Part 2 of Matthew’s 3-part BBC show on genetic engineering

July 27, 2021 • 9:15 am

I was alerted to the appearance of Matthew’s BBC radio second show on genetic engineering from his tweet below. He’s offering a prize, too, if you understand the final music (put your guesses below or tweet them back at Matthew). I’m told the prize will be an autographed copy of Genetic Dreams, Matthew’s book that inspired this show: The book will appear next year.

Click below and then on “listen now” to hear the program. The BBC summary:

Professor Matthew Cobb looks at how genetic engineering became big business – from the first biotech company that produced human insulin in modified bacteria in the late 1970s to the companies like Monsanto which developed and then commercialised the first GM crops in the 1990s. Were the hopes and fears about these products of genetic engineering realised?

The show is based on lots of interviews—conducted by Matthew himself. It’s a good episode, beginning with the creation of venture-capital-funded genetic engineering firms, firms that made scientists wealthy beyond their wildest dreams, and eventually used recombinant DNA technology to manufacture “artificial” human insulin and growth hormone, as well as over 400 other drugs. But there was a downside of genetic engineering: interviewees complain about the secrecy it imposes on scientific research and about the fact that the technology made medicines more expensive. 

The last part of the show concentrates on GM (“genetically modified”) organisms—specifically crops. We all know about Monsanto’s creation of crops resistant to the herbicide Roundup, giving companies a convenient way to sell both crop and herbicide, as well as making it easier for farmers to tend their fields.  Despite these scientific advances, though, Matthew notes that GM crops haven’t led to more food being produced, all the while increasing the use of herbicides and pesticides that may have dire effects on the ecosystem. At the end, Matthew reaches a conclusion about whether GM technology has been more of a dream or a nightmare.

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Matthew’s new BBC show on recombinant DNA

July 20, 2021 • 9:30 am

I knew Matthew was writing a book on genetic engineering, and I knew he was doing a BBC radio series on the upcoming book, but I learned about the show’s first episode, now available, only from a tweet he emitted (below). You can access the 28-minute program, one of three, by clicking on the second screenshot.

Click to listen. This first part covers the advent of genetic engineering, and the huge controversy that took place when I was in graduate school. Did recombinant DNA pose serious dangers to the world. Would some engineered organism escape the lab and kill everyone? This didn’t prove to be the case, but at the time the science was at a very early stage.

A discussion on genetics, evolution, and information with Richard Dawkins

June 30, 2021 • 10:30 am

Reader Luke sent a recently filmed 48-minute discussion between Richard Dawkins and Jon Perry. Luke says “Perry does the excellent Stated Clearly YouTube channel. This was posted on his ‘personal’ site.”

Luke added this, too:
It’s a good conversation. It mostly focuses on River Out Of Eden and the ideas within that book. I know Richard has a new book out, but it’s refreshing here that he takes a deep dive into his past writings. While he touches upon atheist arguments, most of the conversation concerns Darwin, evolution, the genetic code, information theory, computers and function. This, I think, is where Dawkins is at his finest — talking about evolution. There’s a great moment when Dawkins is talking about the genetic code and machine code and Perry pulls out a strip of computer tape! [JAC: this happens at 12:48.] A great illustration of the ideas discussed!
It’s clear Perry is very much inspired by Dawkins, and it’s good to see. His YouTube channel is one of the best and most consistent.

Because of my past as a working biologist, I found the discussion of biology (sexual selection, brood parasitism, etc.) more interesting than the long discussion of code, the genetic code, information, and so on.

I enjoyed the section about whether animal signals evolve via genes that improve “cooperation.”  Whether you answer this “yes” or “no” depends on how you conceive of “cooperation”.  If you mean that cooperative signals evolve even though they reduce the fitness of the replicators within populations (i.e. cooperation as pure altruism), there’s no way that cooperation can evolve by individual selection (more accurately, by differential replication of genes among individuals in a population). Remember, you have to include kin and reciprocity when dealing with the evolution of cooperation within a population.

Most biologists think that the vast bulk of cooperation in animals evolves in a way that increases the fitness of the cooperators in a population. It confers an individual advantage to cooperate. You scratch my back and I’ll scratch yours, ergo you give excess food to your fellows so long as they remember to give excess food to you when you need it. Lions in a pride can gain advantages by cooperating in a hunt by being able to get more per capita food by being able to bring down larger prey or by being more successful at catching prey.

If you want a general increase in cooperation that does not enhance the fitness of individuals, you’ll have to posit forms of group selection.

I know of no examples of cooperation in animals—including any evolved cooperation in primates like ourselves—that cannot be seen as having evolved by individual (or genic) selection. Such examples, to be convincing, would have to show that while they may increase the longevity or “splittability” of a group, would have to reduce the fitness of the cooperators themselves, even when you include their kin. Some aspects of social insect behavior might conform to a group selection model, but recent work refuting such suggestions by Martin Nowak and his colleagues suggests this isn’t the case. At this point we can say that evolutionists know of know adaptations in organisms that must have evolved by group rather than “individual” selection. In the last chapter of my book on Speciation with Allen Orr, however, we describe how some evolutionary trends might be due to a form of group selection, but these are not features or behaviors of individuals.

A post of mine on human genetics gets condemned and labeled “harmful” by a university

June 18, 2021 • 1:45 pm

On May 6 I posted a piece on racism and human genetics, making the point that while some early human geneticists promoted eugenics (this doesn’t happen any more), there were other geneticists who explicitly opposed it. I wrote it to counter an article by Lea Davis in Scientific American (of course), who claimed that white supremacy is baked into the structure of human genetics and that the field still carries the burden of white supremacy. Anyone actually studying human genetics in a university knows that Davis’s accusations are not true.

Here’s a short excerpt from my article that gives the tone of my piece, which is critical but not, I think, uncivil:

Beyond that, we have the multiple Kendi-an accusatons that all human geneticists are complicit in racism and white supremacy. A few samples [from Davis’s piece]:

How do we teach and talk about this incredibly problematic history? Despite the many scholarly texts available, there is rarely an open and frank acknowledgement that the very foundations of our field were rooted in the false and dangerous beliefs of biological race and human racial hierarchies. Today, there is an effort to distance modern genetics from the harms of eugenics. This shameful aspect of our shared history is often separated from the primary curriculum for human genetics trainees, relegated to classes in “ELSI” (ethical, legal and social issues), which are usually electives—or, worse, just one day of training. In large part, we are failing to disclose this startling racist legacy to young scientists entering the field; a sad irony for a discipline devoted to human inheritance. Our failure to acknowledge the racist origins of modern genetics also has repercussions in our (in)ability to attract and retain members of underrepresented communities in genetics and other STEM training programs. Thus, as time marches on, the knowledge of our harmful racist history is fading while the culture of whiteness continues to dominate.

No, there is an effort to teach people about the history of our field. But that should not include the accusation that STEM is racist, for every school I know of is trying to “diversify” STEM as hard as we can. The issue is a “pipeline problem”: few minority candidates have reached the Ph.D. stage. That itself reflects older racism, but not racism imbuing human genetics, for scientists are pretty much anti-racists.

Further, the “very foundations of our field were not rooted in racism”. Yes, some famous geneticists believed that, but by no means all. Was the monk Gregor Mendel a racist? Were the re-discoverers of Mendelism, Hugo DeVries, Carl Correns and Erich von Tschermak, determined to imbue the field with racism? Not that I know of. How about the popularizers of modern genetics: people like T. H. Morgan, Theodosius Dobzhansky, Alfred Sturtevant, Calvin Bridges, Sewall Wright, and J. B. S. Haldane? Nope. You can mention Ronald Fisher in support of racism, but his eugenics was based on poverty, not race, and at any rate never got purchase. No, our field is not founded on racism.

And I gave several articles by famous geneticists of the 20th century who opposed eugenics.

