National Institutes of Health violates academic freedom, restricts dissemination of taxpayer-funded research

October 21, 2022 • 9:20 am

This article just appeared in the (conservative) City Journal, and is written by James Lee, a behavioral geneticist at the University at Minnesota.  What Lee reports made steam issue from under my collar, for he claims that the National Institutes of Health, a U.S. government science institute, has a huge genetics and “trait” database of several million Americans. The genetic data appear to be thorough, based on genome scans, and the traits associated with each person’s genome include education, ethnicity (“race”), intelligence, income, and occupation. You can imagine how rich that dataset is for mining. And yet the NIH is restricting scientists’ access to the data to projects it apparently considers ideologically kosher.

Remember that the NIH is completely funded by the American taxpayers, so those data were accumulated with our money. To me, this means that any researcher with a valid project should have access to the data. But apparently some projects are more valid than others.

Click to read.

Here’s Lee’s description of the hard time geneticists have in getting the data when their project sounds “iffy”, and by that I mean any project that has to do with heredity and intelligence (presumably IQ or a similar measure). Note that none of the attempts to get the data have been to do projects on ethnicity and IQ, which of course are considered taboo by many (readers may want to either echo or refute that taboo). Check out the second paragraph of the excerpt below, which I’ve put in bold.

American geneticists now face an even more drastic form of censorship: exclusion from access to the data necessary to conduct analyses, let alone publish results. Case in point: the National Institutes of Health now withholds access to an important database if it thinks a scientist’s research may wander into forbidden territory. The source at issue, the Database of Genotypes and Phenotypes (dbGaP), is an exceptional tool, combining genome scans of several million individuals with extensive data about health, education, occupation, and income. It is indispensable for research on how genes and environments combine to affect human traits. No other widely accessible American database comes close in terms of scientific utility.

My colleagues at other universities and I have run into problems involving applications to study the relationships among intelligence, education, and health outcomes. Sometimes, NIH denies access to some of the attributes that I have just mentioned, on the grounds that studying their genetic basis is “stigmatizing.” Sometimes, it demands updates about ongoing research, with the implied threat that it could withdraw usage if it doesn’t receive satisfactory answers. In some cases, NIH has retroactively withdrawn access for research it had previously approved.

Note that none of the studies I am referring to include inquiries into race or sex differences. Apparently, NIH is clamping down on a broad range of attempts to explore the relationship between genetics and intelligence.

It’s hard to believe that the NIH is restricting data that might be used to show any relationship between genes and intelligence, even within one ethnic group.  We already have data on genes implicated in academic achievement (which is correlated with IQ); those data are a big part of Kathryn Paige Harden‘s book The Genetic Lottery: Why DNA Matters for Social Equality, a book I reviewed for the Washington Post and also discussed on this website. As I recall, Harden’s genome-wide association study found nearly 1300 genomic sites associated with variation in academic achievement among the American European (“white”) population. Intriguingly, many of those sites were active in the brain. That in itself is of considerable interest, though Harden’s claim that this variation would help us create “level playing fields” for secondary-school students seemed unjustified.  But even finding genes associated with intelligence would tell us a lot about the developmental genetics of an important human trait.

Lee also explains why the NIH should NOT be a censor of valid research projects:

What is NIH’s justification? Studies of intelligence do not pose any greater threat to the dignity of their participants than research based on non-genetic factors. With the customary safeguards in place, research activities such as genetically predicting an individual’s academic performance need be no more “stigmatizing” than predicting academic performance based on an individual’s family structure during childhood.

The cost of this censorship is profound. On a practical level, many of the original data-generating studies were set up with the explicit goal of understanding risk factors for various diseases. Since intelligence and education are also risk factors for many of these diseases, denying researchers usage of these data stymies progress on the problems the studies were funded to address. Scientific research should not have to justify itself on those grounds, anyway. Perhaps the most elemental principle of science is that the search for truth is worthwhile, regardless of its practical benefits.

NIH’s responsibility is to protect the safety and privacy of research participants, not to enforce a party line. Indeed, no apparent legal basis exists for these restrictions. NIH enforces hundreds of regulations, but you will search in vain for any grounds on which to ban “stigmatizing” research—whatever that even means.

This is a no brainer. The NIH has NO business vetting the “political correctness” of research, and since nobody is investigating The Taboo Question—racial (or “ethnic” differences in intelligence—that issue doesn’t even come up. The only reason to prohibit “genetics of IQ” studies is a strict (almost Marxist) anti-hereditarianism based on the fear that there may be a genetic basis to differences in IQ. But we already KNOW that from studies of adoptions and relatives, which show that about 50-60% of variation in IQ among people is due to variation in their genes. The NIH appears to be afraid of being canceled. That is a hell of a way to do scence!

And I can’t imagine why the NIH would even think of restricting the data for any other studies. It seems to be IQ that’s the sticking point here, and that’s unconscionable. The data belong to the American public, and to American scientists, because the American public paid for it.

I’ve always object to the demonization of research that gives results that are politically or ideologically unpalatable, but this goes beyond the pale.  The government cannot withhold data paid for by us on the grounds that it might yield results that could offend people.

If a researcher has a valid reason to request these data, and the NIH refuses because of possible “stigmatizatization,” then I would say that a lawsuit is in order.

The remarkable physiology of hibernating bears

October 11, 2022 • 10:45 am

Have you been voting in Fat Bear Week? If not, today is the final day: the run-off between two heavyweights that will determine the Fattest Bear.

You probably realize that the bears get so fat in the fall because they are about to go into five months of hibernation, and need to stock up on food to sustain their metabolism as they go into winter. The Washington Post article shown below describes the remarkable phenomenon of hibernation, the potential bodily problems it poses, and new biochemical discoveries that help the bears obviate these issues and could also help immobile humans with the issue of atrophied muscles. Click to read:

Quotes from the article are indented:

But for many scientists, the true fascination of Fat Bear Week involves what happens next, when the now beachball-shaped bruins, carrying about 40 percent body fat, lumber into their dens and start hibernating. During hibernation, they remain healthy under conditions that would weaken and sicken mere humans. The bears emerge months later, lean, strong and barely affected by their months of starvation and inactivity.

Until recently, researchers could not explain how. But several fascinating new molecular studies suggest hibernation remodels bear metabolisms and gene activity in unique and dramatic ways that could have relevance for people. The fat bears can advance our understanding of diabetes, muscle atrophy, inactivity and the ingenuity of evolution.

Superficially, hibernating bears seem passive and inert. For five months or more, they do not eat, drink, urinate, defecate or move, except occasionally to turn over or shiver. Their metabolisms drop by about 75 percent. Hearts beat and lungs inflate only a few times a minute. Kidneys shut down. The bears grow profoundly insulin resistant.

If this were us, we would shed much of our muscle mass because of inactivity and probably develop diabetes, heart disease, kidney failure, frailty and other ills.

But the bears maintain their muscle and rapidly reestablish normal, healthy insulin sensitivity and organ function after hibernation.

Insulin functions to allow cells to absorb glucose from the blood to use as energy, or to convert some glucose to fat. It also helps break down fats and proteins. Normally, the onset of insulin resistance would, as the article implies, lead to diabetes and its attendant problems, but the bears are somehow able to tolerate that—as well as the muscle atrophy attendant on not moving for five months. (Muscle atrophy is a problem for people who are either paralyzed or bedridden for long periods of time.)

How do the bears do this? That’s the point of the article, which links to three scientific articles (one given below) explaining how the bears survive hibernation.

The information on fat usage came from blood samples drawn from hibernating and non-hibernating bears at Washington State University (WSU), bears trained to allow a blood draw without being anesthetized. (I guess the WSU bears also go into hibernation.)

It turns out that there is differential activation of genes in the bears during hibernation that protect them from deleterious effects of hibernation. Here are two papers cited:

By comparing the samples, [reserachers] concluded hibernation is biologically uncanny but hardly quiet. In a 2019 study, the WSU scientists and others found more than 10,000 genes in bears that work differently during hibernation vs. in autumn or spring. Many involve insulin activity and energy expenditure and most occur in the animals’ fat, which becomes quite insulin resistant during hibernation and robustly insulin sensitive immediately afterward.

Digging deeper into that process for a new study, published in September in iScience, they bathed fat cells drawn from hibernating and active bears with blood serum taken during the opposing time and watched the fat switch seasons. Fat from hibernating bears became insulin sensitive and genetically similar to fat from the active season and vice versa.

