Dreams and nightmares of the genetic age

April 24, 2022 • 9:24 am

by Matthew Cobb

This is a talk I gave at the Royal Institution in London in March, as an award from the Genetics Society of the UK – the J B S Haldane lecture, which is given in honour of a scientist’s work in popularising genetics.

I chose to give the talk on the subject of my forthcoming book, which will be published this autumn, under different titles on either side of the Atlantic. In the UK, it will be known as THE GENETIC AGE: OUR PERILOUS QUEST TO EDIT LIFE, while in the USA it will be called: AS GODS: A MORAL HISTORY OF THE GENETIC AGE. You can have your own views about which title you prefer. My first book equally had different titles in the UK and the US, and as a result The Lancet reviewed the book twice, not realising it was the same work (both reviews were very positive).

You can watch the talk here, and pre-order the book, should you so wish, from your local bookstore or bookshop.org. I think Jeff Bezos has enough money already.

The RI edited out the musical break from Orchestral Manoeuvres in the Dark I used in the middle of the lecture, to avoid copyright issues. You can listen to the track I played here:

Or you could choose to watch this song by X-Ray Spex, equally called Genetic Engineering, which came out eight years earlier. Spot the difference between the outlooks of the two songs – this reflected the shift in attitudes to genetic engineering I describe in the first part of the talk:

Here’s my DNA results: Surprise—I’m descended from Ashkenazi Jews!

April 15, 2022 • 12:00 pm

I forgot to mention that my 23andMe DNA results arrived just before I left for Antarctica.  Today I’ll just give the general overview of where my genes come from. There will be more later on the physical traits predicted from the DNA, but I deliberately didn’t ask for health information, as I don’t want to know what I’m going to die from!

I paid $100 for this?

Where my genes come from. Well, one thing’s for sure if these results be correct: I have NO IRISH ANCESTRY. So much for that theory about inter-faith copulations! But I have genes from the area that’s now Poland and perhaps Ukraine. Here’s the map:

And the rest—bupkes!

Finally, I’m not even above the median in my Neanderthal gene composition!

Yep, I’m pretty much a full-blown Ashkenazi Jew descended from Eastern Europeans.

In the next installment, when I feel so inclined, I’ll talk about the physical traits they prognosticate for me from my DNA. (Most are accurate.)  I also have a few matches for first cousins once removed, and have to decide whether I should contact them.

Soon I’ll learn my ancestry: is there any Irish in there?

February 25, 2022 • 10:15 am

Well, I’ll learn it at least insofar as the 23andMe tests are accurate. I guess they did get usable DNA out of my second sample, and so the genetic analysis will be coming very shortly, probably when I’m in Antarctica. (I opted out of the genetic health information as I’m neurotic.)

My prediction:  96% Ashkenazi Jew, 4% Neanderthal. The big question is whether there’s any Irish at all in my genome given that one or more of my distant ancestors may be Irish.

Here’s a diagram of what I know of the ancestry on my father’s side (on my mother’s it’s Jewish all the way down.) Below the diagram is what I wrote four years ago after showing my paternal family tree (“Floyd Coyne” was my dad), with information provided by my cousin Jeffrey. Jeffrey was the son of my dad’s half brother Jack. My dad’s birth mother, whom I believe was named “Rose Bloom”, died shortly after he was born, during the influenza epidemic in 1918. His father Joseph remarried.

My father was apparently badly treated by his stepmother and never spoke of her. And he was estranged from his half brother Jack until they reconciled in Sacramento when my folks visited me as a postdoc in Davis, California (early 80s).

What I knew four years ago (slightly revised:

As the diagram at the top shows, Pauline Zoffer (my father’s grandmother) married Peter Coyne, born in New York in 1862. There used to be an announcement online of my paternal great-grandparents’ wedding in Brooklyn, and it was a small piece titled “Jewish wedding”, announcing that Peter and Pauline were married at a synagogue.  (Sadly, that announcement is no longer there, but I remember it.) That comports with Pauline’s religion (after all, her own dad was “Isadore Zoffer”), but what about Peter’s?  [My cousin] Jeff tells me that their marriage “caused a rift within the Zoffer family” because Pauline married a gentile, and that would mean that my name wasn’t Jewish—wasn’t changed from “Cohen” or “Coyne”.  It would also mean that my paternal grandfather Joseph, whom I never met, was Jewish by Jewish law, for his mother was Jewish. But he would have carried a gentile Y chromosome from his non-Jewish father Peter.

But if that’s the case, why do I have a Y chromosome showing Eastern European Jewish ancestry? For that would mean that Peter himself was not of complete gentile ancestry, but that his Y was Eastern European Jewish. (I have his Y.)

It is a mystery. Peter’s parents were Patrick and Catherine Coyne, with Patrick born in 1823 and Catherine in 1831, both in IRELAND. And Patrick’s parents were John and Ann Coyne, both Irish, too, with John born in 1803 in Galway and Ann born in 1805 in Ireland (no city specified). My name, and my Y chromosome, goes straight back to John W. Coyne.