The article certainly provides an opportunity to debate Davis’s claims versus my own, but when someone tried to do that, a ruckus ensued. Here’s a comment that a reader made on my post this morning on “social constructs” (click on the screenshot to go to the comment):

I have been officially condemned! Well, I’m not going to defend myself here; you can read my piece for yourself and judge for yourself. I further deny that it could cause “harm” to anyone who didn’t already have psychological issues, and I assert that a robust debate on these issues is exactly what this benighted university (I don’t know which one) needs but is trying to prevent.

Shame on that department, and shame on that university! For their actions are inimical to the very purpose of the university: to say your piece, adduce what facts you have, and let students hash out the issues in class or even in their own brains.

Punctuated equilibrium is dead; long live the Modern Synthesis

June 13, 2021 • 9:30 am

“If [Ernst] Mayr’s characterization of the synthetic theory [of evolution] is accurate, then that theory, as a general proposition, is effectively dead, despite its persistence as textbook orthodoxy”.—Gould, 1980

“If Steve Gould’s characterization of punctuated equilibrium involves the evolutionary mechanisms that he and Niles Eldredge proposed, then that theory, as a general proposition, is effectively dead, despite its persistence in Gould’s writings.”—Coyne, this post

Punctuated equilibrium (PE) was first proposed in a paper by Niles Eldredge and Steve Gould (“E&G”; reference below) in 1972, the year before I entered graduate school. When I entered Harvard in 1973  it was a huge deal, heavily promoted by Gould, a professor in the Museum of Comparative Zoology, as a replacement for the view of evolution most people held (“neo-Darwinism).  Not a little of the theory’s popularity came from Gould’s nonstop promotion of it as well as his extraordinary ability to write popular science.

At first the theory was largely about the pace of evolution. Instead of imperceptibly gradual change in a species over time (the view Darwin proposed, though Darwin did note in the Origin that evolution could also be rapid), Eldredge and Gould proposed that the pace of evolution was jerky, with big changes occurring relatively rapidly over evolutionary time little evolution happening the rest of the time. (This of course concerned only morphology, and was tested largely using hard parts—the parts most often preserved in fossils.)

Most of us microevolutionists were willing to go with the data, and some fossil data did seem to show an episodic pattern of morphological change. But of course there was argument about this, for what constitutes “big” versus “small” change in fossils? Further, the fossil record is often incomplete, so missing strata can make a gradual change look like a near-instantaneous big change.

Nevertheless, the theory that the pace of evolution could vary widely sat comfortably within the neo-Darwinian paradigm, which predicts that change will be rapid when natural selection is strong, and small when selection is weak or nonexistent. I remain open about the prevalence of the pattern, for I don’t know all the data.

But, over time, PE became more than a hypothesis about the relative rate of evolutionary change in fossil lineages. It morphed into a theory of evolutionary process—a theory that was pretty much “non-neo-Darwinian” and also much more controversial. And while the pattern may be right, the processes proposed by E&G are so wrong that I’d call them “definitively falsified”.

Over time, the following six assertions became part of Gould and Eldredge’s theory, and were proposed by the pair themselves:

a.) The claimed observation that most of the times species in the fossil record didn’t change (i.e., exhibited “stasis”) was not due to weak selection or an absence of selection, nor was it due to “stabilizing selection”: the kind of selection in which the average character in a population is the most fit, and extremes are selected against. That is the classic explanation for a lack of evolutionary change over time. These explanation were rejected by E&G in favor of two other explanations:

1.) Organisms have “developmental constraints”: there may be selection, say, to make individuals of a species bigger, but the species doesn’t get bigger because it either lacked genetic variation for bigger size or, alternatively, attaining a bigger size would have negative effects on the average fitness of the species (for example, if food is scarce, getting bigger might lead to faster starvation).

2.) Gene flow among populations of a species means that no population could change in response to local selection pressures because there was a constant influx of genes from other populations that didn’t experience such selection. This constant mixing of genes from populations undergoing different forms of selection averaged out to no net change in the appearance of a fossil species.

b.) Punctuated change in morphology can occur only when the genome is somehow “shaken up”, and this shake-up occurs during speciation events—when one lineage branches into two or more lineages. Absent such splitting events, a species stays static.

c.) The genomic discombobulation that somehow releases a species from its stasis—that is, loosens the developmental constraints—occurs when, as supposedly happens during most speciation events—a small peripheral population undergoes a form of “genetic revolution”, a kind of speciation in which reproductive barriers arise during an interaction between natural selection and genetic drift (random changes in the proportion of gene variants that are most prevalent in small populations.) At the time of this theory, several evolutionists, including Sewall Wright and Hampton Carson, had proposed that some types of evolutionary change require genetic drift in small populations. Without those population “bottlenecks”, these proponents said, species don’t change much. E&G drew on these ideas to buttress the episodic nature of evolution. One problem here is that there was and is little evidence that this kind of drift-associated change occurs, and almost no evidence that it’s ever associated with the appearance of a new species. Evolutionists have repeatedly put species through extreme bottlenecks—as few as two individuals—and have never seen that lead to even the beginning of reproductive isolation. (Reproductive isolation is the sine qua non of speciation to evolutionists.)

d). These claims all combine in the following way to lead to a punctuated evolutionary pattern. A big, widespread species is resistant to evolutionary change for the reasons mentioned above. Then, a small peripheral isolate population, cut off from the rest of the species, forms. Being small, it undergoes genetic drift, which releases the evolutionary constraints and allows the isolate to undergo rapid and substantial evolution.  Eventually, the isolate rejoins the main population, but by that time it’s evolved reproductive isolation from the other populations and is thus a new species. For reasons unexplained, the isolate quickly replaces the other populations. And voilà!—one sees a big change in the fossil record as the small and changed population supplants its ancestral species.

e.) But there’s another way that big morphological change can occur rapidly, too—one that was promoted by Gould: macromutation. This is the notion that changes in an animal’s appearance, behavior, physiology, and so on, don’t need to occur in small, incremental steps (the “Darwinian” pattern) but can occur via mutations that make big jumps, creating “hopeful monsters” (“saltations”). This idea was popularized by Richard Goldschmidt in the 1930s, and was revived by Gould in PE. Gould, for example, said this in a 1982 paper in Science.

 I envisage a potential saltational origin for the essential features of key adaptations. Why may we not imagine that gill arch bones of an ancestral agnathan moved forward in one step to surround the mouth and form proto-jaws? (Gould, 1980)

When called out for the absence of adaptations based on such huge mutations, Eldredge and Gould backtracked, claiming that PE was “never meant as a saltational theory”.  As you see, and this is true of other parts of PE, Gould in particular waffled about what the mechanisms of episodic fossil change really were.

f.) One of the most important parts of PE, worked out largely by Gould, was the claim that major features of adaptive evolution, and evolutionary trends in general, like the increase in body size in many lineages (“Cope’s Rule”) was due to species selection. This is a process of differential speciation and extinction that is said to occur not within species (that’s just classical Darwinism), but among species.  A further claim was that the changes within species had little to do with selection itself (they may have resulted from drift)—or at least little to do with the process of differential speciation and extinction.

So, for example, an increase in body size among a group of mammals over time would be explained by species selection this way: each species attains its average body size either by drift or by forms of selection that have no relationship with the persistence, speciation rate, or extinction of species. But it may happen that, for other reasons, the biggest species either speciate faster or go extinct more slowly. Over time, then, we’d see a pattern among lineages of an increase in body size, but this has nothing to do with classical Darwinian selection on gene forms.

The problem with this is that species selection cannot account for complex adaptations like jaws so easily. Each feature of an adaptation would have to evolve by a process of differential extinction or speciation, and evolving a complex adaptation would take a gazillion years.  That’s because species selection is much slower than individual Darwinian selection since the former relies on replacement of species over evolutionary time, while the latter relies on the rapid replacement of gene forms within a species, which can occur over a few thousand generations or fewer. Further, the evidence for species selection as a general explanation of evolutionary trends is very thin. In his last big book, The Structure of Evolutionary Theory, a 1400-page, poorly written monster that I actually read (and wish I hadn’t), Gould winds up admitting that he can’t adduce a single good example of species selection. However, in the last chapter of my book with Allen Orr, Speciation, we do make a case that a limited form of species selection may operate in nature and can explain evolutionary trends but not adaptations themselves. Species selection is just not as ubiquitous as Gould thought.