In other words, something in the blood serum of non-hibernating bears restored the insulin sensitivity of hibernating bears, and vice versa. This shows that it is something in the serum, and not in the fat, that changes during hibernation. The article continues:

Perhaps most compelling, they also identified and cross-matched hundreds of proteins in the animals’ blood and found eight that differed substantially in abundance from one season to the next. These eight proteins seemed to be driving most of the genetic and metabolic changes in the fat.

Of course correlation is not causation, and I doubt that 10,000 genes are involved in actually producing hibernation or mitigating its effects. (After all, humans have only about 25,000 protein-coding genes—more if you include as “genes” bits of DNA that do something but don’t produce proteins—and bears can’t differ that much from us. There may be changes in that many genes, but many of these may simply be side effects of natural selection changes the expression of many fewer genes.

But it’s clear that genes involved in insulin usage and sensitivity work differently in hibernating versus nonhibernating bears. What are the cues that turn these genes on and off? I doubt that we know, and the paper doesn’t say, but a good guess is that this has to do with environmental factors indicating the impending arrival of spring or fall: cues based on day length or temperature.

But what about the bears’ muscles? Why don’t they atrophy? Again, it’s due (as it must be) to differential activation of genes. And again, the gene products responsible seem to be circulated in the blood serum.

The paper below from PLoS ONE (click on screenshot to read; pdf here and reference at bottom), implicates both the blood serum and the genes involved in maintaining muscle.

The Japanese researchers bathed cultured human skeletal muscle cells in serum from either hibernating or non-hibernating black bears. What they found was significantly less degradation of protein when hibernating-bear serum was used. This appeared to be based on a gene-induced decrease in levels of two proteins and an increase in the level of another, which act in concert to preserve protein levels in the cultured cells. (The protein made in reduced amount breaks down muscle while the others promote and sustain muscle growth.) Altogether, changes in gene action appears to keep the bears’ muscles fairly intact as they go through hibernation.

Now these are cultured human cells, not bear cells, and the experiment was done in vitro rather than in vivo, but it gives a very promising lead to how bears keep their muscles strong during hibernation.

The Post article also lays out the potential uses of this information in human health.


Potentially, these same eight proteins, which also appear in human blood, might at some point be harnessed pharmaceutically to improve insulin sensitivity or treat diabetes and other metabolic disorders in people, Kelley said. But that possibility lies far in the future and requires vastly more research with bears and us (although perhaps not in close proximity).


The ultimate aim of this research, [author] Miyazaki said, is to isolate and refine all of the substances and processes in hibernating bears’ blood and elsewhere in their bodies that protect them from muscle wasting, with the hope that these same elements might treat atrophy from bed rest or aging in people.

“There is probably no better way to maintain a healthy lifestyle than through physical exercise,” he said, but for people who cannot be active, for whatever reason, the internal operations of slumbering bears might someday provide respite from frailty.

It’s important to remember that these remarkable changes are certainly due to evolution via natural selection, as it’s hard to imagine a random process like genetic drift causing evolutionary changes that are certainly adaptive.

As Ernst Mayr emphasized, many important evolutionary changes in animals begin with a change in behavior. Perhaps bears in cold areas survived better if they underwent a period of low activity during winter when food is scarce (this behavioral change could reflect genetic variation), and then those quiescent bears who also had mutations affecting fat and muscle metabolism would be those most likely to survive hibernation, leaving their genes to future bear generations.


Miyazaki M, Shimozuru M, Tsubota T. (2022) Supplementing cultured human myotubes with hibernating bear serum results in increased protein content by modulating Akt/FOXO3a signaling. PLoS ONE 17(1): e0263085.

Svante Pääbo nabs Medicine and Physiology Nobel

October 3, 2022 • 7:30 am

I had totally forgotten that it’s Nobel Prize season, and the first one, the Medicine or Physiology Prize, was awarded today—to the human evolutionary geneticist Svante Pääbo, a Swede. The reader who sent me the news had these immediate reactions:

  • Highly unusual that there is a single winner nowadays
  • How often has the prize gone to an evolutionary scientist (of any shape or form) ?
  • Probably being Swedish helped a bit!

Yes, the last “solo” prize was given in this field in 2016 to Yoshinori Ohsumi for his work on lysosomes and autophagy. As for the evolutionary biology, I’m not aware of anybody working largely on evolution who has won a Nobel Prize. The geneticist Thomas Hunt Morgan won one, but it was his students who became evolutionary geneticists.  I also remember that when I entered grad school, my Ph.D. advisor Dick Lewontin was helping prepare a joint Nobel Prize nomination for Theodosius Dobzhansky and Sewall Wright, but Dobzhansky died in 1975 before it could be submitted, and posthumous Prizes aren’t given.)

Of course, Pääbo has worked on the evolution of the genus Homo, and a human orientation helps with the Prize, but his substantial contributions fully qualify him for the Big Gold Medal.  As for him being Swedish, I don’t know if there’s some national nepotism in awarding prizes, but again, Pääbo’s work is iconic and no matter what nationality he was, he deserves one. And of course I’m chuffed that an evolutionary geneticist—one of my own tribe—won the Big One.

Click on the Nobel Committee’s press release or the NYT article below to read about Pääbo or go to his Wikipedia page.


Pääbo is the leader of a large team, and has had many collaborators, but it’s clear that, if fewer than four people were to get the prize for work on human evolution, Pääbo would stand out as the main motive force, ergo his solo award.  Sequencing the Neanderthal genome and estimating the time of divergence from “modern” H. sapiens (about 800,000 years)? That was Pääbo and his team. Finding the Denisovans, a separately-evolved group from Neanderthals? Pääbo and his team.  Discovering that both of these groups interbred with our own ancestors, and we still carry an aliquot of their genes? Pääbo and his team. Learning that some of the introgressed genes from Denisovans have conferred high-altitude adaptations to Tibetans? Pääbo and his team. And that some Neanderthal genes confer modern resistance to infections? Pääbo and his team.

The man can truly be seen as the father of human paleogenetics—and he’s five years younger than I? Oy!

Although born in Sweden. Pääbo works mostly in Germany. Here’s his bio from the Nobel Prize Committee:

Svante Pääbo was born 1955 in Stockholm, Sweden. He defended his PhD thesis in 1986 at Uppsala University and was a postdoctoral fellow at University of Zürich, Switzerland and later at University of California, Berkeley, USA. He became Professor at the University of Munich, Germany in 1990. In 1999 he founded the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany where he is still active. He also holds a position as adjunct Professor at Okinawa Institute of Science and Technology, Japan.

A prize for work in evolutionary genetics! Well done, Dr. Pääbo!

Svante Pääbo

And a bit of biography from the NYT article:

Dr. Pääbo has a bit of Nobel Prize history in his own family: In a 2014 memoir, “Neanderthal Man,” he wrote that he was “the secret extramarital son of Sune Bergstrom, a well-known biochemist who had shared the Nobel Prize in 1982.”

It took some three decades of research for Dr. Pääbo to describe the Neanderthal genome that won him his own prize. He first went looking for DNA in mummies and older animals, like extinct cave bears and ground sloths, before he turned his attention to ancient humans.

“I longed to bring a new rigor to the study of human history by investigating DNA sequence variation in ancient humans,” he wrote in the memoir.

It would be no easy feat. Ancient genetic material was so degraded and difficult to untangle that the science writer Elizabeth Kolbert, in her book “The Sixth Extinction,” likened the process to reassembling a “Manhattan telephone book from pages that have been put through a shredder, mixed with yesterday’s trash, and left to rot in a landfill.”

Free BBC broadcast: Three biologists (including Matthew) on their new science books

September 26, 2022 • 9:15 am

I can’t imagine NPR putting on a program like this; it’s long and science-y (without jokes), and intelligent. The moderator is not a radio announcer but a scientist.  What we have are three scientists discussing their new (or upcoming) books about genetics and evolution in a BBC panel moderated by geneticist and science journalist Adam Rutherford. You probably know that Adam himself has written several books on genetics.

The show is 42 minutes of discussion with 8 minutes of live audience questions. Here are the three participants and their new works:

Our own Matthew Cobb, Professor of Zoology at the University of Manchester. Matthew’s talking about his new book on genetic engineering, The Genetic Age: Our Perilous Quest to Edit Life. In the U.S. it’s called As Gods: A Moral History of the Genetic Age (out here November 15). I’ve previously highlighted some positive reviews.