Already, then, at the beginning of the nineteenth century, the name “Coyne” was still “Coyne”, and perhaps it was never “Cohan” or a variant therefore. All this time I’ve been telling people that my name was changed from something like “Cohan,” which was simply a guess.

While there is a small Jewish community in Ireland around Galway, there are also plenty of pure Irish Coynes. So I have no idea if my name was changed from something else, was always “Coyne”, and whether “Coyne” was even a Jewish name. Was the wedding in Brooklyn a “mixed” one? Why do I have a Jewish Y chromosome if my paternal great-grandfather was a gentile?

But of course when I had my Y chromosome tested way back in 2007, it was a Y characteristic of Jews. and thus I had Peter Coyne’s Y, which was also Patrick Coyne’s Y and John Coyne’s Y.

We’ll find out something soon, I guess. One thing is for sure: eating corned beef won’t violate either a Jewish or Irish heritage.

Stay tuned, and if you have your own predictions for me, let me know.

“Luck” vs. genes: is there a moral difference?

January 29, 2022 • 11:00 am

Not long ago, I reviewed for the Washington Post Kathryn Paige Harden’s newish book on genome-wide association studies (GWAS) of human traits and how we can use the results to bring about social change. Click on the screenshot to read my take, or request a pdf:

Harden wrote the book with a social purpose that. she thought, could be implemented through the new technique of GWAS. I explain the method in my review, and so won’t reiterate it here, but it aims to identify many regions of the human genome responsible for genetic variation in a chosen human trait in one population. The trait she concentrates on is “educational attainment” (years of schooling), which is highly correlated with nearly every measure of “success” that you can think of—particularly wealth and income. And indeed, Harden, summarizing previous work, points out that over 1200 regions of the DNA can affect the value of this trait.

What this means is that even in a newborn child, you can predict how well a child will succeed. The predictability isn’t anywhere close to 100%, but still you can “rank” children by their GWAS scores in their likelihood of “success.”

Now this sounds like a hereditarian nightmare, with the possibility of ranking people as Aldous Huxley did in Brave New World: alphas at the top and the useless epsilons at the bottom. But although Harden is a hereditarian, her aims are not stratification or ranking, but equity. Her view is that once we know the genes responsible for academic achievement, we can use that information to help achieve equity in academic achievement.

And that’s where the big problem lies in her book: she couldn’t propose a good a way to use this information to achieve “equity”.  While her description of the genetic work in the book’s first half is excellent, the remedies she proposes in the second just aren’t there. In fact, I can’t see myself how to use this kind of genetic information to promote academic success. Suppose you know from genotyping an infant that that kid has an expected chance of graduating from high school that’s only 80% of the average value. What do you do with that information? Start tutoring the kid as soon as possible? Give more money to schools to boost everyone (this hasn’t worked)? There is no solution that doesn’t involve differential treatment, but Harden doesn’t want that, for it creates classes of “smarter” and “dumber” people, branding them from the outset.  It turns out that I wasn’t the only reviewer to spot this problem. And I’d claim that it’s easier to manipulate the school environment than to genotype a gazillion kids. (All genetically-based interventionsmust be tested empirically, anyway.)

But I’m not writing this to reiterate my review, but to bring up some stuff that I had to leave out of my review. So I’ll put below an argument that I thought was important but omitted from that review, both because I was severely limited by space and because a few people who looked at my draft saw this as superfluous. Now I regret not having written what I say here. Bolding below is mine.

These are quotes from my rough draft about Harden’s argument that we need to pay special attention to inequalities based on genetics because they’re a matter of “luck”.  I had to omit these bits (indented):

Harden’s motivation for using genetic differences to engineer equality comes from the fact that those differences are a matter of luck: the vagaries of how genes sort themselves out during egg and sperm formation. It’s unfair, she says, to base social justice on randomly distributed genes: “People are in fact more likely to support [wealth] redistribution when they see inequalities as stemming from lucky factors over which people have no control than when they see inequalities as stemming from choice.” [p. 206]

But is there really “choice”? Like many scientists and philosophers, I’m a determinist who rejects the idea of free will—at least the kind that maintains that there is something more to behavior than the inescapable consequences of your genetic and environmental history as well the possible indeterminate (quantum) laws of nature. In this pervasive view, at any one moment you could have chosen to do something other than what you did.

But there’s no evidence for this kind of free will, which would defy the laws of physics by enabling us to mystically control the workings of our neurons.  No inequalities stem from “free choice” and so everyone’s life results from factors over which they have no control, be they genetic or environmental.

Harden actually admits this dilemma: “If you think the universe is deterministic, and the existence of free will is incompatible with a deterministic outcome, and free will is an illusion, then genetics doesn’t have anything to add to the conversation. Genetics is just a tiny corner of the universe where we have worked out a little bit of the larger deterministic chain.”  [p. 200] And with that statement she pushes her whole program into that tiny corner.

