in the phenotypically diverse redpoll finch complex (Aves: Carduelinae: Carduelis flammea-hornemanni), Evolution, 49, 962-973.

http://www.jstor.org/stable/2410418?seq=1#page_scan_tab_contents 

Stewart, D.T., A.J. Baker, and S.P. Hindocha. (1993). Genetic differentiation and population structure in Sorex Haydeni and S. Cinereus, Journal of Mammalogy, 74, 21-32.

http://jmammal.oxfordjournals.org/content/74/1/21.abstract 

Yang, T.J. (1996). Parasitic protist of metazoan origin, Evolutionary Theory, 11, 99-103.