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So apart from a) and the presence of genetic drift, virtually every part of PE is “non-neo-Darwinian”: processes that aren’t considered widely as part of the modern evolutionary synthesis. That doesn’t mean that they’re wrong, but when examined closely, the evidence for these ancillary assertions is virtually nonexistent. Although to G&E, PE represented a Kuhnian “paradigm shift”, closer examination shows that these components (peak shifts, connection of morphological change with speciation, restriction of response to selection by developmental constraints, saltation, widespread species selection etc., etc.) are individually not common, and in tandem seem impossible to form the basis of a convincing theory. Despite that, Gould claimed that PE put neo-Darwinism to rest (see his quote at the top of the article).

Now I could write in detail why the assertions above are dubious, and why PE as a mechanism of evolutionary change is almost certainly wrong, bu that case has already been made. It was first made by three of my colleagues, Brian Charlesworth, Russ Lande, and Monty Slatkin, in a 1982 paper in Evolution that pretty much put the mechanism of PE to rest. You can read that paper below; it’s a classic not of modern evolutionary genetics, and also a paradigm of close examination and debunking of a popular theory (click on screenshot for the pdf). The debunking involved a massive mustering of evidence from genetics, population-genetic theory, laboratory experiments, field experiments, artificial selection, and geology. The last bit of their conclusions says this:

We have also demonstrated, as has Orzack (1981), that punctuationists have often severely distorted the neo-Darwinian theory of evolution. Punctuationists are mainly criticizing oversimplified versions of neo-Darwinism (which are currently popular in some fields) rather than the original statements of this theory and the evidence which has been used to support it. Furthermore, some of the genetic mechanisms that have been proposed to explain the abrupt appearance and prolonged stasis of many fossil species are conspicuously lacking in empirical support. Thus, we do not feel logically compelled to abandon neo-Darwinism in favor of the theory of punctuated equilibria.

This paper of Charlesworth et al. was expanded and brought up to date by the new “Perspectives” paper of Hancock et al. in Evolution (reference below, pdf here).


And here is the abstract, supporting the conclusions of Charlesworth et al. (my emphasis)

The Modern Synthesis (or “Neo-Darwinism”), which arose out of the reconciliation of Darwin’s theory of natural selection and Mendel’s research on genetics, remains the foundation of evolutionary theory. However, since its inception, it has been a lightning rod for criticism, which has ranged from minor quibbles to complete dismissal. Among the most famous of the critics was Stephen Jay Gould, who, in 1980, proclaimed that the Modern Synthesis was “effectively dead.” Gould and others claimed that the action of natural selection on random mutations was insufficient on its own to explain patterns of macroevolutionary diversity and divergence, and that new processes were required to explain findings from the fossil record. In 1982, Charlesworth, Lande, and Slatkin published a response to this critique in Evolution, in which they argued that Neo-Darwinism was indeed sufficient to explain macroevolutionary patterns. In this Perspective for the 75th Anniversary of the Society for the Study of Evolution, we review Charlesworth et al. in its historical context and provide modern support for their arguments. We emphasize the importance of microevolutionary processes in the study of macroevolutionary patterns. Ultimately, we conclude that punctuated equilibrium did not represent a major revolution in evolutionary biology – although debate on this point stimulated significant research and furthered the field – and that Neo-Darwinism is alive and well.

So the best you can say about the mechanism of PE, a claim I’ve heard many times, was that it furthered the field of paleobiology—brought paleontology to the “high table of evolutionary biology”, as someone asserted. Well, while it did stimulate debate about the relative frequency of rapid versus gradual change in the fossil record, the falsity of its claims about mechanism was already known to evolutionary geneticists when PE was first proposed! Charleworth et al. simply collected all the theoretical and empirical work that showed the falsity of the mechanism.

I remember debating this issue with Steve Gould in our conference room at Harvard, asking him to explain the details of PE’s mechanism. Gould got more and more exercised, and wound up tarring me by telling me that I was just a “hidebound gradualist.”  I still wear that label with pride.

Later, Brian Charlesworth and I had several exchanges criticizing PE in the journal Science (see Coyne and Charlesworth references below).

It apparently wasn’t enough for E&G to point out a pattern in the fossil record that might have been real (I still don’t know how ubiquitous “jerky” evolution is). No, they wanted to go further—to be Kuhnians and tear down the wall of evolutionary theory, erecting the new paradigm of PE in its place. Well, such an endeavor is fine, but the new paradigm hasn’t worn well, and in fact was stillborn when first proposed.

I’m not sure whether paleobiologists still teach punctuated equilibrium as a viable theory, but if you hear that claim, remember this: PE as a pattern in the fossil record may well be correct, but as a mechanism of evolutionary change is “not even wrong.”

Addendum: I don’t want to go through the Charlesworth et al. and Hancock et al. papers in detail, as you can read them for yourselves. But if you have specific questions about the mechanism of PE that I can answer briefly, put them in the comments.

Stephen Jay Gould (left) and Niles Eldredge (right) flanking their mentor, Norman D. Newell (seated) on the occasion of Dr. Newell’s 90th birthday celebration at the American Museum of Natural History in New York in February, 1999. Photo by Gillian Newell. Source.

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Charlesworth, B.R. Lande, and M. Slatkin1982 A Neo-Darwinian commentary on macroevolutionEvolution 36474– 498.

Coyne, J. A. and B. Charlesworth.  1996.  Mechanisms of punctuated evolution (technical comment). Science 274:1748-1749. (includes response by Elena et al.)

Coyne, J. A. and B. Charlesworth. 1997.  Punctuated equilibria (technical comment).  Science 276:338-340.

Eldredge, N. and S. J. Gould. 1972. Punctuated equilibria:  An alternative to phyletic gradualism. Pp. 82-115 in T. J. M. Schopf, ed. Models in Paleobiology. Freeman, Cooper, San Francisco.

Gould, S. J. 1980. Is a new and general theory of evolution emerging?. Paleobiology 6 119-130.

Hancock, Z.B., Lehmberg, E.S. and Bradburd, G.S. (2021), Neo-darwinism still haunts evolutionary theory: A modern perspective on Charlesworth, Lande, and Slatkin (1982). Evolution. https://doi.org/10.1111/evo.14268

How much variation in human behavior is due to variation in our genes? Answer: quite a bit.

May 24, 2021 • 9:45 am

The only people who claim that behavioral variation among people has nothing to do with their genes are ideologues: “pure blank slaters.” Based on studies of other species, we know that virtually all studies of traits that vary among individuals—be those traits morphological, physiological, or behavioral—show that some or even a lot of the variation in a population is based on variation in the genes of different individuals. (I know of only three studies in animals, out of thousands done, that failed to find a genetic basis for variation among analyzed traits.  Two of the three studies were mine, and all were on directional asymmetry: trying to see if there’s a genetic difference for, say, having more bristles on the right than on the left side of a fly.)

While humans have an extra source of inter-individual variation—culture—there are ways to get around cultural inheritance to see how much of human variation is based on genetic variation. There are several ways to determine and measure the contribution of genetic variation to variation among individuals.

First, though, let’s learn the technical term at issue: heritability. Heritability is a measure that ranges from zero to one (or 0% to 100%), and tells you how much of the observed variation among individuals in a population is based on genetic variation among those individuals.  The higher the heritability, the more genetic determination there is of variation in the trait. So, for example, if the heritability of human height for females is 0.7 (or 70%), that means that if you measure the variation in a population for height of women (the variation is conventionally estimated by calculating the variance—denoted by σ² or s²—then of the total variance for height, 70% of that estimate is due to variation of individual’s genes. In this case, there’s a high degree of genetic control of variation in height. (This is close to the actual figure for female height.) Confusingly, the symbol for heritability is h².