But then Harden adds something like “I’m not going to get into the issue of free will.” By doing that, she punts on the most important issue of her book. Since our lives are completely the uncontrollable results of our genes and our environments, which even a compatibilist will admit, why should we see genes as a matter of “luck” but environment not? The family we’re born into, the people we meet, and all the influences of our lives are a matter of “luck”—and by “luck” I mean “naturalistic factors over which we have no willful control.”  It’s not pure “luck” which way a coin falls when you toss it: it’s actually determined by the laws of physics at play when you flip it (velocity, wind currents, and so on). The outcome, like that of our lives, are determined. Or, in some cases, not absolutely determined by the laws of physics (i.e., theoretically predictable if you had perfect knowledge) but are still absolutely produced by the laws of physics, since quantum mechanics, which so far as we know is inherently indeterministic, can affect some circumstances. But, as we know, quantum mechanics cannot support the common notion of free will: “I could have chosen other than I did.”

People will argue about this, but I don’t really want to argue about free will here; I want to make a point about determinism.  And that point is this. If you think that your genes, which partly determine your success in life, are the result of “luck” (I guess Harden means by “luck” those factors over which we have no conscious control), then so is everything else that determines your success in life.  In other words, as Harden suggests (but then dismisses) the idea that genetic “luck” is somehow physically an morally different from “environmental luck” is a bogus distinction.

And if that be the case, then people’s feeling that you need to be more concerned with fixing genetic inequalities than with fixing environmentally-based inequalities is unfounded.

The point isn’t really how we define “free will”, for all rational people are naturalists, accepting that our wills cannot change the laws of physics that really control our lives. And even if you are one of those rare libertarian free willers—who are largely religious people—I can’t see any rationale for being more concerned with genetically based inequalities than with environmentally based ones. (I note her that “environmental inequalities” can also have a genetic basis, so the distinction isn’t completely clear-cut. For example, we have evidence that there are genetic propensities to choose certain people as your friends, and your friends are immensely important in determining how you turn out.)

I applaud Harden’s motivations; who wouldn’t want to improve everybody’s chance of educational achievement? But by punting on the issue of determinism, it seems to me that Harden undercuts the whole social value of her genetic program. And because she’s a true progressive leftist, she’s more or less forced to evade that issue. But it’s fourth down and 25 yards to a first—what else can you do?

Either I have no DNA or I’m an aberrant hominin

January 11, 2022 • 11:00 am

Several months ago, 23andMe was running a sale on DNA analysis for only $99, which gave you not only a good guess at your ancestry, but also a readout of a large number of nucleotides in your genome—and perhaps the chance to find lost relatives.

I got my kit, spit in the tube, followed all instructions scrupulously, and sent back my material.

During the two months’ wait, I got a fair number of “build up my excitement” emails from the company. I could get my medical information if I wanted—the maladies I’d be most likely to die from! (I said, “No thank you.”). I could find Coynes who shared my genes! The results were on the way! They’re almost here! And so on and so on. . .

And then today I got this:

Apparently my saliva wasn’t good enough. It’s nice of them to offer a free new analysis (I knew that when I paid up in the beginning), but I’ve been waiting for several months for the result. Would I be a Jew? Would I be part Irish? Would I be handsome? Would I be rich? And here’s what they said to me: “Que sera, sera.”

I informed Matthew of this event, and the wag responded, “Why, what happened? Did you come back 50% Neanderthal?”

Very funny, but, as we both realized, the PCR amplification had for some reason failed. I followed the directions carefuly and sent the kit back just a few days after I got it. Frankly, I don’t care if I’m 50% Neanderthal (they’d be able to tell that anyway), as I’ve done pretty well for an early offshoot of modern H. sapiens. (I consider Neanderthals to be H. sapiens rather than a different species because we clearly interbred with them, and the hybrids must have been at least partly fertile.)

So, stay tuned. My Coynezaa present to myself didn’t work out, but there’s still a chance it will.

Daniel Finkelstein defends E. O. Wilson (and mocks Scientific American) in the Times of London

January 5, 2022 • 11:45 am

I don’t subscribe to the Times of London, so I count on my UK readers to alert me to anything interesting there. And today two of them did: Readers Pyers, who said the article below was “a superb piece”, and reader Adrian, who said this of the same piece (quoted with permission):

Been following your posts on E O Wilson and that horrific Scientific American article about him. [JAC: see that article here.]

Just noticed this morning that the Times (UK) has weighed in on the issue via a regular op-ed writer, Danny Finkelstein. Finkelstein is a regular contributor to the paper, and is a Tory peer. He belongs however to a very liberal strand of Toryism, and wouldn’t have much in common with the current Tory party, I imagine. I consider myself centre left, but very much like his writing. He always makes me think and question my own biases. He’s one of my go-tos for getting a sensible conservative view on the world – so in that respect, in my view, he sort of fulfills the same role that Andrew Sullivan does on US issues.

Anyway, his take on the cancelling of E O Wilson is a good one. And he also stands up for Paige Harden too – seeking to build a consensus around the idea that truth is not a left or right wing political issue.

I confess to feeling bamboozled by life at the minute. It seems only a minority of the people I consider to be on ‘my team’, the centre left (there are honourable exceptions of course), are keen to stand up against the revisionism that is currently de rigueur. I do find myself increasingly agreeing with some folk I would once have considered odd bedfellows, on the centre right. Maybe I’m just getting old, or maybe it is the polarised times we live in? I can’t quite decide between these options.