Alison Bashford, Laureate Professor of History at the University of New South Wales and Director of the Laureate Centre for History & Population. Her new book is An Intimate History of Evolution: The Story of the Huxley Familyand deals with both Thomas Henry Huxley and his grandson Aldous Huxley. A positive review of her book is at the Guardian

Deborah Lawlor, a professor of epidemiology at the University of Bristol, is working on a book about the inheritance of diabetes in pregnant women in Bradford of both British and Asian descent. She’s also from Bradford where the show was filmed, and so is a local in two respects.

I recommend listening to it all, but if you want to hear just Matthew, he describes his book beginning at 27:43. But then you’d miss Bashford’s eloquent description of the Huxleys and their contributions.  One fact that I didn’t know was that both T. H. and Aldous Huxley suffered from depression (it was called “melancholia” then), which led Aldous to think about a genetic basis for their condition.

Click below to go to the show’s main page, where you can download the podcast.

And click below to listen to the show. Do it soon if you want to listen, as the BBC doesn’t keep its shows up long.

h/t: Anne

New paper claims to have discovered 17 English Jews killed in 12th-century anti-Semitic attack

September 4, 2022 • 9:20 am

After the Norman conquest of England in 1066, William the Conqueror invited Jews into England. Settling in places like Norwich, York, and Lincoln, they were presumably Ashkenazi Jews, who originated in Europe and the Middle East (my DNA tells me that I’m one of them.)  Their professions were, as a Smithsonian article (second below) recounts, mainly “financiers and moneylenders,” professions that were forbidden for Christians.

But although they were invited in, they weren’t loved, and were ultimately expelled from England in 1290. (Nobody likes the Jews!). History recounts that, around 1190, only 133 years after the Conquest, a group of Jews were killed by Christians who thought they’d do in a bunch of Ashkenazis on their way to the Third Crusade.

Or so the paper below, from a recent issue of Current Biology, tells us. It recounts a genetic analysis of 6 of 17 skeletons—11 adults and 6 children—found in 2004 in a well in Norwich near the location of the city’s ancient Jewish quarter.  This was 18 years ago, and you can see video and photos of mass grave in the “cold case” video below.

The genetic analysis of 6 of these individuals suggests that the skeletons were a group of Ashkenazis, probably ones killed in the 1190 massacre. Click on the screenshot below to go to the Current Biology piece (free access). You can download the pdf here, and I give the reference at the bottom.

First, here’s what was found (photo and caption from 9News.  (You can see a lot more in the video at bottom.)

At least 17 human bodies found at the bottom of a medieval well in Norwich were a group of Ashkenazi Jews who may have been victims of anti-Semitic violence during the 12th century. (NPS Archaeology/BBC)

After the remains were excavated, sorted, and sexed, they found 17 bodies, with 11 adults (a mixture of men and women) and 6 children. The bones were radiocarbon dated to between 1161 and 1216 (95% confidence interval), putting the burial right at the time the Jews of Norwich were killed.

Although a few of the bones were broken, that was from being tossed into the well (head first), which cracked some ribs and vertebrae. As for what killed the individuals, there’s no indication of that: no fractures or indications of blows. They were almost surely killed before being tossed into an empty well, perhaps by stabbing or cutting, or perhaps by smoke inhalation if their houses were burned.

Six of the individuals had DNA extracted from the bones for genetic analysis. The authors didn’t do complete genome sequencing, but did enough to determine that three of them, ranging from 10 years old to young adults, were full siblings—sisters. (You can tell the sex from both the bones and the DNA itself.) These three had identical mitochondrial DNA, showing that they came from the same mother. Another individual was more distantly related to these.

We are also at the stage where we can determine with near certainty the hair and eye color of individuals from DNA, for we know which genes are involved in those traits. As the paper notes,

Two individuals were inferred to have had brown eyes, one with “dark” and one with “light” hair (SB605 and SB676, respectively), while the 0- to 3-year-old boy (SB604) was inferred to have had blue eyes and red hair, the latter of which is associated with historical stereotypes of European Jews.

I wasn’t aware that this is a historical stereotype of European Jews; I would have thought that most of them, like me, had dark hair and eyes, but what do I know from historical stereotypes? And of course two of the three were dark, so what we see is variation, not really a confirmation that these were Ashkenazi Jews. The evidence for that comes from genetic data. First, here’s a reconstruction of the faces of two individuals—a young one and an older one—from both DNA and skulls. These are of course very rough, and don’t tell us much. (I wonder, now that 23andMe has a huge sample of my own genetic data, if they could estimate what I look like from my DNA alone. They already guessed correctly that I have dark hair and eyes.)

The genetic evidence for who these individuals were rests on comparing their DNA with several modern populations from Western Eurasia, as well as looking for sequences of genes that cause disease in modern Ashkenazi Jews. (As an inbred group that probably went through a severe reduction in population size, as well as having substantial intermarriage—”endogamy”—living Ashkenazi Jews have a high frequency of genetic disorders, the most famous being Tay-Sachs disease.

You can see below a plot of where the six individuals whose DNA was analyzed (the black dots) fall in a cluster study—made from what’s known as a principal-components analysis—of the various modern populations. analyzed. Data from living Brits are in the small purple cluster at about 9 o’clock, far away from the Norwich individuals, who fall closer to Southern European and Middle Eastern populations, including modern Ashkenazi Jews, Turkish Jews, and North African Jews. As the authors conclude:

We projected the six Chapelfield genomes on a PCA defined by variation among modern western Eurasian population samples, including modern Jewish individuals. All six Chapelfield [Norwich] individuals project well away from present-day British samples, as well as northern Europeans more generally. Instead, they partially overlap with Southern Europeans, close to Cypriots, modern Ashkenazi, Turkish, and North African Jews. These results are consistent with the Chapelfield individuals having Jewish ancestry (cf. Kopelman et al.)

Click to enlarge:

There’s one more line of evidence that the individuals in the well were Ashkenazim. This is the observation that the six individuals analyzed had a much higher similarity of DNA sequence at the “disease genes” to modern Ashkenazis than to other populations. As the authors note:

To explore this further, we formulated a likelihood function to calculate the exact probability of the six individuals’ observed allele reads at the 159 disease loci, given the allele frequencies of any proposed population.

. . . The maximum likelihood read error rate estimates are notably similar (0.87% and 0.94%, respectively), and crucially these results show that the data are 4,615 times more probable under a model that these individuals were sampled from the modern Ashkenazi population than they were sampled from the modern non-Finnish European population. This approach assumes the six individuals are randomly sampled from either population. Further assessment of the effect of this assumption given that three individuals are siblings suggests that in the case of these data our assumption has a conservative effect on the likelihood ratio

This is scientific jargon saying that, in the end, there’s a much higher likelihood that these genes came from Ashkenazim (modern ones) than from modern European populations. (I’m not sure why they exclude Finns, save that Finns have a high proportion of genes from ancient Siberia.)  The high frequency of alleles that, when homozygous (two copies needed), cause genetic disease, suggest that any “bottleneck” in population size of the Ashkenazi must have occurred before these individuals were killed. That’s several centuries earlier than historians have suggested.

The best guess, then, is that the 17 individuals were Ashkenazi Jews killed by Crusaders who wanted to do in a few Semites on their way to doing in some Muslims in Constantinople. But not every scientist agrees. The Smithsonian piece quotes a dissenter:

Speaking with NatureEran Elhaik, a population, medical and evolutionary geneticist at Lund University in Sweden, casts doubt on the DNA analysis, arguing that the team identified the individuals as Ashkenazi Jews “because that was the only population that they considered.” In response, co-author Ian Barnes, an evolutionary geneticist at the Natural History Museum, tells Nature that local archaeologists and historians know of few other “plausible alternatives” in terms of “other groups that might [have been] in medieval Norwich at the time.”

Given that the paper compared the skeletons in the well with modern populations, most of which were not Jewish, I’m not sure what Dr. Elhaik is on about, but he has published a paper claiming that principal-components analysis is faulty and can be biased to get the results you want. That said, the confluence of the historical and genetic data, and the lack of any other plausible explanation for this slaughter (plus the spot-on estimates from carbon dating to the same period where Jews were being killed in the area), convinces me that the authors are probably right.