Now it’s a bit more complicated than this, for heritability incorporates only what we call the additive genetic variance rather than other kinds of genetic variance (usually minor). And course, there are other obvious sources of variation in height—most prominently nutrition and health.  The more that environment contributes to differences among individuals in a trait, the lower the genetic heritability. So, for example, the heritability of hair color among adults has been reduced by the introduction of an environmental source of variation: hair dyes. Less of the variation in hair color that we see, compared to, say, 200 years ago, is due to genetic variation.

It’s important to grasp several caveats about heritability. First, it is a figure that applies to one interbreeding population at one time—the time of measurement. You cannot apply heritability in one group to a different group that may have different genes and, importantly, different amounts and sources of environmental variation that affect a trait. A population undergoing famine, for example, may show a lower heritability of height because individuals’ heights may be altered by grossly different amounts of food they get.

Second, heritability says very little about how much a trait can be changed, for genetics isn’t destiny. Yes, the heritability of height may be 70%, but that doesn’t mean that we can’t make people bigger or smaller by feeding them a lot of good food, injecting them with growth hormones, or starving them. When people object to measuring heritability of IQ, for instance, they often mistakenly think that because IQ has a sizable heritability, which it does, it therefore can’t be changed. But that’s bogus; there are many possible interventions that can affect IQ.

Third, as implied above, measuring heritability within a group tells us very little, if anything, about the genetic basis of difference among groups. That’s because there may be environmental differences between groups that affect the character in profound ways and make extrapolations from one group to another useless. You cannot conclude, for example, that measures of behavior, mentation, and so on, in one population or ethnic group, even if the heritabilities are large within that one population, must therefore mean that big differences between groups must rest on genetic differences between those groups. The heritability of height in the Japanese population right after WWII, for example, was probably considerably smaller than 70% because of wide variation of nutrition in the Japanese. Thus you can’t conclude that their smaller height than Americans at the time was based on genetic differences. In fact, the average height of Japanese people went up three to four inches in about thirty years! So much for the idea that a substantial heritability for a trait in one group means that that trait can’t be changed!

Fourth, there’s a common misconception that heritability tells you “how much of your height (or weight, or IQ) is genetic”.  A heritability of 80% for height doesn’t mean that, if you’re five feet tall, four feet comes from genes and one foot from the environment. That conclusion is biologically meaningless since the height of an individual involves an interaction between genes and environment. The only sensible way to construe heritability is to say that it tells us how much of the VARIATION we see from individual to individual within a population is based on differences in their genes (or rather, forms of their genes: different “alleles”).

How do we determine heritability? There are several ways. In species like plants and animals in which we can perform artificial selection, we can estimate heritability by seeing how much a population responds to artificial selection for the trait. The bigger the response, the higher the heritability. There is an equation that tells you this: the response to artificial selection is roughly equal to the strength of selection (how much difference there is in the average trait in the group you choose for breeding and that of the population in general) multiplied by the heritability. If the heritability of head-to-tail length in pigs is 50%, and you choose for breeding a group of pigs whose average size is two feet longer than that of the population, you’d expect the next generation of swine to be one foot longer than the original population (0.5 X 2 feet). So if you know how strong you’re selecting, which you do, and what the response is in the next generation, you can back-calculate to estimate the heritability of the trait you selected.

Artificial selection isn’t practiced in humans, of course, so we usually determine heritability by looking at the correlation between relatives, including parent-offspring correlation and the correlation between twins. Parent-offspring correlation is dicey if there’s an environmental component to the trait that can also be inherited. I seem to remember that the two traits with the highest heritability in humans are religion and wealth, and that’s due to the passing on of these traits among generations via culture, not via genes!  In animals that have no transmissible culture, like fruit flies, one can, however, do these kinds of studies.

Humans researchers often use twin studies, comparing the similarity between identical twins (which have the same genes) with the similarity between fraternal twins, which share half their genes. We all know that identical twins are more similar for virtually every behavioral and morphological trait than are fraternal twins (just look at them!), implying that genes play a big role in these traits. You can in fact estimate the heritability of traits by looking at the difference in the correlations of identical vs. fraternal twins (you need a decent-sized sample of twins to do this).

There’s one caveat here, too, however. Identical twins often share more environmental commonalities than do fraternal twins. They may be treated more alike, dressed alike, brought up alike, and educated more alike than are fraternal twins. Thus an increased similarity of identical twins need not reflect the identity of their genes, but a greater similarity of their environments. At least for physical appearance, though, that doesn’t seem to be the case: you can’t “socialize” identical twins to look more alike than do fraternal twins!

One way around the possible environmental similarity is to compare fraternal twins raised together with identical twins separated at birth and raised apart. If the latter still show appreciably greater similarities despite their different environments, that’s a sure sign that the traits measured have substantial heritabilities. However, as you can imagine, there aren’t big samples of identical twins separated at birth.

Finally, we can measure heritabilities using DNA, by “genome-wide association studies”. This is more complicated, but involves finding those regions of the DNA associated with variation in a trait (like height), and then adding up the small effects of all known regions to see how much these known bits of the genome can contribute to variation among individuals. Heritabilities measured in this way are invariably smaller than those measured by correlations or selection, as the latter two methods take into account every region of the genome contributing to variation. Variation in most behavioral traits is due to many genes of very small effect, and it’s nearly impossible to find them all by association mapping.

This is all a very long prologue to a very short figure I’m going to show you—a figure that comes from this new paper in Nature Human Behavior. It summarizes heritability data for a number of behavioral traits, comparing heritabilities from twin studies to those from association studies. Click on the screenshot to see the paper, and I’ve put the full reference at the bottom:

And here’s Figure 2 showing the heritabilities measured both ways. Blue lines and dots give data from twin or family studies, orange lines and dots from association mapping.  You can see that association studies produce, as expected, lower estimates of heritability, but I’d expect the true values to be closer to the family-study data). 26 behavioral traits were measured, ranging from educational attainment, IQ as children and adults, amount of drinking and smoking, neuroticism, to mental disorders like schizophrenia.

Click on the figure to enlarge it.

The values in the colored triangle to the left are the “genetic correlations” between traits, which tells us the degree to which pairs of traits are affected by variation in the same genes. We need not concern ourselves with that.

For the moment, look at the lengths of the blue bars to the right, which are probably pretty close to accurate estimates of heritabilities. And for most traits they are pretty big, with over 25% of the variation in a trait due to variation in the genes within that population. For some traits, like adult IQ, number of sexual partners, alcohol dependence, autism spectrum placement, and schizophrenia, heritabilities are over 50%

What all this does is refute the “blank slate” view that the differences between people in their behavior is completely due to culture and socialization. It also shows that a substantial portion, however, is due to other sources of variation: developmental, post-birth environmental differences, and so on.  It also shows that you could select on any of these traits and get a response, increasing, for instance, the age of first intercourse (Christians take note!) or reducing alcohol dependence. NOTE: I AM NOT SUGGESTING THAT WE SELECT ON THESE TRAITS!

So have a look—and click on the figure!

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Abdellaoui, A. and K. J. H. Verweij. 2021. Dissecting polygenic signals from genome-wide association studies on human behaviour. Nature Human Behaviour. https://doi.org/10.1038/s41562-021-01110-y

Human genetics accused of furthering white supremacy and racism—today

May 6, 2021 • 11:00 am

All geneticists know, and knew decades ago, that we had a shameful period in our history, particularly human genetics. (This was not predominant, but a blind alley.) Some geneticists, like Galton and Davenport, were explicit “negative eugenicists”, urging sterilization or discouraged breeding of the “inferior”, including not only those who were deemed mentally deficient or of lower class but also those of other races. This history has been reemphasized recently with the rise of anti-racism, and it’s good that we’re constantly cognizant of our past history and its racist (and classist) underpinnings. In fact, this history is already widely taught, but there’s no harm in learning about it—as we should learn the entire history of our field.