I currently tell myself that the extreme pathologies on the left and right of politics need to be opposed, and if that means centre left and centre right find common ground, then that is a good thing.

Now you won’t get anything but a few paragraphs if you click on the screenshot below, but the text is available via judicious inquiry. If you do have a Times subscription, you’ll get to see the whole thing. At any rate, I’ll give some quotes to show its tenor. Adrian has already informed us about author Daniel Finkelstein.

It is a remarkably well written and thoughtful piece, which defends Wilson against that idiotic attack in Scientific American, and also defends Kathryn Paige Harden, a left-winger whose recent book argues that the Left cannot ignore the palpable fact of genetic differences among people (my WaPo review of her book is here).  We are not, say Finkelstein and Harden, blank slates.

I can do no better than quote the author himself on a few selected topics (I’ve chosen the quotes and grouped them).

The ideological opposition to sociobiology (now called “evolutionary psychology”):

Last week EO Wilson died, and the world lost one of its leading scientists. The professor had started by studying fire ants and his knowledge of ants was peerless. But he had broadened as he had aged and had begun to consider human beings. Humans are animals too, after all, so our social organisation, our behaviour, our hierarchies, our urges will, to some extent at least, be the product of our biology.

This, the foundation stone of sociobiology, seems an unremarkable observation, but it provoked a remarkable reaction. Marxists and radicals, well represented in American universities, saw it not as a scientific hypothesis but as a political attack. Their argument was that human behaviour was overwhelmingly the product of social and economic organisation. Humans were, in essence, a blank slate, one very much like another. If Wilson was right, then this idea was wrong. If Wilson was right, societies were going to be harder to change. If Wilson was right, people might not come out equal even with all the social engineering in the world. So Wilson simply couldn’t be allowed to be right.

The weapon of choice in the battle to take down sociobiology was the accusation of racism. . .

The Scientific American screed:

Indeed one of the most useful results of studying the genetic and evolutionary basis of human behaviour has been that it has shown that the Nazis and other racists are wrong. And Wilson was quite clear about that. But unfortunately the accusation that Wilson was a racist was not made only by students. It was made by other academics seeking to protect unconvincing leftist ideas about social organisation. And it is still being made. A couple of days after Wilson’s death, Scientific American published an article by a University of California associate professor, reviving the charge of “racist ideas”.

It was an astonishingly muddled article whose vague arguments slip out of one’s hands every time one tries to grasp hold of them. Its appearance owed more to intellectual and political fashion than to rigour.


Kathryn Paige Harden on genetics:  I gave Harden’s book a mixed review. The first part, which shows the substantial genetic differences between individual humans—differences that affect our performance and chance of success in life—is very good, and well worth reading. It is the second part, where Harden discusses what social engineering can be done to make people more equal, that I criticized, for she offered no credible solutions. (Granted, solutions are very hard!).  Finkelstein:

Many of our abilities are heritable.

If we ignore this we are making social policy impossibly hard. As the egalitarian and geneticist Kathryn Paige Harden argues in her recent book The Genetic Lottery: “Genetic differences between us matter for our lives. They cause differences in things we care about. Building a commitment to egalitarianism on our genetic uniformity is building a house on sand.”

We don’t have to live with the outcome of genetic disadvantages. That would be like saying that although I’m short-sighted I shouldn’t be allowed glasses. But we do have to recognise genetic differences, or we end up denying glasses on the grounds that short-sightedness is the fault of capitalism and we need to nationalise the water industry first.

The idea that discovering natural difference in capacity is somehow right-wing is deeply puzzling. The truth doesn’t have a wing, it’s just the truth. But it’s not just that. There is a randomness to genetic inheritance, just as there is in economic inheritance. With the latter it is left-wing to observe this randomness and argue that we should help the disadvantaged poor. Why would people on the left not wish to even acknowledge the randomness of genetic inheritance? It is perverse.

The three reasons to rebut the ideological challenge to evolutionary psychology:

There are three reasons to rebut this challenge firmly. The first is that it is our duty to Wilson, a very great scientist. His contribution to the understanding of animal behaviour — of ants, of humans, of all nature — has been profound and it would be both cowardly and a tragedy to allow his reputation to be attacked when he is no longer here to defend himself against a baseless charge.

The second and even more important reason is that Wilson was achingly, obviously right. How likely is it that human beings are the one species whose capacities and behaviour aren’t largely influenced by biology? If every other animal’s behaviour demands an evolutionary explanation, how can it possibly be that ours does not?

He then refers to ideologically based criticism of palpable truths—like the fact of substantial genetic differences between individual humans adduced by Harden:

. . . Which is the third reason for defending Wilson and the study of sociobiology. Scientific methods and the search for truth matter. The accusation that sociobiology is racist rarely rises above the level of saying that as the Nazis were interested in genetics, genetics must be Nazi. It’s a bit like attacking Linda McCartney’s soya-based sausages on the ground that Hitler was a vegetarian.’