Here is an hourlong “Cold Case” video from 2018 about the finding of the bodies, made before any genetic work was done. I haven’t watched the whole thing straight through, but you can see the discovery of the skeletons, other forensic estimation, and people’s best guess at the time what the mass grave told us: 


Brace, S. et al. 2022. Genomes from a medieval mass burial show Ashkenazi-associated hereditary diseases pre-date the 12th century. Curr. Biol.

The imminent cancellation of Emily Willoughby: a fight to remove her from Wikipedia

August 21, 2022 • 12:30 pm

In a post from Wednesday called “The ignorant and misguided demonization of a behavior geneticist,” I described the mob of people going after Emily Willoughby, a behavioral geneticist and paleoartist (someone who depicts ancient and extinct species). Note that the link to her name is likely to disappear very soon, since it’s an endangered Wikipedia entry that is the subject of this post.

Here’s what you see when you go to her page.

Emily is currently not only drawing, but is a postdoctoral researcher in personality, individual differences, and behavior genetics at the University of Minnesota Twin Cities.

It all started with the bonkers email, below falsely accusing Willoughby of being tied to eugenics, racism and classism (she doesn’t work or approve of those issues). Not only that, but the tweet is doubly slimy in saying that she “believes, or is at least indifferent to, the myth that intelligence has a racial component.” Notice the two alternatives offered, both of which are false (she isn’t tied to that work, and she repudiates racial extrapolations from within-population genetic data). “At least is indfferent to” is about a weaselly as you can get.

Nevertheless, whoever this clown Prehistorica is, he or she set off a tirade of ignorant claims about Willoughby, some of which I highlighted and rebutted in this post. Ignorance, hatred, and innuendo can bring get your cause to go a long way on Twitter!

And below is one of the results: injuries to Emily’s career, based on false accusations. Here, one of her collaborators disassociates himself for her, and for no good reason save that she has been “accused”.  How much less empathic can you get? And of course Naish will not discuss his misguided decision. You’d think he’d check the facts before writing something like this:

But of course nasty words on Twitter or social media are not enough. You have to get the person cancelled—erased. And that’s what people are trying to do to Emily’s Wikipedia page.  A reader (afraid of his/her own demonization), sent me this information about the effort to get Willoughby’s page erased.

I’d like to bring your attention to what’s been happening over the past couple of days to the paleoartist and behavioral geneticist Emily Willoughby. Emily is the co-author and illustrator of the anti-creationism book that you covered here:

The main Twitter thread attacking her is this one:

And Emily posted this thread in response:

The assumption underlying most of these attacks is that all research about the genetic basis of human intelligence is inherently supportive of racism or eugenics. None of Emily’s published research involves race or eugenics directly. Even Eric Turkheimer, a behavioral geneticist who’s known for opposing any research in this field that relates to race, thinks that these attacks are unreasonable.

The reader sent me a subsequent email:

The mention of this [Wikipedia erasure] was buried in the comments to your post about Emily, so I’d like to make sure you’ve noticed that the Wikipedia article about her is about to be deleted. There are currently ten people arguing to delete the article and only one arguing to preserve it, so it’ll be deleted in a few days if nothing unexpected happens.

Most of the people arguing for deletion haven’t directly mentioned the attacks against Emily on Twitter, but it’s obvious that that’s the reason this is happening. There was a previous attempt to delete the article last year which was unsuccessful, and Emily has no less coverage in sources now than she did a year ago, but the thing that’s changed in the past year is that the people who edit Wikipedia’s paleontology related articles aren’t willing to defend her anymore. There’s also been no attempt to delete the Wikipedia articles about paleoartists who are much more obscure than Emily, such as Julio Lacerda or Davide Bonadonna.

I think this is another example of how Wikipedia is increasingly influenced by ideology nowadays, as you recently posted about here.

If you go to the Wikipedia “discussion page” that supposedly gives the reasons she doesn’t belong on the site, none of it is about her work on behavior genetics of intelligence. No, it’s about the claim that her artwork isn’t sufficiently good to merit her a page. Yet on the first attempt to cancel her, this wasn’t sufficient.

What is clear is that mob sentiment is now trying to get her page erased because a few yahoos falsely accused of her engaging in racist work on IQ. Nobody cares about the facts; an accusation is sufficient.

The people trying to hurt her career are reprehensible; humans lacking a crumb of empathy and wallowing in their own ignorance about the person they’re trying to cancel. And if Wikipedia erases her article, it will be shameful.

If there are readers willing to argue her cause on Wikipedia, I’d urge you to jump into the fray.


The ignorant and misguided demonization of a behavior geneticist

August 17, 2022 • 11:30 am

I don’t usually look at Twitter unless a reader sends me a tweet, and I never engage in Twitter battles. But I’ve heard enough about these squabbles—particularly when connected with someone’s “cancellation”—that I know that they’re rancorous, full of ignorance and hatred, and the participants are often anonymous, which is cowardly.

Today we’re going to look at one attempt at cancellation that particularly galled me, for the charges against the accused—genetic researcher and paleoartist Emily Willoughby—are not only unfair, but bespeak the profound ignorance of her critics.

This piling on is what happens when someone studies the genetics of IQ, but doesn’t even mention race.  It’s enough that one studies the genetics of this trait to bring out a pack of howling morons denying that there is IQ, that it has a genetic component, and then you claim that the student is a horrible person who must be a eugenicist or Nazi.

That kind of tirade, of course, derives from the empirical demonstration that ethnic groups differ in IQ, which has become taboo to mention. You don’t even have to mention race: all you have to say is the undeniable scientific fact that IQ (whatever it may be) is highly heritable within a group—that is, about 60% of the variation in IQ among, say, Europeans, is due to variation in their genes—and the Blank Slate Police come knocking. The implication is that if you deny this simple empirical fact, you must also think that variation among groups has a big genetic component (this is a faulty conclusion), and therefore must be a eugenicist hoping to sterilize or kill members of groups with lower IQs.

I wouldn’t have believed this kind of stupid extrapolation had I not seen it for myself.

As I said, Willoughby is a geneticist: a postdoctoral researcher in personality, individual differences, and behavior genetics at the University of Minnesota Twin Cities. She is also a paleoartist, known for depicting extinct creatures. I gave a positive review in 2018 to one of the books she illustrated, a pro-evolution book called God’s Word or Human Reason?: An Inside Perspective on Creationism.

Here’s Emily’s bio from her research webpage (there’s another on her art webpage).


Emily is also engaged in the new genome-wide association mapping (GWAS) of various human traits, a technique I described in my review of a book by Kathryn Harden on the method. It’s a new way to find small regions of the genome that contribute to variation among people in behavioral and physical traits. One of the most well-known papers describing its results is the paper below published in Nature Genetics. As you see, Emily is an author (click to read).

Using a huge sample (1.1 million people), and one “race” (Americans of European ancestry), the authors found fully 1271 variable regions of the genome (“single-nucleotide polymorphisms”, or SNPs) associated with differences in educational attainment (how far you go in school) and cognitive performance (how you perform on tests). These SNPs accounted for about 10-13% of variation among “Europeans” (i.e., U.S. whites). Because the “heritability” of the trait measured by standard methods (parent-offspring correlation, twin studies, and adoption studies) is substantially higher than this (around 0.6), the GWAS results imply that there are a ton of variable regions in our genome that affect academic and cognitive performance within an ethnic group, but have effects to small to measure. Other studies give similar results.

Now this isn’t IQ per se, but these traits are highly correlated with IQ. Whatever IQ measures, there’s no doubt that it’s strongly correlated with various measures of “conventional” success in life, including academic achievement, financial success, income, socioeconomic status, educational attainment (one of the traits measured in the paper below) and occupational level attained. There is no controversy about this, or about whether IQ itself has substantial heritability within a population.

Now, what does someone bent on stirring up trouble and besmirching a genetic researcher’s reputation do with the fact that Emily works on stuff like the above? Here’s what—they issue a defamatory tweet, full of misrepresentations.

Where does one start hacking through this thicket of nonsense? First, how can a measurement be a “pseudoscientific myth”? It is an estimate, and one that is not only highly heritable, but highly correlated with conventional measures of success in life. (Note: I am not saying that people with higher IQ’s are “better”: many of them are jerks, and there are lots of valuable human qualities, like empathy, not measured by IQ. All I’m saying is that IQ measures something that correlates with academic, occupational, and financial achievement.)

“Prehistorica”‘s deliberately misleading slurs go on.  Emily’s research, as you can see by reading her c.v., is NOT “directly tied to eugenics, racism, and classism.” Yes, in the past bigoted researchers have made those ties, but to imply that Emily is doing that is simply a lie. She works on genetic analysis and heritability of behavioral traits within populations.