What bothers me, though, is the complete neglect of the movement against eugenics that was widespread in America, a history exemplified by articles like these (I’ll try to find links online later). This, too, is part of our history:

and this

and this, the Presidential Address at the American Society of Human Genetics in 1961

You never see this pushback mentioned in the histrionic accusations, like the one below by Lea Davis in the increasingly woke Scientific American, that human genetics in America and the UK not only has a racist past (partly true) but also a racist, white-supremacist present (not true). Lea K. Davis is an Assistant Professor of Medicine at Vanderbilt Medical Center.

Now it’s true that in a few places prisoners have been offered completely voluntary sterilization in return for lighter sentences, but this rarely happens. And it’s execrable. But the accusation that human genetics is ridden with racism and complicit with white supremacy is simply false. These are performative accusations, like those John McWhorter mentioned yesterday.

Davis makes a number of overheated statements and at least one contradictory one. The latter involves the existence of “races”. As I’ve written ad infinitum, there are no discrete and easily distinguishable populations that can be classified as “races”, but we do have populations, distinguished by genetic ancestry, that can, if you use many genes, be almost absolutely identified as to self-identified ethnicity as well as geographical location.

Davis argues that “race” is a social construct, a misleading statement that needs considerable explanation, which she neglects to provide.

Together, could we dispel the myth of biological race? Again, we cannot do this alone, as most of us are ill-equipped to confront the rhetorical science misinformation bombarding society on a daily basis. Engaging experts in strategic science communication, along-side of social scientists and geneticists, is mission critical to meaningfully de-biologizing race.

Let’s ditch the loaded term “race” and just use “ancestry” or “ethnicity”, recognizing that there is substantial genetic information in one’s genome that not only tells you what your self-identified race is with substantial accuracy, but also gives you a good idea of your ancestry and geographic origins. “Race” may be a social construct, but “genetic differentiation of populations” is not.  And Davis makes the mistake of saying that “race” (let’s use “ethnicity”) is something completely different from ancestry:

Others routinely, if naïvely, perpetuate the scientifically inappropriate conflation of race and ancestry. The trouble is that most human geneticists know very little about race. Scholars in sociology, anthropology, critical race theory, gender studies, etc. who have a far more sophisticated understanding of the origins of race and racism, have so much to teach us.

She’s dead wrong here. I’d rather talk about “race” (“ethnicity”) with people like John Novembre or Graham Coop, well known human geneticists, than with critical race theorists or gender studies people, who have no training in genetics, an ideological commitment, and, I’d aver, lack a “far more sophisticated understanding of the origins of race.” Ancestry has everything to do with “race” (read “ethnicity”: it’s differential ancestry that results in geographic populations being genetically different!

But the contradiction is when Davis claims that clinical studies of genes that map near disease genes have largely been conducted on white populations—a form of racism. I don’t think it’s really racism, because white populations are what’s largely available to clinicians (at least locally, as they draw participant from their local universities in Europe and the US), but I’ll grant her that we need to do such studies in people of different ethnicities. But if race is a social construct, on what basis can we do “ethnicity-based” genetic analysis of disease propensity? If ethnicity or race are social constructs that have nothing to do with biology, working on one group is as good as another. That’s not the case, of course: groups differ in their genes and their propensity to get different diseases (cultural differences surely also play a role). You need to IDENTIFY ethnicity to do such work!

Note how she throws in the accusation of explicit and systemic racism for this concentration on focal populations:

Lack of diversity in available genetic data is not an accident; it is an inevitable consequence of systemic racism in biomedical research. The difficulty in recruiting non-European populations into genetic research today is a direct result of our history of white centering, gatekeeping by white academics and decades of human rights abuses suffered at the hands of white researchers. White centering is still so embedded in human genetics that even though we recognize these problems, millions of dollars are being invested in programs to capitalize on Eurocentric genetic scores and tests that are primarily effective for people of European descent, potentially leaving communities of color behind in precision medicine advancements.

If we are to do these tests, we must label people by their ethnicities, for we’ll otherwise have no data. In fact, this is being done right now, so Davis is exaggerating.  She simply must recognize a finite number of ethnicities to do this work, for otherwise it’s of no value. (Furthermore, to have full representation, studies should be done in Africa, but white doctors attempting to collect African data are at risk of being accused of racism and colonialism.

Beyond that, we have the multiple Kendi-an accusatons that all human geneticists are complicit in racism and white supremacy. A few samples:

How do we teach and talk about this incredibly problematic history? Despite the many scholarly texts available, there is rarely an open and frank acknowledgement that the very foundations of our field were rooted in the false and dangerous beliefs of biological race and human racial hierarchies. Today, there is an effort to distance modern genetics from the harms of eugenics. This shameful aspect of our shared history is often separated from the primary curriculum for human genetics trainees, relegated to classes in “ELSI” (ethical, legal and social issues), which are usually electives—or, worse, just one day of training. In large part, we are failing to disclose this startling racist legacy to young scientists entering the field; a sad irony for a discipline devoted to human inheritance. Our failure to acknowledge the racist origins of modern genetics also has repercussions in our (in)ability to attract and retain members of underrepresented communities in genetics and other STEM training programs. Thus, as time marches on, the knowledge of our harmful racist history is fading while the culture of whiteness continues to dominate.

No, there is an effort to teach people about the history of our field. But that should not include the accusation that STEM is racist, for every school I know of is trying to “diversify” STEM as hard as we can. The issue is a “pipeline problem”: few minority candidates have reached the Ph.D. stage. That itself reflects older racism, but not racism imbuing human genetics, for scientists are pretty much anti-racists.

Further, the “very foundations of our field were not rooted in racism”. Yes, some famous geneticists believed that, but by no means all. Was the monk Gregor Mendel a racist? Were the re-discoverers of Mendelism, Hugo DeVries, Carl Correns and Erich von Tschermak, determined to imbue the field with racism? Not that I know of. How about the popularizers of modern genetics: people like T. H. Morgan, Theodosius Dobzhansky, Alfred Sturtevant, Calvin Bridges, Sewall Wright, and J. B. S. Haldane? Nope. You can mention Ronald Fisher in support of racism, but his eugenics was based on poverty, not race, and at any rate never got purchase. No, our field is not founded on racism.

And here’s how we’re still racist:

When we identify white supremacy as the paramount problem in our field’s history, it becomes clear that it is still our problem today. Lack of diversity in available genetic data is not an accident; it is an inevitable consequence of systemic racism in biomedical research.

and this; note the reference to structural violence and our complete complicity (my emphasis). The last sentence might has well come from the pen of Ibram Kendi:

Human genetics is a science that I love, a science to which I have devoted my life, and a science that I believe could be a powerful force against racist ideas in medicine and society. But this potential can only be reached if we are willing to reckon with our role, collectively and individually, past and present, in upholding white supremacy and structural violence in science and academia. As educator and author Catrice M. Jackson has observed, “If you don’t have an antiracism plan, you plan to be racist.”

It is ludicrous to claim that if we don’t have an antiracism plan, we plan be racist. Colleges are already doing their best to get women and minorities into STEM by various programs. That is our antiracism plan, and Davis cannot ask more. Society needs a plan that widens the pipeline, allowing equal opportunity for all to pursue their interests, but this has nothing to do with the supposed ongoing racism in human genetics.

An antiracism plan will require challenging everything from the speed to the priorities of human genetics research, but if we are serious about reducing health disparities through precision medicine we must push back on the culture of whiteness in medicine and research. We can begin by explaining that equitable translation of genetic medicine will be a slow process because of the inequity that our field has already created. Efforts to increase diversity among scientists are desperately needed, and unless we are committed to dismantling inherently racist structures and ideas in science, we will never achieve real equity.