Finkelstein’s conclusion:

As we develop our capacity to study our genes we are going to learn more about human nature. We must be allowed to talk about that, even if the things we discover unsettle political activists and the orthodoxy they have adopted. We must defend good science against bad politics.

If the controversy over EO Wilson teaches us that, than the great scientist will have rendered us one final service.

This may be enough of an excerpt to satisfy you. If not, well, you know what to do.

“Jeopardy” shows that the Woke have won

December 16, 2021 • 1:15 pm

I received an email from reader Paul Topping, and I thought it was both amusing and sad. I have his permission to post it, so I’ll give it to you just as I got it:

My wife and I watch “Jeopardy!” regularly. This last Tuesday, they had an answer and question that might amuse you. This week and last they are doing their “Professors Tournament” which, obviously, features college professors. This question/answer was the “Daily double” in the first (single) Jeopardy part of the show.


     Biologist T.H. Huxley was a renowned defender of this theory & in 1893 famously lectured on it ‘& Ethics’

Contestant (English Prof from Penn State U, Hester Blum):

     What is eugenics?


    Sorry, the question is “What is evolution?”

I don’t think this contestant was well-informed on science. She laughed out loud when the subject for Final Jeopardy was introduced: Physics.

When I wrote Paul that this was both sad and funny, he responded:

t’s interesting but not surprising that someone would know just enough science to name scientists to cancel but not much beyond that. If it’s any consolation, she lost the contest.

It would be an English professor, wouldn’t it? (Or a sociologist or cultural anthropologist!)

I’ve written about T. H. Huxley (“Darwin’s bulldog”) several times, and about how his reputation has been unfairly besmirched. Huxley College of the Environment at Western Washington University, for instance, has been renamed because the University deemed Huxley a racist. Now T. H. seems to be more associated with eugenics than with biology, abolitionism, or science education. And he was NEVER a proponent of eugenics!

In which I start to ascertain my genetic ancestry

December 12, 2021 • 10:00 am

Thanks to a friend who told me that the 23andMe company is running a big sale on DNA kits that give you not only a readout of the presumed ancestral composition of your genome, but the much of the sequence itself, and, if you wish, what diseases you’re prone to get.  I have sprung $79 (usually $99) to get the “traits and ancestry” kit.  I didn’t want to know whether I’ll get Alzheimer’s or die from some horrible cancer, so I didn’t choose the $129 (usually $199) “health + ancestry” kit, which includes the DNA data plus those SNPs associated with various diseases.

The cheaper alternative still has lots of useful information, including the ability to scan large parts of your genome if you want to look for particularly interesting genes. It will give you a guesstimate of your ancestry (they have data for 200+ regions) and tell you the probability that you have various physical traits, like brown eyes or attached earlobes. And if you register your DNA at the site (optional), you may be able to find some lost relatives.

All in all, it’s a bargain for $79, and this would have been inconceivable two decades ago.  You can order at the link below. I think it would make a swell holiday gift for someone, as who isn’t interested in their genetic background?

I did this years ago for my Y chromosome to find out if I was a “Kohen“—one of the groups of Jews who have special status in the synagogue, taking care of the Torah and the like. Kohanim are elite Jews, regarded as “priests” and the job is passed from father to son, starting with the supposed Biblical Aaron, brother of Moses. That means that there is an unbroken lineage of Kohanim-specific Y chromosomes going back to the distant past. Yes, there’s been some pollution due to lack of sons or illicit canoodling, but there is a definite genetic sequence of the Y associated with being a Kohen. These people often bear the name “Cohan” or “Cohen” today, but while all Kohanim bear those names, not all Cohens or Cohans are members of the kohanim, as there are pretenders—those who use the name without the job. “Coyne” might have been a corruption of “kohen”, so I wanted to know

Well, I found out that I am a faux kohen: although my Y-chromosome ancestry is Eastern European Jewish, I don’t have the genetic signature of the Kohanim. So it goes.

Now, however, I will get a readout of my entire genome, not just the Y. What will it be? Surely mostly eastern European Jew, but there may be some real Irish genes in me, too, as my lineage does include an Irish goy in the 18th century.  And how Neanderthal am I? Do my brow ridges suggest a higher level of Neanderthal genes than normal (about 2%, I think)?

You can guess below, but I do suggest that a DNA testing kit is a great idea for a present.  All you do is pay the fee, and the kit comes within a few days. You spit into a plastic tube and put a special top on the tube that releases a liquid that mixes with your saliva. Remove that device, cap the tube and shake it, put it into a special plastic bag, and then return it, postpaid, in the box in which it came. Easy peasy!

Click below to order if you wish. And guess what I’ll turn out to be, genome-wise!


Ready to find out what “I” am (LOL):

My review in the Washington Post of a new book on genetics and social justice

November 19, 2021 • 9:45 am

Today the Washington Post put up online a review I wrote a while back on Kathryn Paige Harden‘s new book, The Genetic Lottery: Why DNA Matters for Social Equality. Click on screenshot to read my take, or make a judicious inquiry if you can’t access it.