And saying that Emily is “indifferent to the myth that intelligence is a racial component” is a way of implying that she knows this is true, but doesn’t pay attention to it. In fact, we don’t know whether it’s a myth, because we have very few data. But at any rate, Emily does not deal with the issue of racial differences in cognitive abilities. This is just a smear.

Below is some approbation for one of her papers, which measures the heritability of IQ using correlations between parent and offspring in both adoptive and biological families. (This is one of the better ways to measure heritability, since family environment is presumably similar among the groups but genetic relatedness differ drastically.)

In the graphs below, notice the difference in the heritability using IQs of parents correlated with biological offspring (0.42, or 42%), versus that between parents with their adoptive offspring. (Parents and biological offspring were almost all whites of European ancestry, while adoptive children were 21% white but with 66% Asian and 13% adoptees of other groups. Heritabilities are the slopes of these regression lines.) In contrast to biological parents and their offspring, the heritability of IQ using parents and adopted offspring was much lower: either 10% or 6%, depending on how it was measured. This shows a small “common environment” effect, but a much larger effect of genes—a finding in line with that of previous studies.

These are respectable studies in peer-reviewed journals, conducted using standard protocols, and giving results that are in line with previous work or, in the case of GWAS studies, with contemporanous work.

But that doesn’t matter. Watch the yahoos go to town on Twitter! We start again with Prehistorica, as all the another tweets are responses to his tweets.

The tweet above is hilarious. The correlation (as instantiated through the regression line) is evident to anybody who has studied statistics, yet “magpie” can’t believe that this is a correlation. Magpie is an idiot.

All these people are shocked by the misguided tweet of Prehistorica, though they clearly know nothing about Willoughby’s research. This is how someone’s reputation is taken down by ignoramuses. Note the people who completely write Willoughby off because of what Prehistorica says, yet what he says is ignorant gibberish. Still, all the Twitterites, ignorant of modern behavioral genetics, fall in line like lemmings. (Willoughby does have a few defenders.)

“Vile, spiteful person.”  How did they divine that from Willoughby’s work?

The one below is even funnier in its stupidity than the one about correlations.  My response is “YES, THIS IS HOW PHENOTYPES WORK.” A phenotype is any measurable trait of an organism, and it can be morphological, physiological, and yes, behavioral. For any measurable trait (“phenotype”) you can calculate a heritability, assuming you do the work right and control for common environment, nongenetic inheritance (wealth) and the like.  So, “Lost Ovis”, take a course in biology for crying out loud!. The fact is that every “behavior” in “Lost Ovis”‘s table is a phenotype that one can use to figure out how much variation among individuals in the behavior is due to variation in their genes.

Here’s a graph from one of Emma’s papers showing estimates of heritability in many “phenotypes”, including behavioral ones.  The scientific estimates are on the Y axis, but do correlate pretty well with laypeople’s off-the-cuff estimates. Note that “intelligence” is estimated by both groups to have a heritability (or, for laypeople, “estimate of genetic influence”) of about 0.6.

Now one attacker above mentions a picture commissioned by Willoughby and her boyfriend in 2009. Here’s the “Nazi” picture that was commissioned, used above to further denigrate Emily. I wrote her and asked her what that was about, and she replied (with permission to quote):

The explanation for the drawing of dinosaurs in Nazi uniforms is just that my boyfriend and I were feathered dinosaur artists and chess fans, and thought it was funny to be offensive 13 years ago. We would never think of asking someone to draw something like that nowadays, nor expressing humor about it in public.

Emily has grown up since she drew it, and, truth be told, I don’t find it so offensive myself. Raptors dressed as Nazis is a trope of comparison, and it doesn’t make fun of any group except raptors. But Emily thought it was necessary to explain it.  I, for one, am satisfied with her explanation and regret, but the trolls will never be.

Emily, distressed that she was being taken apart on Twitter for no good reason save ignorance, decided to write a series of tweets in response. I’ve put the ten of them below.

Although it’s clear from Emily’s final tweet that she certainly does not condone eugenics, she decided to email me further to give a clearer statement about her beliefs. Here it is, unsolicited by me.

I unequivocally denounce eugenics and those who advocate for it. I cannot control those who follow me and argue in favor of ideologies I abhor. I did not invite them. The checkered history of my field is part of why I care about improving it by doing good research and methodology commensurate with our modern notions of human rights. But if people start believing behavioral genetics is a racist field of research, only racists will conduct it. Please don’t let that happen.

Good enough for you trolls? Can you see Emily as a good researcher and a human being again?

I didn’t think so.

This has been an object lesson to me on Twitter, and has further confirmed my unwillingness to read comments on my own Twitter posts (they go directly to the site from my WordPress account) as well as my refusal to engage in Twitter fights.

Yes, Twitter can be useful in scientific communication by publicizing new papers or results quickly. But it can also be used by scientific know-nothings to smear researchers. And that was what was done to Dr. Willoughby here. Both Prehistorica and his/her vicious acolytes should be ashamed of themselves. They won’t be, of course, because, being Woke, they think they’re doing God’s work. Ignore them.

Horizontal gene transfer in insects: widespread, but what does it mean?

July 22, 2022 • 12:45 pm

“Horizontal gene transfer”, henceforth “HGT”, is the process whereby a gene is moved between species by methods other than direct reproduction (the latter is called “vertical gene transfer”). Today I’ll write about a new survey published in Cell, trying to find out how often this process moves genes into the DNA of insects.

It’s surprisingly common, and the authors found one case in which a gene transferred into Lepidoptera from bacteria seems to help moths and butterfly males get mates. But HGT is not common enough to screw up the evolutionary trees of insects. As I said, it’s commoner than I thought, but it’s still pretty damn rare.

(I note that you can have gene transfer between species via reproduction, too, if you allow for a little bit of interbreeding between “species”. Although I think that Neanderthals should be considered members of our own species H. sapiens, we did have some vertical gene transfer in the past when members of the two groups mated. The hybrids passed on their genes to modern humans, and the result is that is that many of us carry a few Neanderthal genes. That’s via reproduction, though, not infection, which is the way HGT occurs.)

Typically, in HGT a bacterium, virus, or other microorganism that lives within a eukaryote host transfers some of its own genes into the host genome, or, in some cases, acts as a vector carrying genes from other organisms, including fungi, plants, or other animals.  But HGT is not really a “non-Darwinian process” that results in a drastic revision of the Modern Evolutionary Synthesis. No, Darwin didn’t know about this—he didn’t know about genes, either—but we can consider the introduction of a novel gene from a very different species as a type of mutation (granted, a big one), producing variation in the recipient species that can be acted on (increased or eliminated) by natural selection, or which could be “neutral”, neither enhancing nor reducing fitness.

And although HGT in principle could mess up evolutionary trees if it were very common, that doesn’t seem to be the case. In fact, HGT doesn’t occur that often, and is actually detected by finding a gene in an organism that, via sequencing, looks as if it came from a different species. Seeing such a discrepancy depends, as it did in this study, in knowing evolutionary trees. We wouldn’t be able to detect HGT if trees were all messed up by the process.  So, no, this new paper doesn’t show that “Darwin was wrong”, much as the Kuhnians want that.  I’ll emphasize this at the end!

With that out of the way, what do we know about the process of HGT? We know that it can be effected by various vectors, usually microorganisms, occurs in a lot more species than we thought, is a fairly recent discovery, and on occasion can create “mutations” that are good for the recipient species. It’s especially widespread among bacterial “species,” in which lots of genes, including antibiotic resistance genes (unfortunately for us) can be transferred widely. That’s how bacteria can quickly evolve resistance to new antibiotics: genes for resistance, favored by natural selection, can be spread among several species via HGT.

What about organisms with true cells—the “eukaryotes”? We know about lots of cases of HGT (see the Wikipedia article on HGT for a good summary), but only three in which HGT has transferred a gene that rose in frequency in the new host by natural selection. Here are the examples cited by Li et al.:

In addition to pieces of symbiont genomes introduced into insects via HGT, some studies have reported the transfer of a single or few genes from fungi, bacteria, plants, and viruses (e.g., Boto, 2014Husnik and McCutcheon, 2018Irwin et al., 2022Perreau and Moran, 2022). The functions of these transferred genes appear ecologically important; for example, carotenoid biosynthesis genes transferred from fungi to aphids contribute to aphid body coloration (Moran and Jarvik, 2010), genes that neutralize phenolic glucosides acquired by whiteflies from plants contribute to whitefly detoxification capabilities (Xia et al., 2021), and a parasitoid killing factor gene transferred from a virus to lepidopterans contributes to lepidopteran defense (Gasmi et al., 2021).