We can empower ourselves and each other to acknowledge our own complicity and call on our funding institutions, our professional societies and our departments to make antiracist action a priority in our daily research practices. The long-overdue awakening emerging in American consciousness is incongruent with business as usual in our field, and it is past time to call in the revolution. Human genetics needs an antiracism plan now, otherwise, we must admit we plan to be racist.

I reject her claim that I’m complicit in racism, even though I’m a fly geneticist. Is Davis unaware of what is being done now? I find it hard to believe her claims, for she raising as a new challenge what is largely a problem already being rectified. As for the “calling in the revolution”, that’s like “sending in the clowns”: “Don’t bother, they’re here.”

As for human genetics being inhabited by figures in pointy hats and white robes, Davis is dead wrong. Genetics was not founded on white supremacy, and although we had racists and bigoted episodes that had some serious consequences, they are largely gone, nor do I see them returning. We are not engaged now in propping up white supremacy.

A retrospective look at a paper: Coyne and Orr (1989)

April 4, 2021 • 12:00 pm

The two best-cited pieces of scientific work bearing my name were both done in collaboration with my graduate student, Allen Orr, who was recommended to me by Bruce Grant, my undergrad genetics teacher at The College of William and Mary. Allen had gotten a B.A. in philosophy there, and went on to do a master’s degree with Bruce in Drosophila genetics. Bruce recommended him to me as a good prospect, but wasn’t sure how he’d work out as a Ph.D. student.

At the time I was at the University of Maryland, took Allen on, and the rest was history. I had no idea how to mentor graduate students—Allen was my first—but it turned out he needed no mentoring: he was a self-starter. Over his few years in my lab, he published about ten papers and won the Society for the Study of Evolution’s Dobzhansky Prize in 1993, given to the person the SSE’s committee considers the best young evolutionary biologist.

The two most cited works include a pair of related papers (Coyne and Orr 1989, 1997), and our coauthored book Speciation (2004).

I summarized the main findings of the two papers, and gave a bit of their history, in a post from October of last year, which includes an interview I did about it in 2017 for Reflections of Paper Past.  At that time I didn’t know that two people, including my last student, Daniel Matute, were writing a retrospective of the 1989 and 1997 papers.

At any rate, in honor of the 75th anniversary of the journal Evolution, it’s been publishing retrospectives of notable papers that have appeared there. One chosen for this treatment was the Coyne and Orr duo. The retrospective paper, by Daniel Matute (UNC Chapel Hill) and Brandon S. Cooper, now at the University of Montana, can be accessed by clicking on the screenshot below, or you can get the pdf here. The reference to the retrospective is at the bottom. It will probably be of interest only to evolutionary geneticists, but it’s here for the record.

I have to say that Daniel and Brandon did a terrific job. It’s far more than a “retrospective” of our papers, but a new meta-analysis of existing data on how reproductive barriers between incipient species grow with time. (That was the subject of our original papers, and you can read the summary at the link above.) The new paper highlights where we were right, where we were wrong, what gaps there are in our knowledge about reproductive isolation, and what directions future research on the time course of speciation should take. In other words, it’s a review paper on a growing area of research rather than a discussion of just two small papers.

I’ll end by giving their abstract, which shows what the paper is about. But if you work on speciation, you’ll want to read their whole paper:

Abstract

Understanding the processes of population divergence and speciation remains a core question in evolutionary biology. For nearly a hundred years evolutionary geneticists have characterized reproductive isolation (RI) mechanisms and specific barriers to gene flow required for species formation. The seminal work of Coyne and Orr provided the first comprehensive comparative analysis of speciation. By combining phylogenetic hypotheses and species range data with estimates of genetic divergence and multiple mechanisms of RI across Drosophila, Coyne and Orr’s influential meta‐analyses answered fundamental questions and motivated new analyses that continue to push the field forward today. Now 30 years later, we revisit the five questions addressed by Coyne and Orr, identifying results that remain well supported and others that seem less robust with new data. We then consider the future of speciation research, with emphasis on areas where novel methods and data motivate potential progress. While the literature remains biased towards Drosophila and other model systems, we are enthusiastic about the future of the field.

____________________

Matute, D.R. and Cooper, B.S. (2021), Comparative studies on speciation: 30 years since Coyne and Orr. Evolution. https://doi.org/10.1111/evo.14181

Evolution society renames Fisher Prize; some of us wrote a letter in response

April 2, 2021 • 12:00 pm

I’m putting this up for the record, for it’s likely that not many outside of evolutionary biology will be interested in this kerfuffle, though the wokeness of the Society for the Study of Evolution (SSE) may be a harbinger of a general wokeness in science as a whole.

Not long ago the Society for the Study of Evolution, the premier society promoting the study of evolutionary biology, put up the following statement announcing a renaming of the Fisher Prize given for an outstanding Ph.D. dissertation paper published in Evolution, the Society’s Journal. Ronald Fisher (1890-1962) was one of the founders of evolutionary genetics as well as the modern science of statistics. We still use many of the tests and methods he devised.

But he also promoted eugenics, though not of the racist variety but the “classist” variety, urging the “lower classes” to have fewer children and the “upper classes” to have more. As far as we know, none of his recommendations was ever made into policy. Nevertheless, his views on eugenics were sufficient for the SSE to erase his name from the prize.

Here’s the SSE’s statement.

SSE statement on the Fisher Prize

SSE statement on the Fisher Prize This award, formerly called the R. A. Fisher Prize, was renamed the SSE Presidents’ Award for Outstanding Dissertation Paper in Evolution in June 2020. This prize, first established in 2006, is awarded annually for an exceptional PhD dissertation paper published in the journal Evolution. The award comes with a $1000 honorarium. Nominations are due in January of each year. Learn more about the award here.

The original name of the prize was chosen to acknowledge Fisher’s extensive, foundational contributions to the study of evolution, particularly through his development of population genetic and quantitative genetic theory. Alongside his work integrating principles of Mendelian inheritance with processes of evolutionary change in populations and applying these advances in agriculture, Fisher established key aspects of theory and practice of statistics.

Fisher, along with other geneticists of the time, extended these ideas to human populations and strongly promoted eugenic policies—selectively favoring reproduction of people of accomplishment and societal stature, with the objective of genetically “improving” human societies. Fisher and other geneticists, ignoring logical flaws certain to undermine the efficacy of this program, were highly influential in promoting eugenic policies. Fisher in particular maintained his support for these ideas even after others had abandoned them. The eugenics movement was founded in racist ideologies, and although eugenics has been repudiated by the evolution community, the field of population genetics continues to carry the mark of its historical connections to eugenics (read more here), causing harm to Black, Indigenous, Latinx and other communities of color. We sincerely regret that authors of color may have chosen not to submit their work for consideration for this award because of its name.

For these reasons, the SSE Council voted in 2020 to change the name of the award, shifting its focus to the scholarly achievements of the awardee. The name also acknowledges that the winning paper is chosen by the three current society presidents. Going forward, SSE recognizes the need to continue to invest significant effort toward making our Society and our field more inclusive and more equitable. The Diversity Committee, established in 2017, has galvanized SSE’s major strides towards this goal, and welcomes input and involvement from the membership in prioritizing and carrying out its initiatives (read more here).

In September 2020, SSE Council approved a suite of actions proposed by the Diversity Committee to increase inclusion of and support for members of historically excluded groups in the field of evolutionary biology and through all of the activities of SSE. Updates on the progress of these actions can be found on the SSE website.

Ten past Presidents and Vice Presidents of the SSE, including me, objected to this renaming on several grounds (we do not favor renaming existing prizes), and sent the following letter to the officers of the SSE (I’ve omitted the names of the signers, though one was clearly me).