Harden is a behavioral geneticist and Professor of Psychology at the University of Texas at Austin. You may remember that The New Yorker had a long profile of her a short while ago, and in it was this statement by her grad school mentor Eric Turkheimer:

In Bozeman, Harden seemed anxious that she had not heard from Turkheimer about her book. It took him a long time to get around to reading it, he told me, in part because of the ways their ideas have diverged in recent years, but when he finally did he wrote her an e-mail that said, “I really do think the book is great—in fact I think it will be instantly recognized as the most important book about behavior genetics that has ever been written. You should get ready to be very famous.”

Turkheimer has beefs with some of Harden’s ideas, but I simply had to read a new book about genetics that was likely to make its author very famous. And so I got the book and read it, and the Washington Post asked me to review it. Click below or go for that judicious inquiry.

As you see, my review is mixed. Her explanation of genetics and the use of “genome wide association studies” (GWAS)—a way of determining the expected value of a phenotypic trait from sequencing an individual’s genome—is excellent. She’s a good writer. The problem with the book is that she tries very hard, despite being somewhat of a genetic determinist who sees most human variation as having a sizable component of genetic underpinning, to appeal to the Progressive Left. For Harden is “woke”, as they say, and she’s aware that the other side, conservatives, would love to hear the sizable contribution to the variation of IQ of attributable to variation in people’s genes (it’s about 40-60%). There are large contributions of genetic variation to many other human traits as well.  But Harden carefully explains, correctly, that genetics is not destiny and that even a high genetic component to variation of a trait doesn’t mean that this variation can’t be flattened or equalized (I use myopia and glasses as an example).

But she’s still left with the problem of reconciling genetic inequality with societal equity—in particular how to treat children in school whose variation in academic achievement has a sizable genetic component. And here, in the prescriptive part of the book, she comes a cropper. She offers no plausible solutions about how one can actually use GWAS scores (I explain them in my review) to level the playing field for low achieving students, including minorities like blacks and Hispanics. (She doesn’t favor “tracking” students as she thinks that only perpetuates inequality.) My own conclusion is that, at present, we have no way of connecting GWAS scores to ways of improving education. It’s even worse because we know the genetic contributors of academic achievement only in European populations, and they could differ, as Harden emphasizes, in other populations. My conclusion:

I happen to share much of Harden’s ideology, and I wish her well. As I noted earlier, both the right and the left will find much to object to in this book. The resulting fracas might have been useful had she achieved what she set out to do — establish the fact of genetic unfairness and develop prescriptions to overcome it — yet she does not deliver on her second goal. Harden’s book is a thought-provoking read but in the end demonstrates only the incredible difficulty of using empirical data, both genetic and environmental, to level the educational playing field.

I want to add one thing here that was left out of my review for lack of space. Harden feels that we must rely on genetics to create equality/equity because one’s genetic endowment is a matter of “luck”:—the combination of genes you happen to inherit from your parents.  And Harden claims that she, and many others, feel it’s especially unfair for people to gain advantages simply because they’ve been genetically “lucky”. The implication is that there are things beyond “luck”, like an individual’s dedication and labor, that are a matter of “choice.”

This I find bogus, because, as a determinist, the “luck of your genes” is just as determined as “the luck of your environment” that also helps you achieve. Having the right for high IQ is “luck” in one sense, in that it’s not predictable, but so is the environment you’re born in and experience, which you also don’t choose. Harden actually recognizes this problem (p. 200):

Whether the universe is deterministic, whether such a thing as free will actually exists—these questions are beyond the scope of this book, to put it mildly. We need to put some philosophical guardrails up. If you think that the universe is deterministic, and the existence of free will is incompatible with a deterministic universe, and free will is an illusion, then genetics doesn’t have anything to add to the conversation. Genetics is just a tiny corner of the universe where we have worked out a little bit of the longer deterministic chain.

And, in fact, that’s the way it is. Harden has punted here. It doesn’t matter if you believe in “compatibilist” free will, because the philosophers who do are still determinists (or naturalists). And if you’re a determinist, then genetics is no more important than environment in its reliance on “luck” (i.e., unpredictability). It is just as unfair for someone to succeed because they had a good environment (and not necessarily good genes) than if they had good genes alone. Everything is determined—save the results of fundamental quantum unpredictability—which means that everybody’s fate is always matter of “luck” (unpredictable results of the laws of physics). Therefore, genetic and environmental influences are equally “unfair.” It is a major flaw of the book that Harden fails to take this seriously, but rather avoids it.

That’s all I want to add. The book is worth reading for its lucid genetic explanations, but I don’t think many hard-thinking readers will be convinced of her program to use genetic “inequality” to achieve social justice, though I agree that we need to do way better with schooling. Before you quibble about what I’ve said, though, read my review.

“Black tigers” in a small Indian reserve suggest random genetic drift

October 17, 2021 • 9:15 am

The two greatest forces changing the frequency of gene variants in a population are natural selection and genetic drift. You’d better be familiar with natural selection by now, but genetic drift isn’t widely appreciated by non-evolutionists. It’s simply the change in frequency of genetic variants due to chance alone: the random sorting and representation of variants from one generation to the next, due not to any inherent increment or detriment to reproduction conferred by the genes.