As far as we know, then, the vast majority of adaptations within eukaryotic species arose not via HGT, but via simple mutations in genes already present on a species’ genome: the “Darwinian way.”

However, research on HGT has been spotty, often highlighting single case studies. Now, a group of 13 authors from China have published a systematic survey of insects, examining the possibility of HGT in 218 species taken from 11 of the 19 orders of insects.

Click on the screenshot below to read the article for free, get the pdf here, or click on the reference at the bottom. If you can’t access the article, a judicious inquiry might yield a pdf.

The authors looked for horizontally transferred genes by examining whole-genome sequences of species and looking for regions of the DNA where an insect’s genome was not related to other insects in its group, but to a very distant group: a discrepancy in the “family trees” of genes. They then determined the protein sequences of those putative products of HGT to ensure that the genes that were transferred actually did something—i.e., make a protein.

They found that among the 218 species, 192 had protein-coding genes horizontally transferred from other species. This transfer involved 1,410 genes in 741 transfer events (more than one gene can be transferred in a single event). Most of the genes inserted into insect DNA came from bacteria: here’s the rundown:

Sources of HGT genes in insects:

Bacteria: 79.0% of the transferred genes
Fungi: 13.8%
Plants: 3.0%
Viruses: 2.8%
Other groups: 1.8%

As one would expect—given that virtually every animal harbors bacteria, and because bacteria are good at transferring their genes to other genomes as well as acquiring genes from hosts—we see the bulk of HGT-transferred genes coming from bacteria. It’s likely that genes from fungi or plants were transferred by viruses or bacteria, but there can also be direct transfer in a variety of ways, including ingestion. See the section on “eukaryote to eukaryote transfer” in Wikipedia, which also notes that there’s a possibility that some of our own genes are there because of HGT:

One study identified approximately 100 of humans’ approximately 20,000 total genes which likely resulted from horizontal gene transfer, but this number has been challenged by several researchers arguing these candidate genes for HGT are more likely the result of gene loss combined with differences in the rate of evolution

Not all groups of insects are equally susceptible to HGT. Here’s a figure you should enlarge, showing the phylogeny of insects studied, with the height of the bars representing the number of genes in each species acquired by HGT.  You’ll have to click on this one to see it all. But what’s clear, even in a small figure, is that Lepidoptera (butterflies and moths) carry a lot more horizontally transmitted genes than insects in other orders (look from 3-6 o’clock below):

As the authors note:

. . . . . we found that the order Lepidoptera acquired by far the highest average number of HGT-acquired genes (16 genes per species), followed by the orders Hemiptera (13 genes per species), Coleoptera (6 genes per species), Hymenoptera (3 genes per species), and Diptera (2 genes per species).

Many of the “HGT genes” in different Lepidopteran species are the same ones, implying that they had already been put via HGT into the common ancestor of the group and then were transferred vertically through reproduction, distributed into the various butterfly and moth species that evolved later. One of the transferred genes seemed to have adaptive value in Lepidoptera; more on that shortly.

Here’s a figure of who the donor species are. The overall picture was given in my list above, but this shows which subgroups of bacteria are the major vectors:

This also shows—take my word for it—that (mainly bacterial) groups that are symbiotic with an insect species (i.e., living within it or associated with it) were the most likely sources of horizontal gene transfer. That of course is also expected. You can’t get genes from an unrelated species unless the vector is nearby.

Finally, there’s one possible case of an adaptive HGT. That is the gene LOC105383139, horizontally transferred to the last common ancestor of Lepidoptera from the bacterial genus Listeria.  We don’t know what it does in the bacterium, but it does have one effect on a species of moth. Because LOC105383139 is in the genomes in all lepidopterans, Li et al. used the CRISPR-Cas9 gene editing technology to simply remove it—snip it precisely out of the genome—from one species of moth. the diamondback moth (Plutella xylostella), which can be reared fairly easily in the lab.

Li et al. found no significant effect of gene removal on any morphological or developmental character in the “snipped” moths, but the “knockout species” did have a much lower number of offspring from each mating compared to the normal moth having the gene. Upon further study, which I won’t describe, Li et al. found that the knockout males don’t court any females as ardently as normal males who carry the transferred gene. Normal moths also copulate more often than the edited ones. For some reason, since we don’t know what the gene does in either bacteria or moth, it is a mysterious “Casanova” gene”.

The diamondback moth

The upshot: In insects, at least, horizontal gene transfer is surprisingly common, with 88% of the 218 species examined having at least one gene in their DNA that came from another species. It’s widespread, too—at least one species in each of the 11 orders of insects examined (8 orders weren’t examined) having at least one HGT-acquired gene.

Of the species examined, butterflies are by far the most common carriers of transferred genes, with an average of 16 such genes per species, with the Hemiptera—true bugs—coming in second at 13.  In butterflies—at least in the one species examined—one of the HGT loci appears to have enhance mating and courtship, and that’s how it may have spread when it infected the genome of the common ancestor of all living moths or butterflies.

Finally, the big question: does this show that because evolutionary trees don’t exist, “Darwin was wrong”? Not on your life!

As I wrote in a previous post, there’s a difference between gene trees (the evolutionary history of a particular form of a gene) and species trees: the relatedness of groups of organisms that formed species as populations. Unless HGT is very, very common, the chance that it will mess up population trees—the trees of life that most concern evolutionists—is almost nil. Butterflies have thousands of genes, but each species has on average only 16 acquired from a different species. That is NOT going to mess up evolutionary trees. It’s a very small bit of noise in an overwhelming phylogenetic signal.

So, while Darwin was wrong about some things, we have no sign at all that he was wrong about the existence and importance of evolutionary trees that show how species are related. Nor was he wrong about variation that arose within species being the primary fuel for natural selection. HGT is fun and interesting, and a novel way of getting mutations and adaptations, but it hardly affects our general view of evolution.


Reference:  Li, Y. et al. 2022. HGT is widespread in insects and contributes to male courtship is lepidopterans.  Cell, DOI:

Once again: are “races” social constructs without scientific or biological meaning?

July 19, 2022 • 9:20 am

Every day, it seems, I hear that “races have no biological reality or meaning; they are purely social constructs.” And that statement is somewhat misleading, for even the crudely designated races of “white, black, Hispanic, and East Asian” in the U.S. are, as today’s paper shows, biologically distinguishable to the point where if you look at the genes of an unknown person, you have a 99.86% chance of diagnosing their self-identified “race” as one of the four groups above. That is, if you ask a person how they self-identify as one of the four SIRE groups (SIRE: “self identified race/ethnicity), and then do a fairly extensive genetic analysis of each person, you find that the groups fall into multivariate clusters.

More important, there’s little deviation between one’s SIRE and which genetic cluster they fall into. Over 99% of people in the sample from this paper can be accurately diagnosed as to self-identified race or ethnicity by looking at just 326 regions of the genome.

This in turn means that there are biological differences between different SIREs, so race cannot be simply a “social construct.” This is in direct contradiction between the extreme woke view of “race”, as expressed in the Journal of the American Medical Association, a statement I discussed in an earlier post:

Race and ethnicity are social constructs, without scientific or biological meaning.

Nope, and we’ve known that statement is wrong for nearly 20 years. Of course, if you take “biological meaning” as “data show that there are a finite number of distinct groups with huge genetic differences”, then it is a correct statement. But nobody thinks that any more except for racists or those ignorant of modern population genetics in humans.

The meaning of the biological reality adduced in papers like the one we’re discussing today is this: genes can be used to diagnose biological ancestry, which is surely involved in one’s SIRE. And therefore “races” or “ethnicities” aren’t just made-up groups, but say something about the evolutionary origin of group members.

As I said, the “old concept” of races as a small number of genetic groups that differ strongly in their genes is dead. But there are still groups, and there are groups within groups, and groups within groups within groups. Thus genetic variation in our species is hierarchical, as expected if variation among groups evolved in geographically isolated populations, between which there was some but not complete mixing.

This view of human variation leads me to abandon the use of the word “race” in general and use “ethnicity” instead. I’ll use “race” in this article, though, as I’m addressing the JAMA statement above, and also using individuals’ own diagnosis of their own “race”.