March 23, 2021

To the SSE Council:

While we applaud the efforts of the Society to enhance diversity in science, and to oppose racism and other forms of prejudice, we wish to express our concerns about the statement on the SSE website concerning the reasons for renaming the R.A. Fisher Prize (https://evolutionsociety.org/societyawards-and-prizes/sse-presidents-award-for-outstanding-dissertation-paper-in-evolution/ssepresidents-award-for-outstanding-dissertation-paper-in-evolution-context-statement.html). There are two issues that we feel should be considered.

First, the statement contains significant inaccuracies, which are injurious to the reputation of one of the greatest of all evolutionary biologists. These inaccuracies are listed below; for further details, see Bodmer et al. 2021 Heredity (https://doi.org/10.1038/s41437-020-00394-6). A scientific society surely has the duty to avoid factually incorrect statements.

Second, it is unclear why the Council and Diversity Committee considered only the renaming of the Fisher Prize. The awards named after the following three people should also have been examined in this context. Theodosius Dobzhansky signed the Geneticists’ Manifesto of 1939, which expressed support for eugenic measures (Crew et al. 1939 Nature 144: 521-22). In his book Mankind Evolving, he remarked that “Equality means that all humans are entitled to equal opportunity to develop their capacities to the fullest, not that these capacities are identical” . In his Narrow Roads of Gene Land. Vol. 2. The Evolution of Sex, William Hamilton expressed support for infanticide as a solution to the problem of the accumulation of deleterious mutations in human populations, and a belief that Jews have innately higher mathematical abilities than the English. T.H. Huxley, while opposing slavery, believed that black people were inferior to white people (https://mathcs.clarku.edu/huxley/CE3/B&W.html).

There is a general issue that the Society needs to consider carefully: to what extent do views that were held by eminent people in our field, and are today repugnant to most or all of its members, negate their scientific contributions? To focus attention on just one individual is to fail in this task.

Inaccuracies in the SSE statement about the Fisher Prize

First, it contains the misleading statement that “the field of population genetics continues to carry the mark of its historical connections to eugenics (read more here), causing harm to Black, Indigenous, Latinx and other communities of color”. The founder of eugenics, Francis Galton, never accepted Mendelian genetics, and the mis-applications of genetics by white supremacists and the Nazis had nothing to do with population genetics as developed by Fisher, Haldane, Weinberg, Wright and their contemporaries; indeed, population genetics completely undermines the concepts of racial groups as homogeneous entities. This is the opposite of “causing harm” to ethnic groups who have suffered discrimination or persecution.

Second, Fisher was not “highly influential in promoting eugenic policies”. None of his proposed measures (family allowances for the supposedly better endowed intellectually, and voluntary sterilisation of people with learning disabilities) were implemented in the UK, and he never advocated the type of compulsory sterilisations carried out in the USA, Sweden and Germany.

Third, the policies promoted by the Eugenics Society in the UK, with which Fisher was associated until 1941, were not “founded in racist ideologies”. The Society was concerned solely with improving the genetic quality of the UK population, although individual members may have held racist views, as was common at the time. Many people of liberal and left-wing political views were members of the Society. Indeed the “The Geneticists’ Manifesto” of 1939 (Nature 144:521-22) contained statements about improving the human population that went substantially further than Fisher’s proposals. It was signed by Dobzhansky, Haldane, Huxley and Muller, among others. According to the introduction to the Wellcome Trust Archive of documents concerning the Eugenics Society (https://wellcomelibrary.org/collections/digital-collections/makers-of-modern-genetics/digitisedarchives/eugenics-society/), the society publicly dissociated itself from Nazi ‘race hygiene’ in 1933.

Fourth, the claim that Fisher “maintained his support for these ideas even after other abandoned them” is not accurate; H.J. Muller continued to advocate eugenic improvement as late as 1959 (Perspectives in Biology and Medicine 3:1-43). Fisher in fact withdrew completely from the Eugenics Society in 1941, and his only later publication mentioning eugenics was in the 1958 Dover edition of The Genetical Theory of Natural Selection; the relevant section was virtually unchanged from the 1930 edition.

Fifth, the statement overlooks the work that Fisher did to encourage the development of statistics in India (see his obituary in Sankhya 24: 207- 208). This work probably achieved more to encourage scientific endeavour by people of color than most scientific societies have done in their entire history. Fisher had relatively few PhD students by modern standards; one was C.R. Rao, the noted Indian statistician, and another was Ebenezer Laing, the Ghanaian geneticist. This was very unusual for academics in the UK at the time. Fisher’s last known letter was a very friendly letter to Laing.

Sixth, the statement claims that there were “logical flaws” in his ideas about improving society; there are no logical flaws in these ideas, but they can of course be questioned on both empirical and ethical grounds.

That’s the letter. The response we got from an official of the SSE, though thoughtful, was basically to reject our objections. I am not at liberty to reproduce the letter, as it was a private response to the ten signers, but I will quote one of its statements:

There emerged a consensus, however, that naming of an award after an individual honors all that person’s dimensions.

This “consensus” is completely misguided, both for the SSE and in general. Who among any famous scientists, particularly before 1940 or so, did not have some views that should not be honored? Most scientists before that time expressed some racist, sexist, or politically “offensive” opinions, and that includes four of the greats, Charles Darwin, Thomas Henry Huxley, Theodosius Dobzhansky, and W. D. Hamilton. The latter three already have SSE Awards named after them. Why shouldn’t the SSE ditch those, too? (Note: as I said, we don’t favor that.)

And if you applied this standard to American history as a whole, virtually all of honored politicians and notables, including Washington, Jefferson, Madison, Lincoln, and so on, have dimensions of their actions or beliefs that aren’t worthy of being honored. My own view is that when we honor someone, we honor them for the good things they did, and I’ll add that such honors should be given when the good they did outweighs the bad. Based on these criteria, Fisher clearly deserves an honorific.

Nobody is perfect, for crying out loud. Who could afford to have all their beliefs and statements put before the public eye?

I still maintain that the purpose of the SSE originally was and should still be to promote the study of evolution, not to promote particular ideological, political, or moral statements. That can be left to the individual members speaking for themselves.

Further thoughts, by Greg Mayer. Putting aside the factual errors noted in the letter from the past presidents and vice presidents, the statement about the Fisher Prize from the SSE seems so suffused with cognitive dissonance as to be redolent of doublethink: Fisher is awful and must be degraded; but Fisher is responsible for extensive and foundational contributions that we use to this day– which is it?

It’s the inability to hold two thoughts at once– epitomized by the claim that an award “honors all that person’s dimensions”– that leads to this muddled thinking. Fisher can be a great scientist worthy of honoring and emulating in his science, without endorsing every part of his life. He had a lousy marriage, eight children, overcame really bad eyesight, held grudges, deeply mourned the death of his eldest son (an RAF pilot in WW II), supported the tobacco industry, was a British patriot, and an anti-totalitarian– some people will want to denigrate him for each of these things. But why would we think  anyone today has an exclusive insight into a final revelation of value? We can only imagine what we will be condemned for in the future; John McWhorter has contemplated a future in which those who have not opposed abortion will be retrospectively condemned.

Assessing Ronald Fisher: should we take his name off everything because he espoused eugenics?

January 18, 2021 • 11:00 am

Many consider Ronald Fisher (1890-1962) one of the greatest biologists—and probably the greatest geneticist—of the 20th century, for he was a polymath who made hugely important contributions in many areas. He’s considered the father of modern statistics, developing methods like analysis of variance and chi-square tests still used widely in science and social science. His pathbreaking work on theoretical population genetics, embodied in the influential book The Genetical Theory of Natural Selection, included establishing that Mendelian genetics could explain the patterns of correlation among relatives for various traits, and helped bring about the reconciliation of genetics and natural history that constituted the “modern synthesis” of evolution. His theoretical work presaged the famous “neutral theory” of molecular evolution and established the efficacy of natural selection—the one part of Darwin’s theory that wasn’t widely accepted in the early 20th century.