Teaching genetic drift to students often involves letting them represent a population by choosing marbles out of a sack. If you have ten marbles in a sack, five red and five blue (representing a population with equal frequencies of two genetic variants), and choose five to be the genes in the parents of the next generation (population size must be finite), then you might get three red ones and two blue ones. You then make a new sack with the new population’s frequencies—6 red marbles and 4 blue ones. The frequency of the red variant has risen from 50% to 60%. Lather, rinse, and repeat, and you’ll see the frequencies of the marbles change each generation due to chance alone. Given enough time, all the marbles will be the same color, and then no further change can occur (this is called “fixation”). Thus we see gene-frequency change (which most of us define as “evolution”) occurring, but there’s been no natural selection, no deliberate choosing of marbles of one color. I often gave my students examples of gene frequency change in one population and said “what would you do to determine if this is due to selection?” (Answer: set up replicate populations. Selection will always drive the same variant to high frequency, while with drift you will get diverse and opposite changes among the replicate populations.)

The smaller the population, the greater the changes in gene proportions will occur (i.e., the stronger the “genetic drift”). In fact, if the population is small enough, genetic drift can overcome natural selection, increasing variants that actually diminish reproduction.  When you see small populations with high frequencies of odd variants, or even deleterious ones, you might begin to suspect the action of drift. Inbreeding can be seen as a form of genetic drift in a small population of restricted size, which is why one sometimes sees high frequencies of genetic diseases or defects in small populations of humans (here are some examples in the Amish).

The paper below, from the latest Proceedings of the National Academy of Sciences, shows a likely case of genetic drift involving a gene variant that causes bigger and darker stripes in tigers in India. You can read it by clicking on the screenshot below, or get the pdf here (the full reference is at the bottom of post).

There’s also a PNAS commentary on the paper above if you want the short take. Click on screenshot below, or get the pdf here.

India is home to two-thirds of the world’s tigers, and natural populations are often fragmented because of habitat destruction, and can also be small because of past hunting. A sampling of Indian tigers from wildlife reserves and zoos showed that one area, the Similipal Tiger Reserve in Odisha, had a high proportion of darkly striped tigers called “black tigers”. This is not the same as the melanism we see in black leopards and jaguars—both called “black panthers” though they’re different species. Below is a black tiger (right) compared to a “normal” tiger (click all figures to enlarge them.)

Below is a map showing where the authors sampled tigers. Circles are natural populations, and squares are zoos or captive reserves. The size of the circles and squares represents the sample size of tigers. I’ve put an arrow pointing to the area of interest, the Similipal Tiger Reserve.

Black tigers are seen only in Similipal Tiger or in small reserves or zoos.  The pie charts also show the frequencies of individuals that have zero (yellow), one (orange) or two copies of the mutant gene causing the unusual pattern (black color). The diagram below shows that black tigers “m/m” are found only in the wild in Similipal, but are also seen in two zoos, where they’ve probably been selected for breeding because they’re unusual. Further, the black tigers in the zoos all were founded by at least one ancestral individual from Similipal.

For some reason that one small wild population has a high frequency of the black variant (“allele”). (There are a minimum of 12 adult tigers in Simlipal, which is a minimum estimate. But there can’t be many more than that, as the rangers can identify the tigers.)

(From paper): Fig. 2. Distribution of the genotyped individuals. A total of 428 individuals were genotyped at the Taqpep c.1360C > T mutation site. Wild tigers are shown with a circular marker, and captive tigers (NKB, AAC, and Mysore Zoo) are shown with a square marker. The size of the square/circle indicates the number of individuals genotyped from a given area. In addition to the 399 Bengal tigers shown on the map, we genotyped 12 Amur, 12 Malayan, and five Sumatran tigers from Armstrong et al. (40) These are not shown on the map to allow the figure to focus on sampling within India. The fraction of the three genotypes in samples from the three populations in which pseudomelanistic tigers are present is shown with the pie chart. Similipal is the only population of wild tigers to have pseudomelanistic tigers, and the other two populations are of captive tigers. All wild tigers were homozygous for the wild-type allele at Taqpep c.1360C > T site except for Similipal individuals.

The researchers got samples of captive tiger DNA easily, but getting wild tiger DNA is hard. That involved tracking the tigers and collecting their feces, saliva from prey, or shed hairs. Sequencing can tell you immediately whether you have tiger DNA or something else. I’m not quite clear about how they managed to distinguish the tracks or prey of individual tigers in the wild from that other tigers, but differences in the DNA from different samples would tell you how many tigers you’re dealing with.

If it is indeed a single gene causing blackness, it behaves as a recessive; that is, you have to have two copies of the mutant form to be a black tiger. With no copies or only one copy paired with the “normal” allele, you have the normal tiger pattern. Here’s a genealogy of color from breeding records of captive tigers. Orange represents normal-patterned tigers, while black are “black tigers.” Circles represent females and squares males.