I’ve emphasized this before—in August of last year. There I cited the 2002 paper of Rosenberg et al. reporting that “one can show by using data from many genes and gene sites, and clustering algorithms, that humanity can be shown to form genetic clusters that correspond to geography (different continents or subcontinents), which of course correspond to evolutionary history.” As I also said then,

. . . . the paper of Rosenberg et al.,. . .  shows that the genetic endowment of human groups correlates significantly with their geographical location (for example, if you choose to partition human genetic variation into five groups (how many groups you choose is arbitrary), you get a pretty clear demarcation between people from Africa, from Europe, from East Asia, from Oceania, and from the Americas. (To show further grouping, if you choose six groups, the Kalash people of Asia pop up). This is one reason why companies like 23 And Me stay in business.

This association of location with genetic clustering (and these geographic clusters do correspond to old “classical” notions of race) is not without scientific meaning, because the groupings represent the history of human migration and genetic isolation. That’s why these groups form in the first place. Now you can call these groups “ethnic groups” instead of “races”, or just “geographic groups” (frankly, you could call them almost anything, though, as I said, I avoid “race”), but they show something profound about human history. The statement in bold above could be used to dismiss that meaning, which is why I consider that statement misleading.

The Rosenberg et al. paper was published two decades ago, and since then we are now able to look at more genes (potentially the entire genome of individuals) and use bigger samples over smaller areas. When we do that, we’re able to see the clusters within clusters. Here’s a reference to a 2008 paper:

Even within Europe,a paper by Novembre et al. reported, using half a million DNA sites, 50% of individuals could be placed within 310 km of their reported origin and 90% within 700 km of their origin.. And that’s just within Europe (read the paper for more details). Again, this reflects a history of limited movement of Europeans between generations.

I wanted to delve a bit into the 2005 paper of Tang et al. (mentioned in my earlier post), because it concentrates on self-reported race or ethnicity, not geographic origin, but also looks at variation over space. geography. Click on the title below to read the paper (pdf here and reference at bottom).

Tang et al. got their data from a study of hypertension in which individuals gave blood and also indicated their self-identified race as one of the four groups mentioned above. Then, each of the 3,636 individuals (taken from 15 geographic locales in the U.S., and three from Taiwan) were analyzed for 326 “microsatellite” markers—short repeated segments of DNA. (These segments may not all be independent because of genetic linkage, but certainly a lot of them are independent. The authors don’t discuss this issue, which is relevant but not invalidating.)

Tang et al. then determined whether the microsatellite data fell into clusters using on multiple genes and the clustering algorithm “structure”—the method also used by Rosenberg et al. to show ethnic variation was correlated with geography. Remember, the Tang et al. study took place mostly in American populations, with each SIRE sampled from several places. But the geographic sampling within the U.S. was limited (e.g., “Hispanics” came from only one place in Texas), and this is a potential problem.

Tang et al. did indeed find clustering using multivariate analysis: here are the clusters for all sites and SIRE combinations. Note that there are four clusters: one each for self-identified Caucasians from 6 populations (upper left), East Asians from 7 populations (middle right), African-Americans from 4 populations (lower left), and self-identified Hispanics from a single location (“K” from Starr County, Texas). Clearly we need more data from self-identified Hispanics from other areas, especially because “Hispanic” can denote many diverse ancestries.

The clusters are pretty distinct. Not only do are they distinct, but they match almost perfectly an individual’s self-identified race or ethnicity. As the authors note:

Of 3,636 subjects of varying race/ ethnicity, only 5 (0.14%) showed genetic cluster membership different from their self-identified race/ethnicity. On the other hand, we detected only modest genetic differentiation between different current geographic locales within each race/ethnicity group. Thus, ancient geographic ancestry, which is highly correlated with self-identified race/ ethnicity—as opposed to current residence—is the major determinant of genetic structure in the U.S. population.

As I said earlier “there is almost perfect correspondence between what “race” (or ethnic group) Americans consider themselves to be and the genetic groups discerned by cluster algorithms.  Because these are Americans, and move around more, the genetics reflect ancestry more closely than geography, though, as Novembre et al. found, in Europe geographic origin is also important. Americans move around more than Europeans do!I

In other words, individuals within a cluster are more geographically dispersed than what Novembre et al. found, so that membership in a cluster indicates ancient ancestry, not geographic origin. For example, members of the “East Asian” cluster come from Taiwan, Hawaii, and Stanford.

But to show that there are clusters within clusters, so that “East Asian” can’t be considered a “race” in the old sense, the authors repeated the cluster analysis using only the East Asian sample, and found that those of Chinese ancestry formed a cluster distinct from those of Japanese ancestry.  This is expected if self-identified ethnicity still reflects genetic differences that evolved in Asia. You would doubtless find similar relationships if you dissected Caucasians or African-Americans by the location of their ancestors.

What this shows, then, is that in the US, and in a limited sample of populations whose members self-identified their “race” into one of four groups, those groups can be differentiated using multiple segments of the genome. Not only that, but the differentiation is substantial enough that if you had an individual’s genetic information without knowing anything about them, you could diagnose their “self identified race/ethnicity” with 99.86% accuracy.

The take-home message:

In the U.S.—and in the world if you look at the Rosenberg study—one’s self-identified race, or race (again, I prefer “ethnicity”) identified by investigators—are not purelysocial constructs. Ethnicity or race generally say something about one’s ancestry, so that those members of the same self-identified race tend to group together in a multigenic analysis.

Note that this does not mean that there is extensive genetic differentiation between self-identified races. The old conclusion from my boss Dick Lewontin that there is more variation within an ethnic group than between ethnic groups remains true. But there is enough genetic difference on average that, if you lump all the genes together, the small differences accumulate sufficiently to allow us to diagnose a person’s self-declared race. Remember, these are “self-declared” groupings, so you can’t say they are imposed on the data by investigators. (That of course doesn’t mean that they aren’t social constructs. They may be in some sense, but they’re also social constructs that contain scientific information.)

So, the big lesson is that the JAMA was wrong: if races/ethnic groups can be diagnosed with over 99% accuracy by using information from many bits of the genome, then the statement “Race and ethnicity are social constructs, without scientific or biological meaning” is simply wrong. Race and ethnicity, even when diagnosed by individuals themselves, do have scientific biological meaning: namely, they tell us about an individual’s ancestry and where their ancestors probably came from. This is true in the U.S. (this paper) or worldwide (the Rosenberg et al. paper). Further, if you look on a finer scale, as Novembre et al. did, you can even diagnose what part of Europe a European’s ancestors came from (it’s not perfect, of course, but it’s pretty good).

This is not a new conclusion, and the papers I’ve cited are older ones.  There may be newer ones I haven’t seen, but I’d be willing to bet that their results would be pretty much the same as that above. Though genetic differentiation between groups is not large, it’s sufficient to tell us where they came from, confirming that geographic origin (reflecting ancient geographic isolation) is the source of what we call ethnic or racial differences.

Just remember this: when you hear that human race/ethnicity is a purely social construct, and doesn’t say anything about biology or evolution, that’s just wrong.

I shouldn’t have to point out that these genetic differences in no way buttress racism, for we don’t even know what they mean in terms of individual traits. But they do give us insights into evolutionary history. And that is something of scientific and biological meaning.


Reference: Tang H, Quertermous T, Rodriguez B, Kardia SL, Zhu X, Brown A, Pankow JS, Province MA, Hunt SC, Boerwinkle E, Schork NJ, Risch NJ. Genetic structure, self-identified race/ethnicity, and confounding in case-control association studies. Am J Hum Genet. 2005 Feb;76(2):268-75.

The Freethinker interviews Richard Dawkins

July 16, 2022 • 1:00 pm

I’m not sure about the nature of this website, The Freethinker, but it appears to be a rationalist and humanistic venue. But I haven’t investigated it in any detail as I really don’t care about its politics given that the article at hand is an interview with Richard Dawkins. Nor is the interviewer named; it’s just “Freethinker.”

Much of the interview you may already know about, as a lot of people here follow Richard, but I’ll highlight just a few intriguing questions and answers. The Q&As in the piece are indented, and click on the following to read:

The introduction includes this:

On his sitting room wall, I spotted two paintings that seemed somehow familiar. They turned out to be by Desmond Morris, the zoologist and surrealist painter; the larger one was The Expectant Valley, which served as the cover for the first edition of The Selfish Gene (1976). Dawkins later acquired them from the artist.