Fisher also made advances important to medicine, like working out the genetics of Rh incompatibility, once an important cause of infant death. His statistical analyses are regularly used in modern medical studies, especially partitioning out the contributors to maladies and in analyzing control versus experimental groups (they were surely used in testing the efficacy of Covid vaccines).  As the authors of a new paper on Fisher say, “The widespread applications of Fisher’s statistical developments have undoubtedly contributed to the saving of many millions of lives and to improvements in the quality of life. Anyone who has done even a most elementary course in statistics will have come across many of the concepts and tests that Fisher pioneered.”

That is indeed the case, for statistical methods don’t go out of fashion very easily, especially when they’re correct!

Unfortunately, Fisher was also an exponent of eugenics, and for this he’s recently starting to get canceled. Various organizations, like the Society for the Study of Evolution and the American Statistical Association, have taken his name off awards, and Fisher’s old University of Cambridge college, Gonville and  Caius, removed their “Fisher window” (a stained glass window honoring Fisher’s statistical achievements) from their Hall last year.  Further disapprobation is in store as well.

This article in Heredity by a panoply of accomplished British statisticians and geneticists (Bodmer was one of Fisher’s last Ph.D. students) attempts an overall evaluation of Fisher’s work, balancing the positive benefits against his work and views on eugenics. If you are a biologist, or know something about Fisher, you’ll want to read it (click on the screenshot below, get the pdf here, and see the reference at the bottom.)

The authors make no attempt to gloss over Fisher’s distasteful and odious eugenics views, but do clarify what he favored. These included a form of positive eugenics, promoting the intermarriage of accomplished (high IQ) people, as well as negative eugenics: sterilization of the “feeble minded.” The latter was, however, always seen by Fisher as a voluntary measure, never forced. While one may ask how someone who is mentally deficient can give informed consent, Fisher favored “consent” of a parent or guardian (and concurrence of two physicians) before sterilization—if the patients themselves weren’t competent. But is that really “consent”? Negative eugenics on the population kind (not the selective abortion of fetuses carrying fatal disease, which people do every day) is something that’s seen today as immoral.

Further, Fisher’s views were based on his calculations that the lower classes outbred the higher ones, which, he thought, would lead to an inevitable evolutionary degeneration of society. But he was wrong: oddly, he didn’t do his sums right, as was pointed out much later by Carl Bajema. When you do them right, there’s no difference between the reproductive output of “higher” and “lower” classes.

Contrary to the statements of those who have canceled Fisher, though, he wasn’t a racist eugenist, although he did think that there were behavioral and intelligence differences between human groups, which is likely to be true on average but is a taboo topic—and irrelevant for reforming society. Fisher’s eugenics was largely based on intelligence and class, not race. Fisher was also clueless about the Nazis, though there is no evidence that he or his work contributed to the Nazi eugenics program.

In fact, none of Fisher’s recommendations or views were ever adopted by his own government, which repeatedly rejected his recommendations for positive and negative eugenics. Nor were they taken up in America, where they did practice negative eugenics, sterilizing people without their consent. But American eugenics was largely promoted by American scientists.

My go-to procedure for assessing whether someone should be “canceled”—having their statues removed or buildings renamed and so on—involves two criteria. First, was the honorific meant to honor admirable aspects of the person—the good he or she did? Statues of Confederate soldiers don’t pass even this first test. Second, did the good that a person accomplish outweigh the bad? If the answer to both questions is “yes”, then I don’t see the usefulness of trying to erase someone’s contributions.

On both counts, then, I don’t think it’s fair for scientific societies or Cambridge University to demote Fisher, cancel prizes named after him, and so on. He held views that were common in his time (and were adhered to by liberal geneticists like A. H. Sturtevant and H. J. Muller), and his views, now seen properly as bigoted and odious, were never translated into action.

Of course the spread of wokeness means that balanced assessments like this one are rare; usually just the idea that someone espoused eugenics is enough to get them canceled and their honors removed.  It saddens me, having already known about Fisher and his views, that what I considered my “own” professional society—the Society for the Study of Evolution—and a society of which I was President, is now marinated in wokeness, cancelling Fisher, hiring “diversity” experts to police the annual meeting at great cost, and making the ludicrous assertion—especially ludicrous for an evolution society—that sex in humans is not binary (read my post on this at the link). The SSE’s motivations are good; their execution is embarrassing. I am ashamed of my own intellectual home, and of the imminent name change for the Fisher Prize, for which the Society even apologized. Much of the following “explanation” is cant, especially the part about students being put off applying for the prize:

This award was originally named to highlight Fisher’s foundational contributions to evolutionary biology. However, we realize that we cannot, in recognizing and honoring these contributions, isolate them from his racist views and promotion of eugenics–which were relentless, harmful, and unsupported by scientific evidence. We further recognize and deeply regret that graduate students, who could have been recipients of this award, may have hesitated to apply given the connotations. For this, we are truly sorry.

His promotion of genetics was not relentless, wasn’t harmful (at least in being translated into eugenics, as opposed to being simply “offensive”), and of course scientific evidence shows that you could change almost every characteristic of humans by selective breeding (eugenics). But we don’t think that’s a moral thing to do. And yes, you can separate the good someone does from their reprehensible ideas. Martin Luther King was a serial adulterer and philanderer. Yet today we are celebrating his good legacy, which far outweighs his missteps.

But I digress. I’ll leave you with the assessment of a bunch of liberals who nevertheless use Fisher’s work every day: the authors of the new paper.

The Fisher Memorial Trust, of which the authors are trustees, exists because of Fisher’s foundational contributions to genetical and statistical research. It honours these and the man who made them. Recent criticism of R. A. Fisher concentrates, as we have extensively discussed, on very limited aspects of his work and focusses attention on some of his views, both in terms of science and advocacy. This is entirely appropriate, but in re-assessing his many contributions to society, it is important to consider all aspects, and to respond in a responsible way—we should not forget any negative aspects, but equally not allow the negatives to completely overshadow the substantial benefits to modern scientific research. To deny honour to an individual because they were not perfect, and more importantly were not perfect as assessed from the perspective of hindsight, must be problematic. As Bryan Stevenson (Stevenson 2014) said “Each of us is more than the worst thing we’ve ever done.”

In one of Fisher’s last papers celebrating the centenary of Darwin’s “The Origin of Species” and commenting on the early Mendelian geneticists’ refusal to accept the evidence for evolution by natural selection he said, “More attention to the History of Science is needed, as much by scientists as by historians, and especially by biologists, and this should mean a deliberate attempt to understand the thoughts of the great masters of the past, to see in what circumstances or intellectual milieu their ideas were formed, where they took the wrong turning track or stopped short of the right” (Fisher 1959). Here, then, there is a lesson for us. Rather than dishonouring Fisher for his eugenic ideas, which we believe do not outweigh his enormous contributions to science and through that to humanity, however much we might not now agree with them, it is surely more important to learn from the history of the development of ideas on race and eugenics, including Fisher’s own scientific work in this area, how we might be more effective in attacking the still widely prevalent racial biases in our society.

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Below: Ronald Alymer Fisher, in India in 1937 (as the authors note, Fisher was feted by a colleague for his “incalculable contribution to the research of literally hundreds of individuals, in the ideas, guidance, ans assistance he so generously gave, irrespective of nationality, colour, class, or creed.” Unless that’s an arrant lie, that should also go toward assessing what the man actually did rather than what he thought.

Fisher in the company of Professor Prasanta Chandra Mahalanobis and Mrs. Nirmalkumari Mahalanobis in India in 1940. Courtesy of the P.C. Mahalanobis Memorial Museum and Archives, Indian Statistical Institute, Kolkata, and Rare Books and Manuscripts, University of Adelaide Library.

h/t: Matthew Cobb for making me aware of the paper.

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Bodmer, W., R. A. Bailey, B. Charlesworth, A. Eyre-Walker, V. Farewell, A. Mead, and S. Senn. 2021. The outstanding scientist, R.A. Fisher: his views on eugenics and race. Heredity. https://doi.org/10.1038/s41437-020-00394-6