You see that two orange tigers can produce a black one; in these cases the orange tigers each carried one copy of the recessive “black” allele; they were “heterozygotes”.  This doesn’t absolutely establish that it’s a single recessive gene; it would strengthen the case if they mated two black tigers together and got all black offspring, which is what you predict from a recessive gene.

From paper: (From paper): (B) The pedigree of the captive tigers sampled for this study. The individual labels shown in red are for the tigers whose genome was sequenced for this study (NKB17 is not shown in the pedigree). The genotype values are indicated for the individuals sampled and successfully genotyped at the mutation site (+/+ for wild-type homozygote, +/m for heterozygote, m/m for mutant homozygote, and x/x for missing genotype). Squares represent males, and circles represent females. Pseudomelanistic phenotype is represented in solid black shapes. The dashed line shows the presence of the same individual at two spots in the pedigree.

But how do they know that the black pattern is caused by a single gene? The authors’ whole-genome sequencing found one gene whose variants comported completely with the color: if you had two copies of the mutant, which has a DNA sequence that eliminates formation of the protein coded by that gene, you were black, but if you had no copies or only one, you were normally colored.  This gene is called Taqpep, which has been implicated in making dark variants in other cat species (see below). The full name is “transmembrane amino-peptidase Q”, and the mutant form, which doesn’t function at all, is called Taqpep pH454Y. We’re not sure how the “normal” gene works in pattern formation: the enzyme is involved in degrading other proteins, and also helps form the placenta in humans!

What we do know is that other mutant felids with darker and broader stripes also have mutations in the Taqpep gene. Below is a figure from the commentary paper showing homozygous mutations in that gene in the tiger as well as in the domestic cat and in the cheetah, where it produces cheetahs with dark blotches instead of spots (see below). Each of the three Taqpep mutations is different, so here we have an example of “convergent evolution,” independent species arriving at similar appearances via independent mutations. These mutations must have occurred since the common ancestors of the three cats, which lived 11.5 million years ago for all three, and 8.8 milion years ago since the ancestor of the domestic cat split from the ancestor of the cheetah.

(From paper): Fig. 1. Convergent evolution of broadened stripes/spots in cat species. The phenotype has arisen independently in the domestic cat (Felis catus), cheetah (Acinonyx jubatus), and tiger (Panthera tigris). (A) The phylogeny on the left depicts the relationships among the three species; numbers above branches indicate the divergence times (in million years ago) among their respective lineages; a timescale is shown at the bottom (tree and node dates are from ref. 17). In each of these species, the phenotype is caused by unique mutations in the Taqpep gene, whose positions in the encoded protein are indicated below the respective branch. Coat pattern images are modified from the photos provided in the original articles: ref. 10 for domestic cat and cheetah; ref. 8 for tiger. (B) Schematic of the Taqpep protein indicating the positions of the five pattern-altering mutations shown in A (color coded per species).

Below, a “king” cheetah (right) next to a normal cheetah:

Why the dark tigers in Similipal? Given that the gene is rare elsewhere except in zoos, and that the Similipal population is small, genetic drift is a likely explanation. The mutation could be “neutral” (i.e., conferring neither a reproductive advantage or disadvantage compared to “normal tigers”, or it could even be slightly harmful. If the dark form were selectively advantageous, you’d likely see it in many Indian populations as it increased in frequency. (Further genome analysis shows no sign that the gene has risen in frequency due to selection, but we can’t say that with absolute assurance.)

In fact, the authors did a simulation assuming that the Similipal population was isolated from other populations 10-50 tiger generations ago, and concluded that the population was likely founded by only a couple of tigers: two or three. In Similipal the frequency of the “dark” gene form is about 58%, while the light gene form is at about 42%. If there were random mating, you’d thus expect (0.58)² dark tigers there, or about 34% of all tigers. As you can see for the Similipal pie chart above, that is pretty close to what you get.

This would, then, be a good example to use when teaching about genetic drift, which is a difficult concept to teach well, involving mathematics that students don’t like. But when teaching you always need examples, and we can demonstrate drift in the lab using sacks of marbles or computer simulations. But it’s better to have examples from nature, and this is one that I’d use when teaching, as it satisfies the conditions for drift, there appears to be no selection favoring the black gene, and the population is known to be small and isolated.

The only other question is that of conservation. The Similipal population is endangered, and could be increased by bringing in other tigers. That would reduce the frequency of the black gene and of black tigers. It all depends on what you want to save: the tiger itself or the pattern? I’d go for the tiger, as the pattern genes will always be around in low frequency in the gene pool, but the tigers may disappear.


Sagar, V. Christopher B. KaelinMeghana NateshP. Anuradha ReddyRajesh K. MohapatraHimanshu ChhattaniPrachi ThatteSrinivas VaidyanathanSuvankar BiswasSupriya BhattShashi PaulYadavendradev V. JhalaMayank, M. Verma Bivash PandavSamrat MondolGregory S. BarshDebabrata Swain, and Uma Ramakrishnan. 2021. High frequency of an otherwise rare phenotype in a small and isolated tiger population