You’ll recognize the painting to the right:


‘Please focus on the science in your write-up rather than the politics,’ he said as I was leaving, ‘it’s more interesting.’ But that is the risk of being a public intellectual with a Twitter account: humans are an odd species, and with all the scientific insight in the world, it is hard to predict which ideas will do best in the meme pool. We leave readers to judge for themselves.

Well, the job of the interviewer isn’t to call attention to Twitter scandals, but to illuminate a person. The interview does a creditable job, but concentrates too much on social media and on memes—an idea I still consider clever but unfruitful, as it hasn’t explained much. More later  Here are a few parts of the interview that struck me.

First, and I love this, Dawkins explains what The Selfish Gene is about. It’s a masterpiece of concise summary:

Freethinker: In a nutshell, how would you sum up the book’s thesis?

Dawkins: Natural selection is the differential survival of genes in gene pools. Individual organisms can be seen as survival machines for the genes that ride inside them. When an individual dies, its genes die with it. If it dies before it reproduces, they really do die. Individuals are descended from an unbroken line of successful ancestors, where ‘successful’ means that they reproduced and their descendants therefore inherit the genes that made them successful. That is what makes living creatures such good survival machines for the genes inside them.

So when you look at an animal and ask why it does what it does, the answer is, for the good of its genes. Genes are ‘selfish’ in the sense that they look after their own self-preservation. Individuals do not – they are not selfish, or not necessarily. They may be driven to be selfish by the selfish genes, but the selfish genes may equally well drive them to be altruistic. The ways in which individuals work for the survival of their genes is dependent upon their ecology, and they may do it up trees or underground, or in water or in deserts. They may be predators or prey, parasites or hosts. But it is all fundamentally about the same thing, which is preserving the genes into the distant future.

“Freethinker” asks a lot of questions about memes (it’s the subject of more questions than any other), referring to a word coined by Richard as a “unit of culture” analogous to a gene. Like genes, memes can spread or not spread via selection, in this case cultural or psychological selection. As examples of memes, Dawkins has often used catchy “earworms”: music or phrases that you can’t get out of your head.  And Dawkins notes, as he has before, that religion is a particularly insidious and invidious meme, since it spreads both horizontally (via proselytizing) and vertically (through indoctrination of children). He mentions that religion is, perhaps, a highly successful meme because children are identified by their religion: we speak of a “Jewish child” or a “Hindu child” while we wouldn’t speak of a “Republican child” (poor kid!).

I don’t want to dwell on why I think memes, though a good idea, hasn’t proven especially fruitful. Richard himself—while he thinks the idea has been fruitful—mentions some of the difficulty of analogizing memes and genes. My own view and critique is best summarized in my review of Susan Blackmore’s enthusiastic book on memes, The Meme Machine; that review was in Nature in 1999 and you can read it here.

Another exchange below: “I don’t do movements?”

Freethinker: Looking back on the New Atheist movement in the 2000s, what was the high point of that for you?

Dawkins: I don’t do movements. I suppose when four books came out within a couple of years of each other: The God Delusion, Sam Harris’ End of Faith, Dan Dennett’s Breaking the Spell and Christopher Hitchens’s God is Not Great. By coincidence – there was not a conspiracy or anything. That might have been a high point.

The question below I consider confrontational, which after all is part of an interviewer’s job, but it’s naive and, indeed, trivial. It’s a “gotcha” question. (The whole interview is peppered with stuff like this.) Richard’s writing may sometimes be polemical, but I see it as “passionate”. Indeed, I give the first part of Dawkins’s response:

Freethinker: As a writer who has done a lot to popularise many areas of science, your style has been compelling and vivid, but often polemical. Why did you choose to write in this way?

Dawkins: I am not sure I see it as polemical. It is certainly read as polemical by religious readers. . , ,

But of course all critiques of religion are seen as polemical, just as all critiques of wokeness are seen as polemical. The best way to shut down discussion is to call a critic “polemical” or “strident”. But If you want to see real polemics, read Mencken!

On accommodationism and humanism, Dawkins gives good answers, though “logically speaking” is ambiguous pharasing by the interviewer.

Freethinker: People can be inconsistent, and believe incompatible things at the same time. But logically speaking, is it possible to be scientific and religious?

Dawkins: Many people are, but I am not sure whether that falls under the heading of logic. I suppose I have to say it is possible, yes. You could say the universe is such a mysterious place that it would be foolish to be over-confident one way or the other about whether some monster intelligence lies behind it. That would be, for me, bending over backwards an awful long way. It is very hard to be a logical theist.

Freethinker: Would you describe yourself as a humanist?

Dawkins: My only hesitation in describing myself as a humanist would be that it implies giving too much of a privilege to the human species as opposed to other species. I would like to call myself a ‘sentientist’ or something like that – with a moral regard for sentient awareness. A large part of that would be human, but no doubt there are other animals that are capable of feeling pain and suffering something like the way we are. With that reservation, I would call myself a humanist.

The interviewer asks Richard about the American Humanist Association revoking his Humanist of the Year Award (a rather boorish thing to bring up), and asks “Speaking as a scientist, what are your views about the transgender debate?” Did he expect Dawkins to come of as a transphobe, which he isn’t? You can read Richard’s answer for yourself.

Two more bits:

Freethinker: Over the course of your long career, what is the achievement of which you are proudest?

Dawkins: My second book, The Extended Phenotype (1982), about the visible manifestations of genes, because it has the most of me in it, and the most original thought. It is aimed at professionals rather than lay people, although lay people can enjoy it.

Richard has given this answer many times, and means it. I’ve read the book, and yes, of all his books, this has the most “meat”, and is the hardest to read and the most original. But the meat is savory, and if you’re feeling ambitious, you must read it.  I can understand why he is proudest of this, because I feel the same way about Speciation (written with Allen Orr). I’ve had two fairly successful trade books, but of everything I’ve written, I’m proudest of Speciation, also written for professionals. When I dip into that book from time to time, I think, “Damn! I could really think then!” I don’t think I could write it now, but I was at the right age to do so and my mental faculties hadn’t yet begun their inexorable decline.

However, if you consider everything that Richard has written, and combine literary quality with scientific explanation, I put The Blind Watchmaker at the top. Some of the prose is so lovely that it almost brings one—or at least a scientist—to tears. Those who claim, as E. O. Wilson did, that Richard is just a “journalist”, or that he’s not a scientist but a popularizer, should read The Extended Phenotype. 

Finally, the discussion turns to Dawkins’s next book:

Freethinker: What projects are you working on at the moment?

Dawkins: I am working on a new book called The Genetic Book of the Dead, which is aimed at the same kind of audience as The Selfish Gene. Its thesis is that an animal is a description of ancient worlds, of an ancestral world in which its genes are naturally selected. A sufficiently knowledgeable zoologist of the future should be able to pick up an unknown animal and read it as a description of a palimpsest of ancestral worlds in which its ancestors were naturally selected.

Now that is also an original idea of Richard’s, and in principle a good one. But as a biologist, I would have drilled deeper into this answer (there are no followup questions). How can you be so sure that you can read environments of the ancient past from a DNA sequence?  After all, that sequence is a palimpsest which has been overwritten continuously for three billion years. And don’t you have to know tons of information about developmental genetics to even start such an endeavor? We know that all very young vertebrates develop gill slits, and that’s a clue that we’re all descended from fish and that our ancestors lived in water. But how do you know which bits of the DNA produce the gill slits, allowing us to infer an aquatic ancestor? And how do you know whether the ancestor lived in fresh or salt water? We carry genes from extinct and unknown ancestors that lived in unknown environments; what way can we reconstruct those ancestors and their environments from just a DNA sequence? I’d ask for an example.

In fact, the fossil record combined with a good phylogeny can answer such questions, but I am doubtful about sequencing DNA as a way to infer the environmental forces that impinged on an organism’s ancestors. Dawkins describes DNA as a palimpsest, as it is, but when a document is overwritten millions of times, you lose a lot of the past information.

These are some of the things that I would have preferred to ask Richard about instead of his supposed “transphobia” and “polemic style.” In fact, I’d love to have this as part of a public conversation onstage, which I’ve had the honor of having with Dawkins several times. But I’ll wait until the book comes out, as I anticipate it with keen interest. And my construal of its contents above is purely speculative, as I know nothing about this upcoming book.

h/t: Daniel